Primary Text & Treatment Options
Section 04
Section 4A
Section 4B

Hepatic Generated Neurotoxins are the proximate Causative Factor and Explanation for Alzheimer’s, Primary Dementias, Parkinson’s and Age Related Macular Degeneration.

Jean-Martin Charcot, the Father of Neurology, a French Neurologist, (1825-1893) reported a series of 20 patients whose illnesses were characterized by dramatic and progressive loss of muscle strength with associated muscle atrophy in 1874. Charcot personally developed the term Amyotrophic Lateral Sclerosis based on the unique autopsy finding in the brain of several of his patients. (2) Initial recognition of a single patient with ALS type findings is attributed to Dr. Charles Bell in London, England in 1824, a half century earlier.

This disease is presently abbreviated as ALS, but is equally well known as Lou Gehrig’s disease. In many European countries, ALS is referred to as a “motor neuron disease”. The anatomically precise term, “Amyotrophic Lateral Sclerosis” is much too cumbersome for routine clinical use.

ALS most frequently is diagnosed in white males between ages 40 and 70. ALS is rarely diagnosed in patients less than 20 years old. Diagnosis to death is less than 48 months in 90% of patients with ALS. ALS is uncommon, currently estimated to afflict 4-5,000 Americans per year.

ALS was essentially unknown and undiagnosable in America until one of America’s best recognized Baseball players: Lou Gehrig (1904-1941), developed unexplained muscle weakness at age 35 in the spring of 1939 at the height of his career. He was eventually diagnosed as having ALS, even today a poorly understood disease with no known cause or cure. Gehrig’s clinical course was characterized by rapid and dramatic loss of muscle strength and atrophy secondary to unexplained nerve degeneration. Gehrig had previously established a Baseball Record playing in 2,130 consecutive Baseball games.

Baseball was then America’s leading sport. Lou Gehrig was one of its best known players. His daily activities were reported publically in the leading newspapers of the day. Based simply on the documented decline in his athletic abilities, “his batting average,” it appears that Gehrig’s prodromal clinical course was most likely in the range of a year or less prior to the start of the 1939 baseball season.

Thirty eight years earlier in 1907, Alois Alzheimer, (1864-1915) a German Psychiatrist and Neuropathologist, described the clinical course of his unique patient: Auguste Deter (1850-1906). Her clinical findings were characterized by dramatic loss of her memory associated with increasingly severe psychotic and erratic behavior. Her autopsied brain (1915), personally studied by Dr. Alzheimer, demonstrated unique cerebral cellular changes and “tangles” now diagnostic of its namesake disease.

Her husband institutionalized his wife primarily because of her increasingly erratic and psychotic behavior, rather than because of her memory loss. His wife’s erratic behavior left him no other choice but to hospitalize her at the local insane asylum, where she lived the last five years of her life. It was here that Dr. Alzheimer met Auguste Deter for the first time.

Dr. Alzheimer was so intrigued by the rapid deterioration of Auguste’s D’s memory and her progressively erratic behavior, that he personally recorded, in his own handwriting, a series of simple questions and her totally inappropriate, ever changing answers. One of Dr. Alzheimer’s colleagues referred to Auguste Deter’s illness as “Alzheimer’s disease” shortly after he presented her clinical course at a local medical meeting. (1906-1907)

It appears purely ironic that the name of a German Psychiatrist would now be associated with a disease feared by every educated senior the world over. Alzheimer’s disease is estimated to affect between 35 and 45 million patients on a worldwide basis and 5.2-5.4 million Americans. The incidence of Alzheimer’s is projected to increase commensurate with the ever increasing aging population. There is so little hope for identifying or preventing the development of Alzheimer’s disease, that at least one major financial planning institution has already projected the incidence and cost of this disease 30-40 years into the future.

Dr. Alzheimer once considered diagnosing Auguste Deter with the “Disease of Forgetfulness.” Best estimates are that her memory loss and erratic behavior began more than 5-10 years prior to her being institutionalized at age 50.

Alzheimer’s personal records were lost for a hundred years, only to be rediscovered shortly after the centennial anniversary of his initial public presentation of the clinical course of Auguste Deter. On rediscovery his records were found have been written in an older German dialect uninterruptable except but to a few German linguistic scholars. Today, Auguste Deter would be classified as having “early onset” Alzheimer’s as her disease became manifest prior to age 50. The significance of early onset Alzheimer’s a century later is still not entirely clear. August Dyer is cited as having a daughter herself who apparently had a child of her own. Both were considered to be normal when last seen. Follow up records of Auguste’s granddaughter are unavailable.

