Diseases of Central Nervous System
INTRODUCTION: Treatment of diseases of central nervous system by fetal brain cell transplantation was developed under the leadership of author of https://bio-cellular-research.com in different countries, from 1991 to this date, under the label of different companies: first by International Institute of Biological Medicine, USSR, joint venture of Bio-Cellular Research Organization(UK) 51%, and USSR Ministry of Health 49% (after the breakdown of USSR on December 29, 1991, replaced by Ministry of Health of Russian Federation). Then after the departure of E.Michael Molnar, M.D. from Russian Federation, when that country became the colony of U.S.A., from the end of 1996 to 2016 by Bio-Cellular Research Organization (UK) alone, and from 2016 to this date by E. Michael Molnar, M.D. alone, in different counties of Europe, Asia, Africa, Australia and North and South America. E. Michael Molnar, M.D., with utmost gratitude and humbleness, acknowledges his close friend, without whom this discovery would not be possible, who was the driving force, with his colleagues from Russian Academy of Sciences, of this heroic task: Prof.Dr. Sergei Saveliev, Doctor of Sciences. He is the son of famous Soviet sculptor, who was declared a "dissident" in USSR and as a result of this his genius son was not allowed to study at any Soviet university, instead he was drafted into Soviet army, and placed in the "specnaz" unit, where only similar "politically unreliable" geniuses, because of their genetics like Sergey, served. His unit was sent to Angola. There he suffered gunshot wound of his spinal cord and became quadruplegic. While he was in a hospital, knowing that his condition was a hopeless paralysis below the neck for life, he made a pledge, that if he ever would get well, he would devote his entire life to do everything possible to discover the treatment for his condition. Eleven months after his injury he noticed an improvement, which progressed until he reached a point to become almost well. He kept his promise to mankind: he gave his entire life, his entire genius, to the research of central nervous system, specifically of everything that improved the fate of patients with his un-treatable condition. When he learned about our IIBM, and opening our office in Moscow, he called in, made an appointment and two of us met alone, for a long time. My Russian was not too good yet, his English was about the same, but we found the way to communicate. No one in IIBM knew about my relationship with Sergey and about his group of friends-scientists from the Russian Academy of Sciences, all Sergey's buddies.
On August 22, 2016, the author suffered a severe stroke, which he luckily survived. Since it happened in the country where there were only three patients that had fetal brain cell transplantation done by the author, and his colleague/close friend is a hand surgeon, and as such not familiar with fetal brain cell transplantation at all, and thus not comfortable to do a lumbar puncture, there was no one to help the author-patient. Luckily I was able to pull remnants of my severely failed brain functions together and remembered all that I luckily never forgot: fetal brain cell transplantation. I wrote my own prescription for fetal cell transplantation, which consisted of 4 fetal brain cells and 5 other cells of different organs, my two close friends-veterinary doctors, that worked with me for 19 years, prepared the appropriate fetal brain and other cells for my treatment, the retired anesthesiologist carried out a lumbar puncture and introduced 4 kinds of fetal brain cells into my cerebro-spinal fluid and 5 kinds of fetal cells from appropriate organs sub-cutaneosly into my body. Today my intelect is in order, the only difficulty that I have is the right hemiparesis that requires a continuous physiotherapy/rehabilitation.
Treatment of advanced Parkinson's disease, no longer responsive to L-dopa therapy, by implantation of human fetal adrenal cells into the patient’s brain became a landmark in history of cell transplantation, when a series of such surgical procedures was carried out in Mexico City in 1980's. A term neurotransplantation was coined for such treatment.
Treatment of neurological diseases has always been a sad chapter of medicine due to a lack of effective therapy for a great majority of illnesses. All diseases of central nervous system diseases continue to be incurable, i.e. each such disease means a guaranteed death.
Here Parkinson's disease has been temporarily an exception, because of availability of L-dopa therapy, which controls symptoms of disease quite well for a few years. Ultimately every patient with Parkinson's disease will reach a stage when medications that stimulate production of dopamine by neurons of the basal ganglia of the brain lose effectiveness, whereupon disability becomes severe, progressive, and lethal within a few years. Ideally, already before that happens, each patient should receive fetal brain cell transplantation.
But neurotransplantation treatment of Parkinson's disease was not usable in clinical practice, with a rate of success of only 2 - 3 %, as under experimental conditions, where a success rate better than 95%. Such enormous discrepancy between the high success of neurotransplantation in animal experiment and minimal success in clinical practice of human medicine was unusual. Very same bad results were obtained in Sweden and West Germany with their method of transplantation of human brain tissues.
The completed U.S. National Institute of Health clinical trial of transplantation of human brain tissue ended in a failure. Scientists believed that the reason was that the neurons in adult human brain and spinal cord could not recover from serious damage, and once dead, could not be replaced. Part of the problem was that researchers were more concerned about fulfilling requirements of double-blind study, including unethical and immoral 'sham surgery', than to help severely disabled patients. Fetal cell transplantation, used by BCRO for the treatment of untreatable or incurable diseases, is hardly suitable for 'double-blind' clinical studies. (Read an article by G. Kolata in ‘Science’ magazine of February 8, 1994.)
Our International Institute of Biological Medicine (IIBM) team in Moscow – 51% BCRO and 49% USSR Ministry of Health - along with the team of Russian Academy of Prof.Dr. Saveliev - devoted enormous amount of time and energy to finding the reasons for the reported failures of neurotransplantation in clinical practice worldwide. An extensive experimental research was carried out, and based on that, eventually several patients with advanced Parkinson’s disease were treated by our early IIBM method of fetal brain cell transplantation.
Based on our analysis we set up the following rules:
1/ in order to establish synaptic connections with neurons of the host, it is mandatory to transplant cells with known and firmly pre-determined properties - we learned that not only human fetal brain cells have desired properties, animal fetal cells do as well and their use was giving substantially better(!) results in clinical practice;
2/ transplanted cells must be highly metabolically active, (and here we learned that not only human fetal brain cells can fulfill such requirement, animal do as well and their metabolic activity was greater beyond any doubt);
3/ transplanted cells must be genetically strongly pre-set in the direction of their differentiation, and be independent of environmental influences, and here we learned that human embryonic/fetal cells from the anterior portion of mesencephalon used in Sweden and Germany do not work because they are undifferentiated/pluripotent.
Experiments with xeno-neurotransplantation between non-vertebrates and vertebrates, and with xeno- and allo-neurotransplantation between various species of mammals, showed, that xeno-transplants survived in the host brain three times longer than allo-transplant. Xeno-neurotransplantation between genetically discordant species was much more successful than between genetically concordant species.
Primordial brain cells of various genetic mutants of Drosophila melanogaster fulfilled the best the above three requirements, and their neurotransplantation into brain of various vertebrates, including mammals, was unusually successful. Genom of Drosophila had been known in detail for a number of years, so that it was not difficult to select the mutants with required properties of the primordial brain cells. The mutants selected survived in the mammalian brain a minimum of 2 – 3 months, and functioned as a stimulant of human brain cells, promoting their differentiation and vascularization, as well as the growth of the host‘s neuronal processes toward the donor transplant, and the stimulation of circulation of the adjacent host brain tissue.
The mixture of human fetal brain cells from ventral mesencephalon and basal ganglia and of primordial brain cells of the mutants of Drosophila melanogaster in the weight ratio of 50:1, or higher, was prepared in laboratory and then implanted under stereoscopic control into ventrolateral thalamic nuclei of patients with Parkinson's disease.
Three of the several operated on patients, two of which had had also previous cryodestructive stereotactic procedures to correct severe symptoms of stage 3 and 4 Parkinson’ disease, are described in the published paper. After 12 months’ follow-up there was no recurrence of parkinsonism and overall success was 95%. 
One of eight patient of this series died of unrelated myocardial infarction 8 months later, and a full autopsy of his brain was carried out, that showed the reasons for the complete success of described combined xeno-allo-fetal cell transplantation approach to the treatment of Parkinson’s disease. 
Treatment of diseases of central nervous system by fetal precursor cell transplantation past childhood (actually past 12 years of age when hematoencephalic barrier closes down) requires an implantation into the brain and spinal cord, even though not into the parenchyma of these organs. We advise strongly the 'intrathecal' implantation, i.e. into the cerebrospinal fluid, vitally important for the function of central nervous system, that vigorously circulates in the preformed spaces around and in the brain and spinal cord, and its volume of 750 ml is completely exchanged every 24 hours.
