Dr. Charles R. Sachatello, a retired physician, announced today that he has published the single most comprehensive theory ever developed attempting to identify the inciting causes and the reasons for the progressive course of neurodegenerative diseases, specifically including Alzheimer’s , Amyotrophic Lateral Sclerosis (ALS) and certain forms of Primary Dementis. (Non-Vascular Senile Dementias)

This multi year effort prompted Sachatello to propose that Alzheimer’s, and Amyotrophic Lateral Sclerosis (ALS), aka Lou Gehrig’s disease or “motor neuron disease” in Europe are essentially the same disease having a common cause: “Neurotoxins” produced in each patient’s own liver.

Hepatic generated neurotoxins most likely derive from the inability of the patient’s own liver to completely metabolize a variety of substrates including intact native protein complexes it encounters during the daily routine metabolic processes necessary to sustain life. The great majority of these incompletely metabolized substrates are innocuous. Others could well have varying degrees of neurotoxicity. Specific Alzheimer’s and ALS neurotoxins will vary in both the strength of their neurotoxicity and in the quantity produced by each patient’s own liver.

This basic premise of the Liver-Brain-Theory easily accounts for the prolonged, but variable length of the prodromal period of Alzheimer’s (5-10 years). Likewise it provides a ready explanation for the fact that prodromal period of ALS is much shorter than that of Alzheimer’s, most likely in the range of a year or less.

The author of the liverbraintheory is acutely aware of the heretical nature of many of his ideas to the point that many will question his sanity. Nevertheless the basic premise of the Liver-Brain-Theory is easily testable. The logical conclusion of this heretical theory is simple and straight forward.

A liver transplant (replacement) may very well immediately arrest the further production of these specific neurotoxins resulting in a dramatic decrease in any further loss of muscle strength typically seen in patients with ALS.

A liver transplant will not be able to restore previously lost muscle strength or strengthen atrophied muscles, but is very likely to give an ALS afflicted patient a more normal life expectancy. A liver transplant should have minimal effect in Alzheimer’s because of the extended prodromal course of this disease.

If only a single patient with ALS is confirmed to have documented cessation of additional muscle loss following a liver transplant, the basic premise of the Liver-Brain-Theory will have been validated: “Hepatic generated neurotoxins are the proximate cause(s) of ALS”.

Confirmation of this theory should encourage others to concentrate on isolating and identifying the exact chemical composition and structural configuration of the ALS neurotoxin(s). A secondary corollary of the Liver-Brain-Theory is that nearly identical neurotoxins will be found to be the proximate cause(s) of Alzheimer’s and certain forms of Primary Dementia.

Once the specific neurotoxin(s) causing ALS are identified with absolute certainty, worldwide attention must be directed to finding the nearly identical hepatic generated neurotoxins that Sachatello predicts will be confirmed to be the proximate cause of Alzheimer’s. All subsequent research efforts should focus on studies of the spinal fluid, hepatocytes, glial cell cultures and brains of recently deceased patients with Alzheimer’s attempting to isolate and identify the specific Alzheimer neurotoxin(s). (Sections 3 -5)

This theory also predicts that it should be relatively easy to synthesize protein blocking or neutralizing agents precluding the development of additional neurotoxins eliminating or minimizing their neurotoxic effects. Such agents should be able to prevent further symptomatic progression of both ALS and Alzheimer’s in currently afflicted or newly diagnosed patients.

"January 7, 2015 (via email)
Dr. Charles Sachatello

Dear Charles:

I always enjoy hearing from you and especially reports about your liver-brain-theory. As you have emphasized, the ultimate test of the hypothesis would be liver replacement.

Thus, it would be very difficult, particularly in today’s climate to justify liver transplantation for the indication of ALS. Be that as it may, I continue to watch your initiatives with lively interest.

With best regards,

Thomas E. Starzl, M.D., Ph.D.
Professor of Surgery
Starzl Transplant Institute
Pittsburgh, PA"

CRS, additional comments:

Repetitive Plasmapheresis has to potential to mimic a liver transplant with respect to neurodegenerative diseases on a short term basis by reducing the quantity of circulating neurotoxins as evidenced by a marked and measurable reduction in the rate of muscle loss and corresponding loss of muscle strength in patients afflicted with ALS.

Only a liver transplant will permanently arrest the production of additional hepatic generated neurotoxins until specific blocking agents can be discovered and manufactured.

- CRS MD FACS, 9/25/2016