Alzheimer’s disease is now considered to be the fifth-sixth leading cause of death in America, and certainly the most expensive disease to treat, manage and care for, currently known to exist.

With respect to ALS, it is easy to calculate that when viewed as a distinct neurodegenerative disease, it will soon be 194 years that we have been aware of the existence of this disease and 110 years that we have been aware of Alzheimer’s in addition to a variety of other forms of dementias. Cumulatively these neurodegenerative diseases have been known to exist for three centuries. Nevertheless they are each still without known cause or cure. Why?

Most serious students of neurodegenerative diseases consider ALS and Alzheimer’s to be distinct and unrelated diseases. These diseases differ in several major respects: Alzheimer’s affects neurons associated with memory: ALS affects motor neurons and their peripheral nerves directing motion.

The author of this paper chooses to consider both diseases to be “related”, if not essentially identical, primarily because of the similar pattern of neuronal cell death. All neurodegenerative diseases share several characteristic features: specific neurons gradually and insidiously lose function, degenerate and die. Similarly, these neurodegenerative diseases have a progressive course, leading to profound disability and a shortened life span for each afflicted patient.

This theory, as proposed, has no explanation for the selection of targeted receptor neurons in separate but specific areas of the brain, unless they are designated by the unique similarity of structural and spatial configuration of their specific hepatic generated neurotoxins.

“Every key is not designed to open every door.”

In the complete and total absence of any other comprehensive and inclusive theories concerning neurodegenerative diseases, the author again proposes the following theory: (his best educated guess), in simple declaratory (but unproven) sentences. (1-3)

“The neuronal cell damage and clinical course seen in most neurodegenerative diseases such as those specified below result from the inability of an aging, but histologically normal liver, to completely metabolize normal substrates it encounters in daily life functions, resulting in a variety of incompletely metabolized byproducts, some of which are neurotoxic.

These hepatic generated neurotoxic byproducts are the direct proximate cause of the initial neuron-glial degeneration and their ultimate cell death. The quantity and variety of neurotoxic metabolites produced may well determine whether any given patient develops ALS, Alzheimer’s, Primary Dementias, Parkinson’s or age related macular degeneration or any other neurodegenerative disease.”

Amplification of this hypothesis will readily support the clinically observable manifestations for most neurodegenerative diseases.

1. The earlier the onset in life, the more severe the disease: the more rapid the progression, the shorter the functional lifespan of specific foci in the brain or other vital motor nerve connections.” (This proposition is based on the premise that the higher concentration of neurotoxins, the more the extensive resulting nerve damage will develop. Likewise, the more extensive the resulting nerve cell damage, the more severe the resulting illness; and the more rapid the death of vital nerves and the patient himself.) Lou Gehrig’s brief illness, prior to his death supports this proposition for ALS quite accurately.

2. The incidence of Alzheimer’s increases with age, due to the fact that hepatic generated neurotoxins are being produced continuously, the higher the probability that any given patient will have some degree of memory loss.) This proposition appears to be confirmed by the observable, progressive memory loss in many elderly patients.

3. The rate of progression of memory loss, erratic or psychotic behavior, increases with age, due to the continued production of neurotoxins resulting in progressive glial- neuronal cell death.

4. Delayed recognition of Alzheimer’s, (the duration of the prodromal period) may be due to a number of factors:

4A. the total number of neurons at risk: (e.g.) those in the cerebral cortex)

4B. the quantity of neurotoxins produced

4C. the relative toxicity and specific neurotoxins produced

4D. innate intelligence

4E. dietary factors (as yet undetermined)

4F. prior cerebral damage (e.g.) individuals who have ingested specific hepatotoxins, (excess amounts of alcohol (e.g.) over a prolonged period of time) would appear to be much more likely to manifest memory loss much earlier than those with minimal prior ingestion of hepatotoxins. It is much more likely that an individual with greater innate intelligence would be more likely to manifest Alzheimer’s type symptoms later in life than a person with much less innate intelligence. Similarly individuals who have damaged their liver by life style choices, alcoholism,” would most likely show signs of Alzheimer’s are much earlier in their life.