Our extensive experimental work on xeno-fetal brain cell transplantation in Moscow led to a discovery of clinical effectiveness of ‘intrathecal’ implantation. There are two approaches to intrathecal implantation of fetal brain cell transplants in human medicine: via a lumbar puncture, or via a ‘ventricular tap’. "Lumbar puncture" implantation is technically simple for any properly trained physician, while "ventricular tap" is easy for a neurosurgeon.
Lumbar puncture, or ‘spinal tap’, is non-traumatic method of neurotransplantation, while there is a minimal trauma to the brain tissues of the patient in the course of intra-ventricular implantation. There is no trauma whatsoever when fetal precursor brain cells are implanted via lumbar puncture.
Due to a very narrow connection between a system of four ventricles in the brain, brain parenchyma and a subarachnoid space around the brain and spinal cord, via foramina Magendie and Luschkae in the 4th ventricle, an opinionated discussion went on between two of our teams for some time: one group believed that intrathecal implantation via lumbar puncture is dangerous, because clusters of fetal brain cell transplants could obstruct foramina Magendie and Luschkae and cause obstructive hydrocephalus. The other group believed that it could not possibly happen. Eventually the matter was decided in favor of the 2nd group after 100 moribund patients due to gun shot wounds of the brain were treated with intrathecal implantation of fetal brain cell transplants prepared by our method, and subjected to a detailed autopsy of the brain after their death and nothing unusual was found, in particular there was no evidence of obstructive hydrocephalus, while there was a complete patency of foramina Magendie and Luschkae.
Subsequently an intrathecal implantation of fetal cell transplants was carried out on many patients with prolonged coma due to various causes, with remarkable success, i.e. patients were waking up from coma within 16 – 18 hours, until we began to treat patients suffering from a variety of incurable neurological diseases not in coma(!), such as amyotrophic lateral sclerosis, Friedreich's ataxia, other spino-cerebellar degenerations, Parkinson's disease, etc. At our First International symposium in December 4-7, 1995 in Moscow, several presentations were made about the clinical results, and the total number of patients included in six different reports exceeded 500+ patients, including those 100 moribund, 8 already described, and countless not mentionad here. All those patients were treated by intrathecal implantation (’spinal tap’) of fetal brain cell tissues.
The initial published study of 14 patients, from 29 to 82 years of age, 7 females and 7 males, 4 with cerebrovascular accident, 4 with Parkinson’s disease, 2 in coma after clinical death for 18 days or more, 1 with toxic encephalopathy, 1 with vascular collapse, 1 with post-traumatic encephalopathy, 1 with Alzheimer’s disease, treated by intrathecal implantation of fetal brain cells via lumbar puncture, gives detailed case histories of 6 patients, and overall results. Only one patient had no response: a 52 years old female with Alzheimer’s disease. All other patients were improved, some spectacularly.
The first patient was a 29 years old female developed anaphylactic shock 30 seconds after I.M. Ampicillin. A resuscitation and intensive care restored spontaneous breathing and improved cardiac function, but deep coma persisted. On 18th day an intrathecal implantation via lumbar puncture of 5 – 6 million of fetal brain cortex cells was carried out. Around 18 hours later the patient opened eyes, recognized her mother, and began to answer questions in simple words. Left-sided hemiparesis, urinary and fecal incontinence, and dementia persisted. Gradual improvement was observed, and 10 weeks later a 2nd intrathecal implantation of fetal brain cortex cells was done. Two days later a dramatic improvement was observed. Athetoid movements of left hand and arm disappeared, spasticity on the left side substantially diminished, improvement of speech, reading, writing, comprehension, gait, EEG, was noted.
The second patient was a 45 years old male was undergoing an uneventful surgery for retinal detachment of the left eye, when a few minutes before the end of the operation a sudden bradycardia and blood pressure drop were observed. After the recovery from an operation the patient remained in stupor, and akinesia with rigidity quickly developed. On 22nd day the patient was transferred to a psychiatric ward for rehabilitation of psychic functions. On 25th day an intrathecal implantation of human fetal brain cells from cortex and peri-ventricular medulla alba of brain was carried out. Two days later a dramatic improvement took place: speech, writing, drawing, all. Then 4 months later a 2nd intrathecal implantation was carried out followed by a continuous improvement.
Then others followed: a 36 years old male suffered a massive head injury in a car accident. There was a huge intracranial hematoma and AV malformation. Patient was left with left hemiplegia. Around 6 weeks later an epilepsy developed. A diagnosis of subdural hematoma was made. While patient was under aggressive medical therapy, 16 months after an accident an intrathecal implantation of ~ 12 millions of fetal brain cortex and peri-ventricular medulla alba of brain fetal cells was carried out. Epilepsy disappeared, EEG slowly returned back to a rhythm, and there was a gradual improvement of neurologic findings.
A 39 years old female was treated for right hemiparkinsonism by L-dopa, without any effect, and so intrathecal implantation of fetal brain cells of basal ganglia was carried out. At 3-month’ follow-up a dramatic improvement was noted. There was no tremor in the extremities, the function of right hand was normal, gait improved. The effect has somewhat diminished subsequently, and 5 months after the first the 2nd intrathecal implantation was done. One month later again improvement was noted, tremor disappeared, gait and writing improved.
A 65 years old female suffered a cerebrovascular accident. Intrathecal implantation of fetal brain cortex cells was carried out immediately. There was a dramatic improvement, so that rehabilitation could begin already 18 hours after intrathecal implantation of fetal brain cells, i.e. the next day after the stroke. Two days later hemiplegia improved to the level of minor hemiparesis. On the 8th day the patient began to walk with a walker.
A 50 years old male survived an extensive cerebrovascular accident 2.5 years ago and was left with hemiparesis, aphasia, and Jacksonian epilepsy. Patient received intrathecal implantation of 12 million of fetal brain cortex cells. Three weeks later he observed an improvement of speech, writing, began to read, and count. Movements of right hand improved noticeably. EEG showed less epileptogenic activity.
Apallic syndrome is a persistent vegetative state after the loss of pallium function due to injury, poisoning or anoxia. There was a complete aphasia, apraxia and agnosia, decerebration rigidity, absent corneal reflex, absent
papillary reflex, absent deglutition reflex, seizures, trophic disturbances, marasmus, immune deficiency. CNS functions were reduced below those present at birth. Eyes were open, starring upward and sideways, or vaccilating.
Optical and acustic stimuli were not registered. In all 33 patients between 1 and 12 years of age, with coma of less than 12 months’ duration, cell transplantation terminated coma, and the conscious patients recovered with a
residual neurological damage. The first step was the removal of all life supports, then implantation of fetal precursor cell transplants of various parts of the brain, and placenta, and specific metabolic stimulation,
followed by peripheral training to substantially recover speech and gross motor functions. None of these patients was treated by intrathecal implantation, which is not mandatory during the first 12 years of life(!), since
hemato-encephalic barrier is not completed yet.
The existing treatments of all degenerative diseases in contemporary medicine suffer from one common problem: no attempt at regeneration of degenerating cells of diseased organs and tissues is ever made. The sole treatment
capable of direct stimulation of regeneration is fetal precursor cell transplantation. and that applies primarily to degenerative diseases of central nervous system.
In 1996 Diacrin Inc. carried out in U.S. a clinical trial in which 12 patients with Parkinson’s disease and subsequently 12 patients with Huntington’s chorea underwent unilateral xeno-neurotransplantation of porcine fetal brain cells. Patients with Parkinon’s diseases received 12 million of ventral mesencephalic cells, while those with Huntington’s chorea 24 million of cells from striatum.
At one year’s follow-up the Parkinson’s disease patients had an average of 19% improvement in the Unified Parkinson’s Disease Rating Scale ‘off” state scores. Some patients had an improvement of as much as 30%. At one year’s follow-up of Huntington’s chorea patients there was no change in the functional capacity.
In the above study of Parkinson’s disease six patients received an immunosuppression by cyclosporine, and six patients by a monoclonal antibody directed against MHC class I. There were no adverse effects. No transfer of endogenous viruses was detected.
One of the patients from the above Parkinson’s disease study died of unrelated causes 7 months after the neurotransplantation. Histological analysis of the putamen-caudate nucleus area proved a graft survival: pig dopaminergic neurons, and other pig neurons and glial cells were present and pig axons extended from the graft site into the host brain.
We have never used any immunosuppressants, steroids, even antihistamins.
Our advice at that time was that Parkinson’s disease patients receive intrathecally fetal precursor cell transplants of basal ganglia and mesencephalon, and sub-aponerotically hypothalamus, liver, placenta, adrenal cortex.
