CONTENTS

In order of relevance



Excellence Award



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THEORIES & RESEARCH
that may be relevant to ALS/MND
(ALS) Amyotrophic Lateral Sclerosis or (MND) Motor Neurone Disease are referred to as ALS/MND.

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The man with a new idea is a crank until the idea succeeds.
Mark Twain

Information here may help in the treatment or understanding of ALS/MND. It is provided for your information only and I leave you to form your own opinions and conclusions.

I have included brief articles here that respond to questions I am frequently asked or that I feel are of particular relevance. As the ALS Research Digest and its archives provide a wealth of information I shall only be adding the occasional article to this page from the start of 2006. For all other current theories I would strongly urge you to subscribe via the links below.

If you wish to discuss these or other ALS/MND related ideas further, the ALS Digest and Braintalk offer good forums. You can subscribe to the ALS Digest, free of charge or participate in the Braintalk discussions (select ALS forum).

The ALS Research Digest, now compiled and updated by Danny Dandignac and Jeff Lester, is an ongoing memorial to Will Hubben's original selective and extremely useful source of ALS-relevant research information. Links to the latest ALS-relevant research articles and abstracts is delivered, free, directly to your computer.

Sign up to receive The ALS Research Digest
Access the ALS Research Digest Archives

For the latest breaking news on ALS/MND Research go to http://www.braintalk.org and then select ALS. You can join the online forum at the same website to ask questions or discuss matters relevant to ALS/MND.
Eric Edney has succeded in treating and, to some extent, reversing the symptoms of ALS/MND.

He has written a book about his experience and his program to beat ALS. It contains details about his experiences over more than ten years with ALS. To order the book see Eric's website

Abnormal Gene: Toxic Cause of ALS/MND

Australian scientists headed by Prof Garth Nicholson from the ANZAC Research Institute believe they have discovered what causes ALS/MND.

An abnormal gene has been shown to kill the nerves from the brain to muscles in the body. It was found that a protein called TDP43 was present in large amounts in the spinal cords of people with ALS/MND and dementia, which can also occur with ALS/MND.

It was not known whether the TDP43 protein was trying to help the body recover from the disease or was actually poisoning the body. In families that have ALS/MND with a mutation in this gene, TDP43 seems to cause ALS/MND.

Many people have thought that ALS/MND might be caused by an environmental poison but it has been demonstrated that it is a poison in the body itself actually becoming dangerous and leading to the death of motor neurones.

If this is indeed the protein that's causing damage in the majority of patients with Motor Neurone Diseases, reducing the TDP43 protein could potentially prevent or cure the disease.

As ALS/MND is probably many diseases with wide variations this may reflect all different varieties of ALS/MND with different mechanisms. But if there's an underlying mechanism that's common to all, and because this protein is generally found in all MNDs, this does offer hope that a general treatment can be found for all types.

For more info and interview with Prof Nicholson.

This is wonderful news and Prof Nicholson, et al, are to be congratulated but, for the record, I would be astonished if this protien alone is the sole cause of such a variety of neurological symptoms. Steven Shackel Feb 2008. [See My Theory for why I think this is so].

In my opinion, the following article is one of the more significant findings in ALS/MND research for many years. Although this has been predicted on this website and elsewhere, this is the first scientific paper supporting the hypothesis.

Cell Environment's Important in ALS
Don Cleveland and Larry Goldstein, The Packard Center for ALS Research at Johns Hopkins Journal: Science 10.2.03

Cells that surround motor neurons, that aren't themselves nerve cells, can play a major role in advancing or limiting the disease.

A principle for extending survival or, perhaps, overcoming ALS, based on how many healthy cells surround an ailing motor nerve cell. Delivery of normal, non-neuronal cells to spinal cords, including stem cell therapies could prove completely protective, even without replacement of motor neurons.

In animal tests, although 75% of the motor neurons in spinal cords carried the mutant gene SOD1 (a known cause of familial ALS) all the motor neurons remained healthy, apparently from having healthy non-neuronal cells nearby.

A small number of normal cells effectively eliminated damage to motor neurons from the ALS-causing genetic error. The opposite effect also appeared: normal motor neurons surrounded by cells carrying an SOD1 mutation showed early signs of disease. Normal neurons can apparently acquire something toxic from at-risk non-neuronal neighboring cells.

A bad cellular environment can damage healthy cells. More importantly, surrounding neurons with healthy adjoining cells can significantly lessen toxic effects. In some cases, having normal cells completely stops motor neuron death.

See Archived Abstract

I believe this is a significant hypothesis that is consistent with my own theories as to what causes ALS/MND.

Hypothesis: A motor neuron toxin produced by a clostridial species residing in gut causes ALS 

We hypothesize that a yet-to-be-identified motor neuron toxin produced by a clostridial species causes sporadic ALS in susceptible individuals. This clostridial species would reside undetected in the gut and chronically produce a toxin that targets the motor system, like the tetanus and botulinum toxins.

After gaining access to the lower motor neuron, the toxin would be transported back to the cell body, as occurs with the tetanus toxin, and destroy the lower motor neuron - the essential feature of ALS. Again like the tetanus toxin, some of the toxin would cross to neighboring cells and to the upper motor neuron and similarly destroy these motor neurons. Weakness would relentlessly progress until not enough motor neurons remained to sustain life. If this hypothesis were correct, treatment with appropriate antibiotics or antitoxins might slow or halt progression of disease, and immunization might prevent disease

Longstreth WT Jr, Meschke JS, Davidson SK, Smoot LM, Smoot JC, Koepsell TD. Department of Neurology, School of Medicine, University of Washington, Seattle, Washington, USA; Department of Medicine, School of Medicine, University of Washington, Seattle, Washington, USA; Department of Epidemiology, School of Public Health and Community Medicine, University of Washington, Seattle, Washington, USA. Med Hypotheses. 2005;64(6):1153-1156.

Coenzyme Q10 Levels and ALS

Increased mitochondrial oxidative damage and oxidative DNA damage contributes to the neurodegenerative process in sporadic ALS.

A study involving 17 patients with sporadic ALS revealed the percentage of oxidized coenzyme Q10 and the concentration of 8-OHdG in the cerebrospinal fluid (csf) of the PALS was significantly greater than that found in 17 age-matched controls. The percentage of oxidized coenzyme Q10 in the csf was inversely associated with the duration of illness and the concentration of 8-OHdG in the csf was positively associated with the duration of illness.

The percentage of oxidized coenzyme Q10 was associated with the concentrations of 8-OHdG in the csf of PALS. The authors, who had set out to investigate whether mitochondrial oxidative damage or oxidative DNA damage contribute to the neurodegenerative process of ALS, conclude, "…both mitochondrial oxidative damage and oxidative DNA damage play important roles in the pathogenesis of sporadic ALS.
Murata T, Ohtsuka C, Terayama Y, Free Radic Res, 2008; 42(3): 221-5. (Address: Department of Neurology, Iwate Prefectural Ninohe Hospital, Iwate, Japan).

Lithium to Treat ALS/MND?