5. The prodromal course of Alzheimer’s disease may be 5-10 years or longer based on retrospective clinical observation. The prodromal course of ALS appears to be much shorter, almost certainly less than a few years. The best explanation for this disparity in the development of these diseases is to estimate the number of neurons at risk. Alzheimer’swould primarily affect memory neurons, the exact number of which is currently undetermined, but is estimated to be in the multiple billions, if not more. ALS would be limited to specific motor neurons. It would appear only logical that ALS would have a much shorter prodromal phase, simply based on the greater ratio of neurotoxins to targeted motor neurons.

6. The extended duration of the prodromal phase in Alzheimer’s is best explained by considering (a) that causative neurotoxins in Alzheimer’s are relatively weak individually. Relatively weak neurotoxins would require an additional extended period of time before they are sufficiently numerous to destroy a critical portion of the uncountable billion number of targeted memory glial-neurons complexes.

7. This theory predicts that the duration of the prodromal phase of Alzheimer’s will prove to be substantially longer than that currently estimated as soon as this disease is diagnosable by simple blood tests. It is highly probable that there will be a time in the future when the length of the prodromal phase can be calculated with precision by objective laboratory studies. The author anticipates that diagnostic laboratory findings will be confirmed in some teenagers prior to their ability to vote. (Age 18)

8. ALS has a much shorter prodromal phase, based purely on clinical observation. This much shorter prodromal phase is a direct consequence of the fewer the number of targeted motor neurons at risk. Currently there are no objective numbers to calculate this ratio. Cortical neurons are estimated to be in the multiple billions. Specific motor neurons must be only a tiny fraction of the number of cortical neurons.

In summary, the length of the prodromal phase in specific neurodegenerative disease is best explained by calculating the ratio of neurotoxins to targeted neuronal glial complexes: The greater the ratio, the longer the duration of the prodromal phase. A logical squeal of this theory is that there will be ample time to initiate therapy to prevent the progressive loss of memory neurons as soon as the disease specific neurotoxins responsible for the prodromal phase of Alzheimer's is discovered.

Admittedly, these assumptions are extraordinarily speculative and certainly will be heretical to most investigators. Nevertheless, they provide a testable hypothesis, never provided before, by any other previously published theory attempting to identify the inciting cause(s) and progressive clinical course of neurodegenerative diseases.

This theory has no ready explanation for the difference in sex distribution or the slight difference in age at initial diagnosis in either disease other than those previously cited unless the individual’s hormonal environment or presently unidentified genetic factors influences the degree of toxicity or quantity of hepatic generated neurotoxins.

9. Simple data collection, documenting the age of onset of menopause, the duration or use of supplemental post-menopausal hormones as well as blood levels of male hormones at initial diagnosis, in addition to use of supplemental male hormones, might well provide important clinical data: conceivably explaining why some patients with Alzheimer’s have more psychotic symptoms than others.

10. The incidence of psychotic symptoms or erratic behavior is appears to be greatly under emphasized in many reports, presumably to protect the name and reputation of the surviving family members. Every observation noted above will likely be applicable to ALS, with several exceptions:

A) ALS patients are recognized to have minimal or insignificant memory loss. Current estimates are that less than 20% of ALS patients have minimal to mild memory loss, while only 10 % or less, will manifest severe Alzheimer’s type memory loss. There is no reason to assume that the presence of either of these neurodegenerative diseases is mutually exclusive.

B) ALS patients presenting with motor nerve degeneration affecting respiration, (phrenic nerve involvement) will succumb more rapidly than those presenting with primary peripheral nerve involvement alone.

C) Patients with ALS presenting with an inability to swallow will be challenged with recurrent aspiration pneumonia, resulting in a shorter life span.

D) ALS patients appear to have a dramatically shorter prodromal course than that generally associated with Alzheimer’s. Lou Gehrig’s publically documented clinical course is the best authenticated record in terms of estimating the relatively short length of his prodromal period.

E) If one documents the first manifestation of ALS, solely by the initial and measurable loss of muscular coordination, (the ability to hit a ball, traveling at 80-90 mph, with a stick), Gehrig’s prodromal course would appear to be in the range of a year or less.