Huntington’s chorea patients should receive intrathecally fetal cell transplants of basal ganglia, diencephalon, and subaponeurotically hypothalamus, liver, placenta, adrenal cortex, intestine, exocrine pancreas. The success rate was zero.
Next to Alzheimer’s diseases, the most common disease of central nervous system in the western countries is a cerebrovascular accident., which in 85% of such patients is due to blood clot in the branch of intracerebral
artery and in 15% due to hemorrhage from intracerebral artery. In those 85% of patients when cause of brain damage is obstruction of a branch of intracerebral artery the fetal brain cell transplantation ought to be carried out
as soon possible. In the remaining 15% of patients with intracerabral hemorrhage fetal brain cell transplantation should be done as soon as the hemmorhage stopped.
In the chronic stage, 3 months after the stroke, an intrathecal BCRO fetal cell transplantation must be carried out.
In January 2004 we received a SOS E-mail from South Africa by a desperate parents of a 19 years’ old man that following a pool diving accident damaged his spinal cord and became quadriplegic. We offered help but the President
and Minister of Health of that country did not give us a permit to treat the patient by fetal precursor cell transplantation there. Eventually he was treated by BCRO in Germany 8 months later. The pleas by his parents aroused
the consciousness of the South African white population and the patients with old spinal cord injuries flooded our communications lines and eventually 55 such patients, including those with untreatable neurodegenerative
diseases, came to Germany for BCRO fetal cell transplantation.
Subsequently, we began to treat patients with old spinal cord injuries by BCRO fetal cell transplants implanted intrathecally, usually of spinal cord and brain stem, or of cauda equina in case of lack of urinary
bladder or anal sphincter controls, and subaponeurotically cell transplants of all other of the cell types known to us as necessary for each individual case.
All 55 patients have had no bladder and anal sphincter control before BCRO fetal cell transplantation and there was no improvement after the treatment. But one, a motocycle racer, re-gained an erection.
In all but two patients there was a significant improvement, against our expectations(!) since the CT scan of all patients (but the first two where CT scan was not done) showed a complete transssection of spinal cord.
In recent spinal cord injury patient treated in South Africa after the emergency surgical repair and debridement, plastic catheters must be left in the area of injury for gentle irrigation of area of fractured vertebrae by BCRO
type of fetal cell transplants every 6 – 12 hours.
After an old injury of spinal cord an intrathecal implantation of BCRO fetal cell transplantation (via lumbar puncture) should be carried out every 6 months with vigorous specialized rehabilitation.
Let’s present case histories of some other neurological patients treated by our BCRO method of fetal precursor cell transplantation.
C.H., 46 years’ old male, from London, U.K., a sportsman, developed 9 years ago encephalitis, following which he lied in bed motionless, no diagnosis was made and no treatment offered, eventually was placed in a
psychiatric hospital when his wife took him home against medical advice. After 6 weeks long metabolic preparation to build up his physical stamina on July 25, 2002, BCRO intrathecal fetal precursor cell transplantation of
brain stem, hypothalamus, thymus, lymphnodes, spleen, mesenchyme, adrenal cortex, liver, testis, stomach/intestine, was carried out. Within 3 months the patient was able to move with assistance, and attend an intensive
physiotherapy program. During a follow-up examination in October 2003 he was able to walk short distance without assistance, and capable of self-care in wheel chair. In June 2004 the patients was walking without any assistance,
gained weight, and in October 2004 became a father of a healthy boy.
A 31 years old male physician from South Africa, nationally known rugby star, suffered a fracture of cervical spine. After his surgery in the recovery room a massive embolization of his carotid arteries took place, first one,
and following the removal of the embolus, also the other carotid, following which such tragic mishap he developed a ‘locked-in-syndrome’, i.e. a total paralysis of all muscles in his body with the exception of extra-ocular
ones. His attending physician, a professor of neurosurgery in Pretoria, told the patient’s parents (father is a physician) that their son will never swallow, breathe or speak on his own. A very intensive rehabilitation was
carried out for 12 months in South Africa. When he arrived at the clinic in Germany, his breathing was very shallow, and he could not clear any bronchial secretions. His deglutition reflex was absent. He could say a word only
when someone squeezed the air out of his lungs. All muscles of his body were paralyzed. On November 18, 2004, he received intrathecally via lumbar puncture BCRO fetal precursor cell transplantation of brain cortex, medulla
alba of brain, subaponeurotically: liver, peripheral myoblasts, brain stem, placenta, and deeply subcutaneously mesencephalon, frontal lobe of brain, occipital lobe of brain. Five days after the BCRO fetal precursor
cell transplantation he was able to stand up with assistance, cough up bronchial secretions, speak, swallow, move his hands. In January 2005 he began a horse riding training, and today he can maintain the balance in the saddle
on his own. His speech dramatically improved as well as swallowing and breathing and the same applies to his eyesight in terms of extraocular muscle function, and accommodation. When the author lectured to the patient's Alma
mater in Pretoria, South Africa, the patients equipped like Prof. Stephen Hawking, was the master of ceremonies exceptionally well.
Let’s now focus on the diseases of ‘white matter’ of the brain.
Ability to accept information from one neuron, and pass it on to another one, requires a participation of membrane receptors activated by neurotransmitters. Activity of ion channels is controlled directly or via
intracellular transport mechanisms. Acetylcholine opens in respective target cells the non-specific cation channels first, that enable passage of Na+ and K+. This leads to depolarization of cell membrane
and thereby opening of voltage controlled Na+- and Ca2+-channels. Ca2+ mediates release of neurotransmitters by the target cell. In the long term also cell metabolism and gene expression are
modulated in the target cells, and thereby production and storage of neurotransmitters.
When axon is interrupted, its distal part dies, i.e. Wallerian axonal degeneration. Axons of central neurons do not grow back but undergo apoptosis. One of causes is a lack of nerve growth factor released by innervated post-
synaptic cells, that normally keeps pre-synaptic cell alive via axonal transport. Interruption of retrograde axonal transport with intact axon leads to apoptosis as well.
As compared with central neurons, in peripheral axons the proximal stump can grow back: the necessary proteins are produced in the neuronal cell and transported to the location of injury by axonal transport.
Due to an interruption of axon not only primarily damaged neurons die, but the lack of innervation often leads to the apoptosis of target cell, i.e. ‘anterograde transneuronal degeneration’, and sometimes also to apoptosis
of cells innervating the damaged cell, i.e. ‘retrograde transneuronal degeneration’.
Due to demyelination of nerve fibers more electric energy is required for reversal of polarization of internodium, and losses of electric energy are increasing further by loosening of ion channels.
If the electric current produced at internodium 1 is not sufficient to depolarize the next internodium 2, then transmission of the stimulus is interrupted. Lighter lesions of internodia cause slowing down of transmission because
it takes more time to reach the threshold at internodium 2. The rate of slow-down can vary in different nerve fibers, and thereby time dispersal of signal ensues.
Eventually, the damaged locus along the demyelinated nerve fiber can spontaneously generate action potentials, with jumping onto the neighboring fibers, or with a retrograde transmission. Such ‘shorting’ causes symptoms of
Genetic defects of structural proteins of myelin sheath or gap junctions of Schwann cells cause Charcot-Marie-Tooth disease, Dejerin-Sottas syndrome, Pelizaeus-Merzbacher disease, for example.
In etiopathogenesis of neurodegenerative diseases the environmental factors are very important. It is not only the effect of measles, whooping cough, herpetic infections, enterocolitis, but also vaccinations, that
sometimes trigger neurodegenerative diseases, and it is often a result of faulty nutrition. It is recognized that due to a poor nutrition in the first 3 years of life, especially deficient in protein, the brain maturation and
intelligence development suffer enormously. But disturbances of the gastrointestinal tract are perhaps even more important. For a long time it was believed that constipation, flatulence, peptic ulcer, mucosal atrophy, and
dystrophy, in the face of adequate food intake, are the result of neurodegenerative diseases, but today there is a growing awareness that gastrointestinal disturbances cause neurodegenerative diseases.
When multiple sclerosis is 5 times more prevalent on Orkney Islands north of Scotland than in the Netherlands and 20 times more frequent than in south of France, or when the incidence of intestinal cancer in Iceland is extremely
high, or when the prevalence of neurodegenerative diseases in Quebec and Ontario provinces of Canada is the highest in the whole world, it is not due to a racial disposition, as the population in Ontario and Quebec is a mixture
of English, Irish, French, Italian, and German immigrants of the past 200 years, for example. The problem is a lack of fresh food, in particular of fresh fruit and vegetables, in Orkney Islands as compared with the south of
The reason for the short discourse on the malfunction of gastrointestinal system and on faulty nutrition is to explain that fetal precursor cell transplantation as treatment of neurodegenerative diseases has to focus on the
treatment of gastrointestinal system and metabolism as well besides central nervous system pathology. Such changed approach to therapy finally brought on a success in the treatment of some of untreatable illnesses.