Lou Guerig Stats

Estimated onset of Gehrig’s disease: (late summer 1938 - Early Spring, 1939) Gehrig’s batting average in his first 79 games was slightly less than in his last 78 games in his 1938 season. The fact that Gehrig had only 4 singles in the 1938 World Series adds credence to an insidious loss of muscle strength in late summer 1938. There is no mention of Gehrig having any type of neuromuscular incoordination or dysfunction during his 1938 season. He is reputed to have told one of his team mates “he did not feel as strong as usual”, in mid-season 1938.

F. A few ALS patients have an unexplainable variation in the rate of progression of their disease: (a very small number of patients appear to live 2 to 4 times longer than others.) Many serious students of ALS cite specific instances during which there is minimal progression of the underlying disease for months or even years, without explanation. (Unfortunately there is minimal published evidence confirming that these specific patients actually had ALS.)

This theory has a possible explanation for the variation in longevity. Hepatic generated neurotoxins could easily vary in both quantity and the strength of their relative neurotoxicity due to as yet undetermined dietary factors.

G. Primary Dementia: It is only natural that there would be a number of various manifestations of primary dementias. Some neurotoxins would primarily affect one aspect of behavior, while others would be more likely to affect other aspects of memory or various other forms of antisocial behavior. These differences would be dependent on a combination of the chemical structure and quantity of neurotoxins produced in addition to innate intelligence and prior education of each afflicted patient.

It is most likely that the chemical structure, spatial configuration and quantity of specific neurotoxins will prove to correlate directly with the characteristic type of observed dementia or specific neurodegenerative disease diagnosed.

H. The single most obvious neurotoxin is excessive alcohol intake. Not only is alcoholism recognized by friends and family, it is generally recognized by the patient himself. Most importantly, it is recognized by law, to the extent, that the quantity of alcohol present in the patient’s blood provides legal evidence for conviction of a crime/ misdemeanor.

Revised and Updated 11/15/2017, 03/09/2018

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Proposed Treatment Options

Hepatic Generated Neurotoxins are the Proximate Cause for Neurodegenerative Diseases, including Alzheimer’s, ALS, Parkinson’s, Multiple Sclerosis and Age Related Macular Degeneration.

A logical extension of these heretical ideas, should they prove to be correct, lies on uncharted waters. Proposing this idea will lead many fellow professionals to openly question the sanity of the author.

4B-1. A liver transplant (replacement) in a patient afflicted with ALS will very likely prevent the inevitable progression of ALS giving afflicted patients a more normal life expectancy.

There is minimal probability that any benefit would be seen in Alzheimer’s patients primarily because of the extended duration of the prodromal period prior to diagnosis of this disease. A very high percent of the memory neurons in Alzheimer’s patients would have already died during the prodromal period.

It should be a foregone conclusion, that when a young, intelligent, otherwise healthy patient, is diagnosed with ALS, and is informed he has a 95-100% of dying within a few years, he might opt for an experimental liver transplant. In the past decade, the number of liver transplants has remained relatively constant in the range of 5,000 – 6,500 per year. Average survival is in the range of 15-20 years, greatly dependent on the patient’s willingness to take care of themselves.

Liver transplants are painful, expensive and fraught with unforeseeable complications. At present they are reserved exclusively for patients with, terminal liver disease who would be dead without one, within a matter of days or weeks.

The probability of peri-operative death resulting from a liver transplant is currently in the range of less than 1 %. Other complications, such as unanticipated drug reactions causing life threatening complications are well documented. Infections occurring in an immuno-suppressed patient are well recognized complications. A few might prove fatal.

In view of the fact this proposal for an experimental liver transplant is so far outside what most might consider rational thought the author feels obligated to expand on the pros and cons to any prospective patient considering such a decision.

When an attending physician speaks to a patient and his family with ALS he is obligated to present all relevant facts: ALS is a debilitating and inevitably fatal disease with death occurring in less than 48 months in more than 90 % of afflicted patients. In several Scandinavian countries suicide is an acceptable alternative treatment for patients with ALS. (10)

The author conceived this currently heretical idea that a liver transplant will arrest the progression of muscle weakness in ALS purely by deductive reasoning. There are no experimental animal models in which to test this theory in a laboratory.

Should the premise of the “Liver Brain Theory” prove to be correct, as the author believes it will be, a new healthy liver will not continue to produce the hepatic generated neurotoxins he theorizes to be the proximate cause of ALS. Should this theory be validated, a successful liver transplant in an ALS patient would likely give an ALS patient a more normal life expectancy

4B-2. Approximately 5,000 to 6,500 liver transplants have been performed annually in the past decade in the US. The number of transplants is limited only by the number of healthy transplantable livers. Because of the paucity of transplantable livers, the recent trend is for a family member to donate part of his liver to a related patient near death from end stage liver disease. Current estimates are that 3-5% of liver transplants are now from live donors. The first patient to receive part of her dad’s liver recently celebrated her 25th post-transplant anniversary. The human liver is the only human organ that can regenerate itself.

Total debunking of this heretical theory will have major benefit: it will allow others to be willing to propose new ideas, without acquiring the stigma of being labeled as “crazy” as this author anticipates he will be.

(1) Suggested Clinical Studies
Selection of Patients

Although the incidence of Alzheimer’s is approximately 50-100 times more common more than ALS. Alzheimer’s patients have no easily quantifiable disease related factors amenable to measurement, with assured reproducible accuracy. As such, patients with Alzheimer’s disease are not suitable for most initial clinical studies.

Patients with ALS have a distinct and unique disease related measurable factor, “muscle strength.” Muscle strength can be measured repetitively with decimal like precision over time. Even more important, these measurements can be made with simple readily available noninvasive techniques and instruments repetitively at minimal cost. (15)

Biting strength, merely another form of muscle strength should be easily quantifiable. It specifically measures the primary muscles of mastication: “temporalis, medial and lateral pterygoids.” This measurement is unique in that these muscles are innervated by an intracranial nerve: the third (V3) division of the trigeminal nerve. By recording these measurements and systematically plotting their natural course of progressive muscle weakness over a period of time, one can measure the rate of decline in muscle function of both somatic and cranial nerves separately, but simultaneously.

As noted elsewhere, these simple measurements could have been completed for a pittance more than 50 years ago. Even today there is minimal, if any, published data recording whether cranial or somatic nerves degenerate at the same or differing rates in patients afflicted with ALS.

The author suggest it would be far more advantageous and cost effective initially to study ALS in specific detail, rather than embark on a random, directionless and most likely futile study of Alzheimer’s or other degenerative brain or nerve diseases.

The very first clinical studies must attempt to measure, quantify, retard or alter the rate of progression of loss of muscle strength in patients with ALS, both by age of onset and sex.

Several simple dietary studies in patients with ALS are mandatory. (a) Does altering the amount of specific proteins affect the rate of muscle loss and strength?

Simply confirming that the rate of progression of ALS can be altered should provide an additional impetus for further evaluation of dietary factors. If such simple studies confirm that diet alone, can alter the rate of progression, in matched controls in patients with ALS, this seemingly insignificant study will provide the first real evidence ever; ALS might be amenable to treatment.

Another simple question pertinent to diets is: Do absolute vegetarians have the same, lesser or greater incidence of ALS in particular? An equally important question: If an absolute vegetarian does develop ALS, does it progress at the same or lesser rate than in non-vegetarians?

It is imperative to appreciate that there may be substantial differences between various types of vegetarian diets as determined in a recent study of the incidence of colorectal cancers in vegetarians. (12)

The Liver Brain Theory predicts that certain types of vegetarians (yet to be determined) would have both a decreased incidence of ALS as well as a decreased rate of progression compared to non-vegetarians. The exact type of vegetarian diet that might influence the rate of progression of ALS can be determined only by additional study using the parameters noted in the references cited. (12)

Another simple inexpensive clinical study, specifically related to Alzheimer’s is as follows: does the amount, duration, frequency or age of onset of alcohol abuse, correlate with the age of onset, or incidence or rate of progression of Alzheimer’s? The liver brain theory states the answer should be self evident: Suggestive evidence should be manifest in almost every homeless shelter!

One more question seeking an answer. Do children raised by mother’s (mother’s milk) or children raised with prepared “milk” have the same incidence of Alzheimer’s? The answer to this simple question may provide additional insight addressing the question: Which type of cells, glial cells or neurons are the primary target cells of neurotoxins? Very recent studies by Zang and Sloan appear to have the potential to answer this question in short order. (12)

Current studies suggest that the overwhelming majority, if not nearly 100%) of intracranial neurons are formed in utero or early in the neonatal period. Other studies suggests that a high percentage of glial cells (if not the majority) are formed post-partum. Even more relevant is the observation that the majority of glial cells continue to maintain their ability to replicate. Equally important is recent but unconfirmed observation that certain types of glial cells may replicate (or migrate) in response to specific stimuli.