Fetal precursor cell transplants of small intestine, stomach/duodenum, liver, exocrine pancreas, colon, adrenal cortex, placenta, peripheral myoblasts, are recommended, as well as cerebellum and mesencephalon, for
ataxias, frontal lobe and basal ganglia, for coordination abnormalities, cardiomyoblasts and peripheral myoblasts, for muscle dystrophies, cell transplants of various parts of CNS implanted intrathecally.
List of incurable/untreatable diseases of central nervous system that can be treated by BCRO fetal precursor cell transplantation:
- Metachromatic leukodystrophy,
- Globoid leukodystrophy, Krabbe disease,
- Cancellous marrow degeneration, Canavan disease, or van Bogaert and Bertrand disease,
- Sudanophilic leukodystrophies, Pelizeus-Merzbacher disease.
B. Demyelinization diseases:
- Diffuse sclerosis, Schilder encephalitis periaxialis,
- Multiple sclerosis,
- Neuromyelitis optica, Devic syndrome.
Myelin is the main component of the ‘white matter’ of the brain. It consists of lipoprotein layers which surround the axons to insulate the nerve fibers and thereby assure that the impulses are transmitted from the ‘grey matter’
of the brain to the effector organs, without any interference or ‘shorting’. This white matter is immature at birth. Even though all neurons are present already at birth, and no new ones are formed during the later stages of
development, the brain is the sole organ in the body that is not ready for an independent existence at that time. Only after the maturation of the secondary structures, i.e. dendrites, axons, synapses, glia, and insulation of
nerve fibers by myelin, is the full functioning of brain assured and that takes place in the 4th year of life.
Since the myelination takes place during the first four years of life, the first faults in medullary sheath maturation occur only after that time. When diagnosing myelination defects it is necessary to distinguish between the
more serious generalized demyelination diseases in early life as a result of inadequate myelination, and the more localized manifestation in later life as an expression of myelin degeneration. Inbetween, in the middle
decades of life, there are no generalized demyelinations, although demyelination may be extensive, such as in Friedreich’s ataxia, which occurs between 10 and 30 years of age, or multiple sclerosis, which is prevalent
between 20 and 40 years of age, that are the most common of all degenerative diseases of medulla alba of the brain.
Multiple sclerosis is an autoimmune disease with a typical onset of various neuronal deficits in different parts of CNS at different, variable, unpredictable, time intervals. After inflammation has subsided, a repair
of damage takes place and nerves are re-myelinated. It is often a familiar disorder, more common in HLA3 and HLA7 carriers.
In multiple sclerosis the main symptoms are disturbances of gait, speech and eyesight, along with manifold neurological symptoms. Periods of progression, of an arrest, and even an improvement of clinical course, make an early
diagnosis very difficult. Fetal precursor cell transplantation of liver, intestine, exocrine pancreas, adrenal cortex, mesenchyme, placenta, peripheral myoblasts, are recommended, but no fetal cell transplants from
central nervous system whatsoever'. Multiple sclerosis is primarily an enzymopathy of the intestinal mucosa, that leads to an abnormal breakdown of proteins and lipids from food in the intestinal wall into pathologic
nucleotides and mono- and di-glycerides, toxic to neurons, that are capable to pass through hemato-encephalic barrier to damage the nerve cells.
The most remarkable patient with MS treated by the author was his female classmate from medical school, who received fetal cell transplantation in 1998, already quite disabled. She got first attack of MS during her first
pregnancy at the age of 26 and had been disabled at the age of 33. She died recently in 2018, 50 years after the onset of her illness. The further progression of her disease was completely stopped after her fetal cell
My grandfather, a governor of Upper Hungary of the Austrian-Hungarian Monarchy from 1909 until the end in 1919, got MS at the age of 39, became completely bedridden 2 years later and died at the age of 51.
MS occurs in 85% of women, but in men it is a much more aggressive disease, they die much faster.
C. Cerebro-ocular degenerations:
- Amaurotic idiocy, infantile form, Tay-Sachs disease,
- late infantile form, Bielschowsky,
- juvenile form, Spielmeyer-Vogt disease,
- Tapeto-retinal degeneration.
D. Spino-cerebellar degenerations:
- Friedreich’s ataxia,
- Ataxia-telangiectasia, Louis-Bar syndrome,
- Abetalipoproteinemia, Acanthosis, Bassen-Kornzweig syndrome,
- Refsum syndrome,
- Myoclonus encephalopathy in children, Kinsbourne syndrome.
In Friedreich’s ataxia, AR disorder with a high penetration, clinical findings are the results of progressive degeneration of cerebellum and spinal cord, in particular of spinocerebellar and corticospinal tracts, and
dorsal funiculi of spinal cord, i.e. gait disturbances, coordination disturbances of arms, speech impairment, hammer fingers, flat feet, scoliosis, and also cardiomyopathy. Fetal precursor cell transplantation of cerebellum,
mesencephalon, liver, intestine,stomach/duodenum, placenta, exocrine pancreas, adrenal cortex, peripheral myoblasts, cardiomyoblasts, kidneys, colon, are recommended.
E. Cerebro-cutaneous degenerations:
- Tuberous sclerosis, Bourneville syndrome,
- Neurofibromatosis, v. Recklinghausen’s disease,
- Angiomatosis retinae et cerebelli, v. Hippel-Lindau disease.
F. Spino-neuro-muscular degenerations:
- Neural muscle atrophies: Wolfrath-Kugelberg-Welander,
- Progressive muscle dystrophies: Duchenne, Becker,
- Myatonia congenita,
- Thomsen myatonia,
- Carnithine myopathy,
- Myasthenia gravis,
- Amyotrophic lateral sclerosis, Motor neuron disease,
Disorders of motor unit
Motor unit consists of motoneuron in spinal cord, (or in nuclei of cranial nerves,) appropriate axon and all muscle fibers innervated by the collaterals of the same motoneuron. Function can be disrupted by damage to the
motoneuron, interruption of nerve conduction or by a muscle disease.
An alpha-motoneuron can be attacked by polio virus, and partially irreversibly destroyed. In spinal muscle atrophies, the group of neurodegenerative diseases with unknown etiology, these motoneurons are dying.
Damage or destruction of axons is caused by autoimmune disease, diabetes mellitus, lead intoxication, alcohol intoxication, genetic defects.
Peripheral muscles can be damaged by autoimmune disease along with other tissues, i.e. dermatomyositis.
Genetic defects cause muscle diseases directly, as in myotonias, or muscular dystrophies.
The outcome of lesion of motor unit is a localized paresis of involved musculature regardless whether it is due to lesion of motoneuron, axon, or a muscle proper.
With a primary destruction of alpha-motoneurons there are typical fasciculations, while with primary destruction of musculature there are fibrillations.
Amyotrophic lateral sclerosis, a disease of unknown etiology, although heavy metal poisoning, trauma, especially by electric current, have been implicated, with incidence of 4:100000 (in Gomoros from Guam 4:1000),
three times more frequent in males, with onset after 40 years of age. It develops probably on the basis of genetically induced disorder of axonal transport. which secondarily leads to demise of motoneurons in spinal cord, as
well supraspinal mtoneurons. Progressive degeneration of pyramidal tract, motor neurons of anterior horn of spinal cord and of cranial nerves, and their axons, with spastic-atrophic muscle pareses, starting distally, muscle
fasciculations and spasms, eventually bulbar paralysis with speech and swallowing difficulties, pre-terminally sphincter disturbances, vision difficulties, dementia, and death due to paralysis of respiratory muscles. Death
ensues after a few years from onset, or after 1 to 2 years from the first symptoms of bulbar paralysis. Fetal precursor cell transplantation of spinal cord, peripheral myoblasts, liver, stomach/duodenum, exocrine pancreas,
adrenal cortex, placenta, intestine, must be given immediately.
The author treated by fetal cell transplantation 4 patients from South Africa, 3 males and one female' from 31 to 56 years of age, from 8 to 30 months since the onset of symptoms.
48 years old male received BCRO fetal cell transplantation intrathecally and under the aponeurosis of rectus abdominis muscle in 2002 and again in 2004. The progression of ALS had stopped as of 2005.
31 years old male developed ALS in 2003, received immediately BCRO fetal cell transplantation in April of 2oo4 and again in March 2005.