Although there appears to be minimal agreement concerning the ratio of glial cells to cerebral neurons in various and specific areas of the brain, this author would favor the proposition that it is the primary death of glial cells that precipitates Alzheimer’s, by the simple process of starvation of their anatomically adjacent, nutritionally dependent memory neurons.

(2) Suggested Laboratory Studies
In Pursuit of the Proximate Cause of ALS

The simplest and least expensive initial laboratory experiments would entail obtaining liver tissue from recently diagnosed or deceased patients with all types of neurodegenerative diseases, in addition to patients with alcoholic cirrhosis.

Aliquots of fractioned homogenized liver specimens should be added to glial-nerve cell cultures. The end point would be documenting the presence of neuronal-glial degeneration, deformation or cell death in otherwise once thriving nerve- glial cells cultures.

The importance of obtaining specimens from younger patients with neurodegenerative diseases cannot be over emphasized. This theory predicts that the younger the patient, the greater the concentration of neurotoxins, or that those that are present, are much more neurotoxic.

May I ask each serious researcher in this field a simple question? Could you be opened minded enough, to accept the possibility, however remote, that many neurodegenerative diseases including Alzheimer’s, ALS, Parkinson’s, Multiple Sclerosis and some forms of macular degeneration are secondary to an aging liver, producing neurotoxins?

Additionally I humbly suggest to every student of neurodegenerative diseases, if you are unwilling to consider this theory worthy of further study, you have a personal obligation to develop one of your own!

We would be honored to publish your theory here without further review!

3) Proposed combined clinical and laboratory studies

An initial two pronged effort is mandatory, especially in young recently diagnosed patients with ALS. While one group seeks to verify the presence of neurotoxins, as outlined above, another team should attempt to remove them by vigorous and repetitive plasmapheresis using standard techniques.

It is more than reasonable to speculate that a certain percent of neurotoxins would be circulating continuously. Some neurotoxins, already intracellular, but unattached, might possibly be eluted due to a difference in concentration gradients, resulting from vigorous plasmapheresis. Any statistically significant data, confirming the slowing of the rate of progression of ALS, must be pursued with renewed vigor.

In summary, a few simple inexpensive studies may well provide the first real clues to the causes of neurodegenerative diseases. Should only a tiny fraction of this hypothesis be confirmed, many forms of neurodegenerative diseases could possibly be of historical interest only in less than a decade or two.

4) A simple logical question without a simple answer: Is it conceivable that vigorous mental gymnastics can delay, retard or possibly preclude the development of Alzheimer’s

Could there possibly be a biologic similarity between what weight lifting does to the muscle mass, and what repetitive cognitive function means to brain function? Weight lifting does not increase the number of muscles cells, but does increase the number of muscle fibers in individual muscle cells. It is generally accepted that most neurons do not replicate after birth, but on the other hand glial cells can and do so.

Could it be reasonable to ask a simple question? Can maximum cognitive function (E .g) playing chess, backgammon or bridge) stimulate the replication of glial cells rendering their associated neurons more efficient in processing increased data while providing them an additional level of sustenance.

Many students of Alzheimer’s appear to have adopted their own plans to reduce their personal likelihood of developing this terrible disease: vigorous mental gymnastics on a regular basis: reading, writing, playing chess, or other demanding cognitive functions such as serious investing of one’s own money.

No better example of this latter endeavor could be found in that of the recent public virtuoso performance on TV station CNBC by one the worlds’ most sophisticated investors and wealthiest men: Warren Buffet. This 85 year old gentleman recently presented his overview of the world’s economy and in doing so discussed the pro and cons of investing in a variety of public companies, while citing specific balance sheet figures, essentially hieroglyphics to all but a few. In addition he proudly admitted to playing chess (online) at least 10 hours a week.

Is Buffet’s exceedingly astute mental function at age 85, purely happenstance, a derivative of family genetics, (His dad was a Congressman.) or is it demonstrable and definitive proof that there is real validity in routine mental gymnastics?

The exact same question can be asked of his 94 year old business partner, Mr. Charles Munger. This gentleman is cited as being one of Mr. Buffet’s closest advisors. His mental gymnastics appear to have kept his thought processes equally astute.