56 years old female got ALS in Summer of 2003 and her ALS progressed extremely fast. In March 2004 she got intrathecal BCRO fetal cell transplantation and her disease stabilized till March 2005.
41 year old male got ALS in October 2003 and his disease progressed very fast. In July 2004 he received intrathecal BCRO fetal cell transplantation in already very bad condition. His condition improved but did not become free of
symptoms like the other treated patients.
ALS must be treated by intrathecal BCRO fetal cell transplantation immediately after the diagnosis is made, and must be treated so repeatedly, as necessary.
Genetic defects of ion channels are a frequent cause of muscle diseases. Normally, depolarization of muscle membrane is triggered after stimulation by voltage dependent Na+-channels which control opening of voltage dependent Ca2+-channels. Inflowing Ca2+ activates Ca2+-channel in the membrane of sarcoplasmatic reticulum. This leads to release of intracellular Ca2+ which mediates
Re=polarization is accomplished by inactivation of Na+-channels, flow of Cl- into the muscle cell and outflow of K+. Repolarization causes inactivation of Ca2+-channels, so that
intracellular concentration of Ca2+ is decreased and muscle relaxes.
Delayed inactivation of Na+-channels due to a mutation of gene for channel protein can lead to delayed relaxation, increased excitability and spasms, i.e. in Na+-channel myotonia, and
On the basis of another defect of Na+-channels or defective K+-channels, with high extracellular concentration of K+, a paralysis takes place, i.e. Hyperkalemic periodic paralysis, AD
disorder, caused by another mutation of the same gene that causes Paramyotonia congenita.
Genetic defect of voltage dependent Ca2+-channels leads to Hypokalemic periodic paralysis.
With defects of Cl-- channels myotonia develops. Depending upon the severity of molecular defect its inheritance is AD in Thomsen congenital myotonia and Myotonia Levior, or AR in
Becker generalized myotonia, all due to the malfunctions of Cl- channel, caused by different mutations of the same gene.
In some defects of sarcoplasmatic Ca2+-channels of ryanodine type of receptor an anesthesia gas Halothane can activate this channel independently of the change of potential. Such massively increased use of muscle
energy for heat production leads to hyperthermia, i.e. malignant hyperthermia. Malignant hyperthermia develops during general anesthesia in 1:15000 children and 1:50000 adults. In 50% of cases it is an AD disorder, in
20% AR, and in 30% a sporadic condition.
In Duchenne and Becker muscular dystrophies, XR disorders, one component of cytoskeleton, dystrophin, is defective. In Duchenne dystrophy, with incidence of 1:3500 newborn boys, only short and non-functioning fragments
of dystrophin are produced and disease is severe and progressive, with lethal outcome in the first 20 years of life. In Becker’s dystrophy with incidence of 1:35000 newborn boys, dystrophin is defective, but to a lesser degree,
so that it is still functioning, and the disease begins later in life than Duchenne muscular dystrophy and runs a much less severe clinical course. Fetal precursor cell transplantation of peripheral myoblasts, liver,
intestine, spinal cord, exocrine pancreas, placenta, is recommended.
Ion channels are specific proteins which can ‘open and close’, and thereby control movement of ions Na+, K+, Ca++, Cl-, across cell membranes.
Clinical entities caused by ion channels abnormalities, called canalopathies, are becoming better known and some, those of muscle fibers and peripheral neurons, have a well defined clinical picture already.
Disorders of neuromuscular transmission
Action potential transmitted to the nerve ending by Na+-channels depolarizes its cell membrane and thereby opens voltage dependent Ca2+-channels. Ca2+ flows into nerve ending and mediates
connections of vesicles containing acetylcholine with pre-synaptic membrane so that acetylcholine subsequently pours out of vesicles into the synaptic cleft. Next, acetylcholine binds to the receptors of sub-synaptic membrane
and thereby opens non-specific cation channels there. Depolarization of membrane in the area of synapse transmits onto surrounding sarcoplasmic membrane, where opening of voltage dependent Na+-channels triggers action
potential, which quickly spreads to the whole membrane of muscle cell. Acetylcholine is broken down by acetylcholinesterase, the split off choline is re-taken up by the nerve ending, and used for re-synthesis of acetylcholine.
Myasthenia gravis is the most important disease of neuromuscular synapse. It is a muscle paresis caused by inability to transmit signals from nerve to muscle. The reason is the development of antibodies against
acetylcholine receptors of sub-synaptic membrane, which suppress the binding of acetylcholine and speed up the breakdown of acetylcholine receptors. This autoimmune disease can be triggered by viruses, and is found in patients
with benign thymoma. Repeated simulation of motor nerve leads in patients with myasthenia gravis at first to development of normal muscle summation action potential, but later on with growing tiredness of neuromuscular
transmission the amplitude of muscle action potential slowly but steadily diminishes. Fetal precursor cell transplantation of thymus, peripheral myoblasts, spinal cord, liver, intestine, adrenal cortex, placenta, is advised.
Myasthenic syndrome of Lambert-Eaton is another autoimmune disease of neuromuscular synapse that occurs in patients with lung cancer of small cell variety.
G. Degeneration of basal ganglia:
- Hepatolenticular degeneration, Wilson’s disease,
- Dystonia musculorum deformans, Torsion dystonia,
- Huntington’s chorea,
- Pigmentary degeneration of globus pallidus, Hallervorden-Spatz syndrome,
- Parkinson’s disease.
Alzheimer’s disease is characterized by the following clinical triad: organic brain disturbances, depression, loss of vitality, that start between 20 and 30 years of age.
Organic brain disturbances are the cause of Alzheimer’s disease, while depression is just a symptom of the basic disease, although often a dominant one, and a lack of vitality is the main clinical feature of the disease. The
dynamic aspects of mental and spiritual processes are the criterion of psychic vitality, and the most important are: inner drive, mood, sensitivity to stimuli, adaptation ability, stress handling ability, behavioral contact.
Psychopathologic symptoms of a syndrome of brain atrophy can be in general described as lowering of the entire spiritual performance level.
The main goal of therapy is an improvement of loss of vitality, in line with teachings of A. Kment of Vienna, Austria, who succeded after decades’ long animal experimentation to objectively prove the ‘revitalization effect’
as the working cytobiological principle. According to Kment, the revitalization is a preservation of vitality over an extended period of time, or the re-gaining of lost vitality in the later years of life, as objectively proven
by statistically significant changes of several parameters of aging, that document an attainment of younger biological age as compared with the chronological age.
The earlier in the course of brain atrophy is fetal cell transplantation carried out, the better will be the results. However, the improvement is possible also in the advanced stages with dementia, as fetal cell
transplantation even then increases the vitality with an overall beneficial effect for the patient, so that it appears that even dementia, i.e. irrepairable loss of intellectual abilities, is improved.
An aggressive treatment of Alzheimer’s disease by fetal cell transplantation is today possible but it is of value only when the patient is really not in the terminal stage.Since fetal cell transplantation is able today to
directly regenerate CNS cells and tissues, there is a new hope for the success of the BCRO fetal precursor cell xeno-transplantation in patients with 4th stage of dementia.
DEMENTIA, aka SENILITY, is a large group of brain diseases, that include the gradually decreasing ability to think, reason and remember, thereby interfering with daily functioning of the patient. There is a more rapid worsening
of the usually expected mental decline of the aging human being, i.e. greater decline than one would expect as a result of the usual aging process.
The most common kind of dementia is Alzheimer’s disease, that comprises 50% to 70% of cases of dementia, followed by vascular dementia (25%), Lewy body dementia (15%), and fronto-temporal dementia, while cases of dementia due to
normal pressure hydrocephalus, Parkinson’s disease, progressive paralysis due to syphilis, Creutzfeldt-Jacob disease, are uncommon and those due to a variety of incurable genetic diseases are quite rare. Regardless of cause,
dementia is progressive, even though usually slow.
Contrary to advertisements and medical publications to support it, there are no drugs or nutritional supplements that would slow down the progress of dementia, or improve the clinical status of the patient. But BCRO type of
fetal precursor brain cell transplantation has been proven to help every patient with dementia.
Dementia affects 36 million of the world’s population, or 10% of people develop dementia at some point of their lives. It becomes more common with age: 3% of people have dementia between the ages 65 – 74, 19% between 75 and 84
years old, 25-50% past the age of 85. In 2013 as many as 1.7 million patients died in the world from dementia and it became one of the most common causes of disability among the old people.
Alzheimer’s disease (AD) was the first disease of the dementia group described in 1906 by the German professor of psychiatry Alois Alzheimer as ‘pre-senile dementia’. It was a triad of clinical findings starting slowly in 20 –
30 year old patients, that caused a decrease of the entire spiritual performance level:
1) organic brain disturbances: cause of AD +
2) depression – a symptom of the basic disease +
3) lack of vitality – main clinical feature of AD.
The main goal of therapy has been an improvement of the diminished vitality.
Prof.Dr. A. Kment, former chief, Department of Physiology of Vienna Medical School, Austria, devoted his entire career to the most comprehensive study of aging disease. He defined the treatment of aging disease, i.e.
revitalization, as a preservation of vitality over an extended period of time, or the re-gaining of lost vitality in the later years of life, objectively proven by statistically significant changes of several parameters of
aging. This documented an attainment of a younger biological age as compared with the chronological age. (The term ‘aging disease’ was created by the author in his first book ‘Forever Young’, published in the U.S.A. in 1984.)
A major problem in the modern era is that psychometric diagnosis of dementia, or cognitive testing, stopped being considered a sufficient proof of diagnosis of Alzheimer’s dementia (as it used to be in USSR, for example), and
only CT scan or MRI of the brain has been usually accepted as proof of brain atrophy and Alzheimer’s disease. Waiting to start therapy with BCRO FCT until there is brain atrophy shown by CT or MRI frequently means that the
patient has deteriorated beyond the stage of real possibility to repair the damaged brain.
The fact remains, that BCRO fetal cell transplantation is of greatest therapeutic benefit when carried out at the early stages of the dementia, or when the patient ‘repeatedly cannot find his car keys’. But, the decision to
treat the patient with BCRO fetal cell has to be left in the hands of an expert in this therapeutic method and cannot be based on any simple test or CT scan showing an atrophy of the brain cortex or any other finding.
The earlier in the course of brain atrophy that BCRO fetal cell transplantation is carried out, the better are the results. However, in the author’s experience, improvement is possible also in the middle stages of dementia, when
the patient no longer can function outside of his own home, and should not be left alone, because he does require an assistance with personal care and hygiene. But BCRO fetal cell transplantation will increase the vitality even
in the late stages when the loss of intellectual abilities appears non-repairable, and the patient requires 24-hour supervision to ensure personal safety, to cope with incontinence, and inability to recognize even the closest
Without deep knowledge of human and veterinary embryology, cytology of human diseases (never studied in medical schools), detailed pathophysiology of human diseases, even availability of the BCRO fetal precursor cell
transplants is of minimal value for the patient with incurable and untreatable disease(s), especially of central nervous system.
BCRO fetal cell xeno-transplantation is an individualized therapeutic method, i.e. each patient receives the necessary BCRO fetal cell transplants in accordance with the pathophysiology of his disease(s) as analyzed on a
cytological level that has never been taught in medical schools.
Case history No. 1 – Late Stage Dementia
An 83 year old male was a retired gynecologist, author’s very close friend, one of the directors of International Institute of Biological Medicine in Moscow, an athlete and a car buff. This man retired 12 years ago and soon after was diagnosed with colon cancer, mostly as a result of intractable constipation that he never took time to pay attention to. He underwent 4 years of very involved cancer treatment before getting into a remission. As a side effect of his cancer treatment, he got myocardial infarction with residual congestive heart failure and arrhythmia. But the worst side effect of years of heavy chemotherapy was his dementia.
When he reached the late stage of dementia his wife finally requested the author to carry out BCRO fetal cell transplantation which was done on July 30, 2015 at the University Hospital in Bratislava, Slovakia. Treatment consisted of: 1) intrathecal (via lumbar puncture) implantation of cell clusters of 3 different parts of fetal brain from rabbits that originated from a closed colony set up in 1973 as per World Health Organization. 2) subaponeurotic (under the aponeurosis of rectus abdominis muscle) implantation of cell clusters of 3 organs for treatment of colon cancer in remission and 1 organ for cardiac arrhythmia from rabbits originated from the same closed colony; 3) subcutaneous implantation of cell clusters of 4 organs for treatment of colon cancer in remission, 1 organ for myocardial regeneration after MI, 1 of tissue fragments for knee cartilage repair, 1 organ for testicular regeneration, and 1 part of extra-thecal fetal brain from rabbits originated from the same closed colony for treatment of dementia.
The whole procedure took 45 minutes.
By the fourth week after BCRO FCT, there was a dramatic improvement in level of vitality, diminished depression, much improved memory, which was unusually fast response to BCRO FCT in a patient who never had BCRO FCT before. Such degree of improvement would have been normally expected only after 4 to 5 months.
The author visited with the patient 75 days after BCRO FCT and observed his friend happy and talkative, the way that he had not been seen for several years.
Case history No. 2 – Parkinson’s Syndrome and Dementia
In 2007 the author treated a 91 year old man in Hong Kong with BCRO fetal cell transplantation because of Parkinson’s syndrome, dementia, lack of vitality and depression. The clinical picture of Parkinson’s syndrome is the same as that of Parkinson’s disease, but the cause is arteriosclerosis of cerebral arteries of the Willis circle at the base of the brain.
He was treated by sub-aponeurotic and subcutaneous implantation of nine BCRO fetal cell transplants necessary for arteriosclerosis and aging disease as well as three intra-thecal implantations of BCRO FCT for treatment of dementia.
When the author saw the patient in a follow-up two months later, it was a hilarious scene. His son reported that 2 weeks earlier his father told his valet to prepare his clothing so that he could go to the casino at night (as this used to be his favored past time all of his adult life). There was no way to stop him. He spent most of the night in the casino and did not lose any money but actually won some. The patient was acting 20 years younger. The fact that he dared to gamble and gambled successfully was the best indication of the success of his BCRO FCT treatment of dementia. The symptoms of Parkinson’s Syndrome visibly improved as well.
Case history No. 3 – Parkinson’s Disease
In 2007 in Hong Kong the author treated a man with an advanced Parkinson’s disease using intrathecal implantation of 3 BCRO fetal cell transplants of necessary parts of brain with a very good result. Encouraged by the results of the first treatment, in 2009, the patient’s wife called their physician and asked him if the repetition of the treatment would not give him further improvement so that he would be able to go back to work. The physician did not consult with the author but instead, ordered the fetal cell transplants in accordance with the prescription used by the author for the first treatment. Being a surgeon, he did the lumbar puncture implantation himself. Three months later, the surgeon called the author to report that this time the patient showed no improvement whatsoever.
After verification, it became obvious that 3 months earlier BCRO did not prepare any fetal cell transplants for this patient. But the label on the vials was an exact copy of BCRO labels. Once the surgeon learned that he was cheated, he recalled that the cell transplants that he received from the Malaysian Chinese husband/wife team looked different since they were black (dead) rather than pink (live).
The origin of those ‘cell transplants’ was a German manufacturer of ‘fresh frozen cell-therapeutica’ in Hamburg whose technology of freezing was decades behind the times, as a result of which, the frozen cells turned ‘rotten’ while in the electric freezer, rather than in a liquid nitrogen one. The surgeon claimed that there was no pathological reaction to an implantation, which was fortunate for the patient.
These two Malaysian Chinese criminals became multimillionaires, bought themselves noble titles ‘Dato Sri’ from one of the Malaysian sultans, and the degree of ‘Professor Doctor’ from one of the U.S. online universities, although they are both high school drop-outs (he from 6th grade, she from 8th grade).
Today unfortunately, most patients seeking fetal cell transplantation are defrauded since they are not given the real fetal cell transplants such as has been prepared by Bio-Cellular Research Organization since 1998.
In 2010 the author wrote a 12 page letter to Mr. Najib, Prime Minister of Malaysia, warning him about the danger that these two criminals present to the public of his country and of the world, but he has not responded to this day. These two criminals were kicked out of Switzerland as ‘personas non-gratas’, but their Swiss website is still active.
Case histories No. 4 – 126 (123 cases of 158)
Here is the discussion of our innovations in the patients’ treatment as they evolved step-by-step in Moscow:
Fifty parts of human fetal brain cells from ventral mesencephalon and basal ganglia with one part of primordial brain cells of the respective genetic mutant of Drosophila were implanted into ventro-lateral thalamic nuclei of eight no longer treatable Parkinson’s disease patients, and the treatment of all of them included also a variety of neuro-cryo-surgical procedures to alleviate various symptoms and signs of Parkinson’s disease, with a phenomenal overall success rate of 95%.
One of those 8 patients died 8 months later from myocardial infarction and detailed autopsy of his brain showed the key reason for such unbelievable 95% success: use of a combination of human fetal brain tissue with brain tissue of genetic mutant of Drosophila for intra-parenchymatous (into the brain) transplantation.