From a strictly personal point of view, these assumptions appear to be worthy of further study. Unfortunately, the author was unable to find a single controlled study addressing or supporting this premise.

Here again it is very sad to recognize that a near definitive answer to this simple question could have been achieved for only a pittance as long as a half century ago. How? Simply by comparing the statistical probability of developing Alzheimer’s in two age controlled groups: those who read, write and think versus those who snooze, sleep, and snore!

The very concept that merely using one’s brain could possibly influence the development of a neurodegenerative disease appears biologically improbable. Nevertheless it is imperative to recognize that the cellular composition of the brain is substantially different than any other organ system. The brain basically has two distinct types of cells, neurons and glial cells. There is little evidence that neurons retain their ability to replicate postpartum. Glial cells definitely do retain this ability on a near life time basis. Is it conceivable to assume that vigorous mental gymnastics have the ability to stimulate the replication of glial cells and in doing so preserve and prolong the life and function of their adjacent neurons?

“A multimillion dollar question”

Does the presence of Amyloid Plaques commonly associated with Alzheimer’s, play a causative role in the development of this disease, or are they nothing more than the tombstones of an aggregation of dead neurons and their physically adjacent dead glial cells?

There is insufficient data to attempt to answer this question at this time. The liver brain theory suggests that Amyloid plaques might well prove to be nothing more than tombstones, marking the graveyard site of an aggregation of dead neurons, a variety of glial cells, most frequently astrocytes and microglial cells.

Concluding Remarks:

I openly hypothesize: (my best educated guess) is that the inciting cause of neurodegenerative diseases originates in the patient’s own liver, leading to a cascade type reaction possibly playing a major role in formation of tau Proteins.

The Alzheimer’s brain is most likely to be an innocent victim of its own aging liver.

The very first question any neurologist-- physician might ask: Why would a retired surgeon, now an octogenarian, have wasted his time for the previous -8 plus years, seeking a solution to these complex diseases that have defied a definitive answer for the past century?

“He would have been much more likely to have been successful had he gone fishing instead!”

The first answer is simple: I had no other choice, for reasons sufficient to myself, but to proceed to study Alzheimer’s disease in detail. I did so, but from an entirely different perspective from that of a budding neurology resident, hoping to pass his boards the first time around. I studied these diseases from the perspective an experienced, knowledgeable retired surgeon:

(1) Everything has a cause!
(2) What is the cause (etiology) of Alzheimer’s or ALS?

In the author’s opinion, it is just a question of a relatively short time, before someone with an open mind, using the scientific method, will soon discover the answers to questions 2 & 3.

The more I read, the more I was convinced of two things in particular:

(1) The cumulative knowledge of causation of ALS, Alzheimer’s and most forms of neurodegenerative diseases is minimal at best.
(2) Shared ignorance is the rule among the so called “experts“.

Another reasonable conclusion appears to be quite apparent: it is highly unlikely that any meaningful progress can be made in the study of Alzheimer’s disease simply because of the fact there is nothing to measure with any degree of accuracy over time.

Variables such as innate intelligence, education, family support, including financial resources, and the ready availability of medical care, are so significant, that it is highly unlikely any reliable control groups can be established. The importance of innate intelligence cannot be over emphasized

Were one individual tested be in the upper decile of innate intelligence be compared with a similarly aged individual in the lowest decile of intelligence, sustain the loss of 10% of memory neurons, the resulting clinical course could very well result in a dramatically different outcome. The more intelligent individual would most likely be recognized as being less sharp than usual. The less intelligent individual could possibly require institutionalization!

Patients classified with primary dementias are much too amorphous as a group to warrant further intensive study at this time. To do so would be folly and a waste of valuable resources.

A logical conclusion of this theory would predict that is very likely that the proximate causal factors of ALS will be recognized long before the etiology of Alzheimer’s is even imagined.

Restating this proposition in the NEGATIVE, in the author’s opinion: The proximate causes of Alzheimer’s will never be determined prior to elucidating the proximate cause of ALS.

Sometime in the near distant future, the primary cause of Alzheimer’s and many other forms of neurodegenerative diseases will almost certainly be determined: The definitive answerer will most likely include the following sentence:

“The proximate cause of Alzheimer’s disease is directly attributable to: primary, age related, hepatocyte dysfunction”.

Rev: 3/20/2015, 2/14/2016--- 04/17/2016—7/16/2017, 03/0//2018

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