Intra-thecal implantation, intra-ventricular at first, then via standard lumbar puncture, has been used by us from then on in all patients over the age of 12, after such treatment was proven to be completely non-traumatic by clinical testing and by autopsies of 100 patients with GSW of brain, in deep prolonged coma: there were no untoward reactions toward lumbar puncture implantation itself, and there were no negative reactions to or complications due to the implanted cell clusters of various parts of human fetal brain.
As the next step in our research, patients with prolonged coma not due to GSW of brain were treated by a combination of human fetal brain cells from various anatomical parts of brain, without addition of brain cells of any kind of mutant of Drosophila fly. The initial published study of 14 patients, from 29 to 82 years of age, 7 females and 7 males, 4 with cerebrovascular accident, 4 with Parkinson’s disease, 2 in coma after clinical death for 18 days or more , 1 with toxic encephalopathy, 1 with vascular collapse, 1 with post-traumatic encephalopathy, 1 with Alzheimer’s disease, treated by intrathecal implantation of fetal brain cells via lumbar puncture, gives detailed case histories of 6 patients, and overall results. Only one patient had negative result, a 60 years old female with Alzheimer’s disease. All other patients were improved, some spectacularly.
A 29 years old female developed anaphylactic shock 30 seconds after I.M. Ampicillin. A resuscitation and intensive care restored spontaneous breathing and improved cardiac function, but deep coma persisted. On 18th day an intrathecal implantation via lumbar puncture of 5 – 6 million of brain cortex cells was carried out. Around 18 hours later the patient opened eyes, recognized her mother, and began to answer questions in simple words. Left-sided hemiparesis, urinary and fecal incontinence, and dementia persisted. Gradual improvement was observed, and 10 weeks later a 2nd intrathecal implantation of brain cortex cells was done. Two days later a dramatic improvement was observed by everyone. Athetoid movements of left hand and arm disappeared, spasticity on the left side substantially diminished, improvement of speech, reading, writing, comprehension, gait, EEG was noted.
A 45 years old male was undergoing an uneventful surgery for retinal detachment of the left eye, when a few minutes before the end a sudden bradycardia and blood pressure drop were observed. After the recovery from an operation the patient remained in stupor, and akinesia with rigidity quickly developed. On 22nd day the patient was transferred to a psychiatric ward for rehabilitation of psychic functions. On 25th day an intrathecal implantation of human fetal brain tissues from cortex and peri-ventricular medulla alba of brain was carried out. Two days later a dramatic improvement took place: speech, writing, drawing, all. Then 4 months later a 2nd intrathecal implantation was carried out followed by a continuous improvement.
A 36 years old male suffered a massive head injury in a car accident. There was a huge intracranial hematoma and AV malformation. Patient was left with left hemiplegia. Around 6 weeks later an epilepsy developed. A diagnosis of subdural hematoma was made. While patient was under aggressive medical therapy, 16 months after an accident an intrathecal implantation of ~ 12 millions of brain cortex and peri-ventricular medulla alba of brain fetal cells was carried out. Epilepsy disappeared, EEG slowly returned back to α rhythm, and there was a gradual improvement of neurologic findings.
A 39 years old female was treated for right hemiparkinsonism by L-dopa without any effect, and so intrathecal implantation of fetal cells of basal ganglia was carried out. At 3-month’ follow-up a dramatic improvement was noted. There was no tremor in the extremities, the function of right hand was normal, gait improved. The effect has somewhat diminished subsequently, and 5 months after the first the 2nd intrathecal implantation was done. One month later again improvement was noted, tremor disappeared, gait and writing improved. There were 3 other Parkinson’s patients among the initial 14 patients treated, all with pronounced improvement. A 65 years old female suffered a cerebrovascular accident. Intrathecal implantation of brain cortex cells was carried out immediately. There was a dramatic improvement, so that rehabilitation could begin already 18 hours after intrathecal implantation of fetal brain cells, i.e. the next day after the stroke. Two days later hemiplegia improved to the level of minor hemiparesis. On the 8th day the patient began to walk with a walker.
A 50 years old male survived an extensive cerebrovascular accident 2.5 years ago and was left with hemiparesis, aphasia, and Jacksonian epilepsy. Patient received intrathecal implantation of 12 million fetal brain cortex cells. Three weeks later he observed an improvement of speech, writing, began to read, and count. Movements of right hand improved noticeably. EEG showed less epileptogenic activity.
Case history No. 127- Cerebrovascular Accident (Stroke)
Next to Alzheimer’s diseases, the most common disease of central nervous system in the western countries is a cerebrovascular accident.
In 2009, the author examined an Austrian politician (the husband of a physician). This politician had diabetes and hypertension and 6 months earlier survived a major stroke but had residual hemiplegia and expressive aphasia. He was depressed due to his disability and persistent pain from spasticity. The patient was treated with three BCRO fetal brain cell transplants via lumbar puncture and nine BCRO fetal cell transplants sub-aponeurotically and subcutaneously. The entire treatment took 45 minutes. His hemiplegia improved 50% and speech 70%, as did his diabetes, hypertension and depression as well. He was the first post-stroke patient in Western Europe treated by the author.
Subsequently several similar patients were successfully treated in China, Indonesia, India, etc.
Case histories No. 128 – 182 – Spinal Cord Injuries
In January 2004, the author received a desperate E-mail from South Africa from parents of a 19 year old son, who just became quadriplegic after cervical spine fracture from hitting his head against the bottom of a pool diving. Since authorities of South Africa did not allow an emergency treatment by BCRO fetal cell xeno-transplantation in their country, the patient was treated 8 months later when he was able to fly to Germany. This triggered a public scandal and we soon treated in Germany 55 patients from South Africa with old spinal cord injuries with a complete trans-section of the spinal cord diagnosed by CT scan(!), with success in terms of a significant improvement of mobility in the opinion of patients, in all but two oldest males from the group, the first 58 years and the second 73 years old. These were quite unbelievable results when considers a complete trans-section of spinal cord, which was beyond any medical logic.
The duration of paraplegia or quadriplegia was from 18 months to 12 years (it was 12 years in the 58 year old, who did not improve).
There was no improvement of anal and urinary sphincter control in any of the patients, however, but erection returned in one, a motorcycle racer, who after a substantial improvement, went right back into racing. The loss of anal and urinary sphincter control was not caused by trans-section of spinal cord(!) but by damage of parasympathetic plexus around spinal cord.
Regretfully due to a lack of funding, mostly for the first class airplane tickets for the patient and the nurse to transport patients to Germany, the project did not include more patients, and repeated treatments in all patients with an improvement of mobility after the first treatment. (The second treatment was done in 3 patients only with an additional improvement of motor functions in all three.)
All patients stated to the author, that if there could be a way to improve their incontinence, their satisfaction with the results of BCRO fetal cell transplantation would have been complete.
In 1995 the author received an emergency request from a neurosurgeon from Pretoria University Hospital, who attended his lecture a few months earlier at the Pretoria Medical School to explain the details how to use BCRO fetal cell transplants during an emergency surgery for fresh transsection of spinal cord, as well as urgent . The adult male, who while driving a car on the freeway from Jo-burg to Cape Town, along with his 12 year old daughter, was shot in the neck, suffered cervical spine fracture and quadriplegia with urinary and fecal incontinence, as well as how to deliver the BCRO fetal cell transplants urgently delivery to Jo-burg.
In recent spinal cord injury, after the emergency surgical repair of a cervical fracture and debridement of cervical spine, the surgeon left plastic catheters in the area of injury and gently irrigated it by BCRO fetal cell transplants every 6 – 12 hours.
When the patient recovered from the spinal shock and realized that his daughter was killed by the gangsters, he instantly immersed into a catatonic state, lost the will to live and ended in a psychiatric hospital forever.
Based on the author’s experience, after old cervical spinal injuries, intrathecal implantation of BCRO fetal cell xeno-transplantation (via lumbar puncture) should be carried out every 6 months with vigorous, specialized rehabilitation.
Case history No. 183 – Total Paralysis From Embolic Strokes During the Acute Stage of Recovery Post-Surgery to Repair Fracture of Cervical Spine
One of those patients with cervical spine fracture was a 31 years old male, a physician and a top rugby star of South Africa. In 2002 he suffered a fracture of cervical spine. After his surgery, in recovery room a massive embolization of right carotid artery took place. He was taken back to the operating room to remove the embolus when an embolization of the left carotid artery occurred as well. Following all that, the patient developed a ‘locked-in-syndrome’, a total paralysis of all muscles in the body with the exception of extra-ocular muscles, i.e. patient could move only his eyes, could not swallow, breathe or speak on his own. A 12 months’ long very intense rehabilitation followed. Upon arrival in Germany, his spontaneous breathing was very shallow, he could not clear any secretion, swallowing reflex was absent and he could say a word only when someone squeezed the air out of his lungs. Essentially all muscles of his body were paralyzed. On November 18, 2004 (more than 2 years after his paralyzing strokes), he received via lumbar puncture three BCRO fetal cell xeno-transplants of three parts of brain, and seven other non-CNS BCRO fetal cell xeno-transplants sub-aponeurotically and subcutaneously. Five days later the patient was able to stand up with assistance, cough up secretions, speak, swallow and move his hands.
Back in South Africa he began horseback-riding training and 2 years later he could maintain balance in the saddle on his own. His speech dramatically improved, as well as swallowing and breathing. Some months later when the author lectured at his medical school of the University of Pretoria, the patient was the Master of Ceremonies. With the equipment like used by Professor Stephen Hawking, he handled a large auditorium full of students like a professional.
Case history No. 184 – Chronic Paralyzing Encephalitis
In 1992 a 36 years old male from London, U.K., a sportsman, developed encephalitis of unknown etiology, following which he was in bed for 9 years, motionless. No diagnosis was ever made and no treatment given. His wife took him home against medical advice. On July 25, 2002, he received in Germany BCRO fetal cell xeno-transplantation, two preparations from CNS via lumbar puncture and eight non-CNS preparations sub-aponeurotically and subcutaneously. In 3 months he was able to move with assistance and start intense physiotherapy. In October 2003, he could walk a short distance with assistance, and in June 2004 without assistance. He gained weight. In October 2004 he became a father of a healthy boy.
Case history No. 185 - Multiple Sclerosis
Multiple sclerosis is an autoimmune disease with a typical onset of various neuronal deficits in different parts of the CNS at different, variable, unpredictable, time intervals. After inflammation has subsided, a repair of damage takes place and nerves are (partially) re-myelinated. It is often a familiar disorder, more common in HLA3 and HLA7 carriers.
In multiple sclerosis the main symptoms are disturbances of gait, speech and eyesight, along with manifold neurological symptoms. Periods of progression, of a disease arrest, and even an improvement of clinical course, make an early diagnosis very difficult. BCRO fetal precursor cell transplantation of liver, intestine, exocrine pancreas, adrenal cortex, mesenchyme, placenta, peripheral myoblasts, are under consideration for treatment. Under no circumstances should any fetal cell transplants from central nervous system be implanted(!), since multiple sclerosis is primarily an enzymopathy of the intestinal mucosa that leads to abnormal breakdown of proteins and lipids from food in the intestinal wall into pathologic nucleotides and mono- and di-glycerides, toxic to neurons, that are capable to pass through hemato-encephalic barrier to damage the nerve cells.
The most remarkable patient with MS treated by the author was his female classmate from medical school who received BCRO FCT in 1988 already in the condition of a total disability. She got the first attack of MS during her first pregnancy at the age of 26 and had been completely disabled since the age of 33. She died in 2018, at the age of 76, 50 years after the onset of her illness, in the same condition as at the age of 33, which is remarkable.
Author’s paternal grandfather got multiple sclerosis at the age of 39, became completely bedridden at 41 and died of his disease at the age of 51.
In men multiple sclerosis is less frequent - only 15%, but with much more vitious clinical course, as was the case of my grandfather. After only 12 months he was tptally bedridden.
Case histories No. 186 – 189 – Amyotrophic Lateral Sclerosis
Amyotrophic lateral sclerosis, a disease of unknown etiology, although heavy metal poisoning, trauma, especially by electric current, have been implicated, with incidence of 4:100,000 (in Gomoros from Guam 4:1000), three times more frequent in males, with onset after 40 years of age. Progressive degeneration of pyramidal tract, motor neurons of anterior horn of spinal cord and of cranial nerves, and their axons, with spastic-atrophic muscle pareses, starting distally, muscle fasciculations and spasms, eventually bulbar paralysis with speech and swallowing difficulties, pre-terminally sphincter disturbances, vision difficulties, dementia, and death due to paralysis of respiratory muscles. Death ensues within a few years from onset, or after 1 to 2 years from the first symptoms of bulbar paralysis. BCRO fetal precursor cell xeno-transplantation of spinal cord, peripheral myoblasts, liver, stomach/duodenum, exocrine pancreas, adrenal cortex, placenta, intestine, are each considered for an individual patient.
The author treated, by BCRO fetal cell transplantation, 4 patients from South Africa, 3 males and one female, from 31 to 56 years of age, from 8 to 30 months since the onset of symptoms.
A 48 year old male received appropriate BCRO FCT intrathecally and subaponeurotically in 2002 and again in 2004. The progression of the ALS disease had stopped as of February 2005.
A 31 year old male developed ALS in February 2003, received appropriate BCRO FCT intrathecally and subaponeurotically in April 2004 and was well as of March 2005.
A 56 year old female developed symptoms of ALS in the summer of 2003 and the ALS disease was progressing very fast. In March 2004, she received appropriate BCRO FCT intrathecally and subaponeurotically, and her condition stabilized until March 2005.
A 41 year old male developed ALS in October 2003, and disease progressed very fast. In July 2004, he received BCRO FCT intrathecally and subaponeurotically but was already in a very bad shape. The patient improved over the next 9 months, but remained symptomatic.
ALS requires BCRO FCT as soon as the diagnosis is made and may require more than one treatment.
Case histories No. 190 – 202 – Muscular Dystrophies
In Duchenne and Becker muscular dystrophies, XR disorders, one component of the cytoskeleton, dystrophin, is defective. In Duchenne dystrophy, with incidence of 1:3500 newborn boys, only short and non-functioning fragments of dystrophin are produced and disease is severe and progressive, with lethal outcome in the first 20 years of life. In Becker’s dystrophy with incidence of 1:35,000 newborn boys, dystrophin is defective, but to a lesser degree, so that it is still functioning, and the disease begins later in life than Duchenne muscular dystrophy and runs a much less severe clinical course. Our IIBM treated in Moscow 10 boys with Duchenne’s dystrophy with a minor success and 2 boys with Becker’s dystrophy with success with fetal precursor cell transplantation of peripheral myoblasts, placenta and liver given subaponeurotically while intestine, spinal cord, exocrine pancreas, were under consideration.
Case history No. 203 - Cerebrovascular Accident - mine
On August 20, 2016 I got a "stroke". Cause was the arterial obstruction due to blood clot. It was the very severe case: my wife was told by attending neurologist, my old friend, that "I was on my way out of this world...". There was no one around who could give me "my" intrathecal treatment of fetal cell transplantation. My fate came to my rescue. After 3 months I put together all my remaining intelect and I was able to organize with the help of my friends my own fetal brain cell transplantation. I made my own prescription for fetal cell transplantation, my friends, who prepared all fetal cell transplants from 1998 when I had to leave Russian Federation courtesy of U.S. until now for all of my patients worldwide, did their usual excellent job, my best friend/chief of surgery at our medical school recruited retired anesthesiologist for intrathecal implantation of 4 kinds of brain cells, and do it his department that he was the chief, so that my treatment was done on December 12, 2016. Two months later the improvement of my status was begun. No one who saw me after my stroke wants to believe the "miracle" how good is the intellectual functioning of my brain.
The success of our study at Helmholtz Russian Research Institute of Eye Diseases Of Russian Academy of Medical Sciences on treatment of myopathies of extraocular muscles by cell transplantation in 8 patients was reported at the 1st Symposium on Transplantation of Human FetalTtissues in Moscow, December 4 – 7, 1995, under the title: “First experience with treatment of endocrine myopathies by cultures of human fetal myoblasts“. At the same research center also a study of treatment of post-radiation eye perforations by cell transplantation was carried out.
54 years old male noticed at the age of 33 a decreased visual acuity and two years later in 1971 underwent operations for retinal detachment on both eyes. Next year a panniculus was removed on the left eye. In 1981 laser coagulation was carried out near the fovea centralis of the right eye. In March 1982 a cataract was removed on the left eye. In 1976 an ophthalmologist advised the patient to have cell transplantation. Between 1976 and 1990 the patient had cell transplantation every year, i.e. 15 times. The retinal disorder stabilized, there was no further decrease of visual acuity and the patient advised in 1977 to enter the school for blind was still working in 1990 in the mail room of a large corporation.