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Alzheimer's: a neurodegenerative disease


"I consider it ironic, that the pharmaceutical industry is investing vast resources in the development of glutamate receptor blockers to protect CNS [central nervous system] neurons against glutamate neurotoxicity in common neurological disorders, while at the same time the food industry, with the blessing of the FDA, continues to add great quantities of glutamate to the food supply."

-- Richard C. Henneberry, Ph.D.
    Director, Neuroscience Program
    Conte Institute for Environmental Health

    Bethesda, MD,  April 7, 199

There is an area of research for which the food industry, to date, has had no comment, contradiction or excuse. These are studies, designed to identify drugs with which to treat neurodegenerative diseases such as Alzheimer's and Parkinson's disease -- diseases in which glutamic acid seems to play some role.

Discovery that MSG caused lesions in specific areas of the brains of laboratory animals and concomitant proliferation of neuroendocrine dysfunction came through interest in the brain. It was brain research that identified glutamic acid as a possible, probable, and now certain neurotransmitter, transmitting nerve impulses. Likewise, it was study of the brain that suggested that a group of these neurotransmitters, specifically the excitatory amino acids (EAA), possess properties that very likely play an important role in the development of certain neurodegenerative diseases.(172, 229-236)  Glutamic acid and aspartic acid are among the EAA that have great potential for involvement in neuro-degenerative disease. Aspartame is approximately 40% aspartic acid.

At the present time, significant headway in the study of neurodegenerative disease is being made. "Three EAA receptor subtypes that mediate excitotoxicity have been identified, drugs with anti-excitotoxic actions have been discovered, and evidence for the complicity of both exogenous and endogenous excitotoxins in neurodegenerative disorders has begun to unfold. There now is substantial evidence for the involvement of each EAA receptor subtype in one or more human neurodegenerative syndrome, and recent findings suggest that EAA receptors are sensitive mediators of excitotoxicity at both ends of the age spectrum."(231)  All forms of MSG are exogenous sources of glutamic acid; and many foods that contain MSG also contain neurotoxic free aspartic acid. This includes the MSG produced when protease enzymes or reaction flavors are used in manufactured or otherwise processed food. Processed free glutamic acid (MSG) always contains free glutamic acid, an EAA.

It has been suggested, and there is evidence to support the suggestion, that the EAA might well play a role in the following neurodegenerative conditions: sulfite oxidase deficiency; epileptic, hypoglycemic and hypoxic/ischemic brain damage; central nervous system trauma; dementia pugilistica; domoate dementia; olivopontocerebellar degeneration; neurolathyrism; amyotrophic lateral sclerosis (ALS), parkinsonism, Alzheimer's dementia; Huntington's disease; and Wernicke/Korsakoff syndrome.(231)  Together, these conditions are referred to as the glutamate cascade.

In October, 2003, the U.S. Food and Drug Administration (FDA) approved Namenda, the first drug developed for people with advanced Alzheimer's.  According to an article in the AARP Bulletin (AARP Bulletin /July-August 2004, p13) "the drug blunts the brain chemical glutamate [glutamic acid] which can accumulate abnormally and kill brain cells."

Memantine (Namenda) for Moderate to Severe Alzheimer's Disease

March 15, 2004 American Family Physician
ADRIENNE Z. ABLES, PHARM.D., Spartanburg, South Carolina

Synopsis: Memantine (Namenda) is an N-methyl-d-aspartate (NMDA) receptor blocker indicated for the treatment of moderate to severe Alzheimer's disease (AD). The NMDA receptor is activated by glutamate, the primary excitatory neurotransmitter in the brain. Overstimulation by glutamate may result in neuronal damage and has been implicated in neurodegenerative disorders such as AD. Memantine is the first pharmacologic agent approved by the U.S. Food and Drug Administration for the treatment of moderate to severe AD. (Bold words added for emphasis.)

According to an article in the St. Petersburg Times (Lynn Stratton, September 25, 2005, St. Petersburg Times Perspective Online), "...the same company [Ajinomoto] that produces a food additive linked to neurological damage and obesity [monosodium glutamate] is also involved in producing a drug [Memantine] that can block the effects of that additive after we consume it."  According to the article, Ajinomoto's pharmaceutical arm, Ajinomoto Pharma, partners with a company called Daiichi Pharmaceuticals. Daiichi partners with Merz Pharmaceuticals. And Merz produces Memantine.  That's right.  Ajinomoto, the worlds' largest producer of free glutamic acid and also the world's largest producer of the food ingredient called "monosodium glutamate," has a financial interest in Memantine (Namenda), the first drug developed for people with advanced Alzheimer's -- a drug which, according to the AARP (AARP Bulletin / July-August 2004, p 13), "...blunts the brain chemical glutamate [glutamic acid] which can accumulate abnormally and kill brain cells."

According to the Internet's adam.about.com, "...a number of experimental drugs are [also] being investigated for Parkinson's disease because they block the actions of glutamate, an amino acid that is a particularly potent nerve cell killer. Some of these drugs block a receptor group to glutamate called N-methyl-D-aspartate (NMDA). Investigative NMDA antagonists include remacemide, memantine, riluzole, and budipine." (http://adam.about.com/reports/000051_7.htm)


172.  Olney, J.W. Excitatory neurotoxins as food additives: an evaluation of risk. Neurotoxicology 2: 163-192, 1980.

229.  Olney, J.W. Excitatory amino acids and neuropsychiatric disorders. Biol Psychiatry 26: 505-525, 1989.

230.  Choi, D.W., and Rothman. S.M. The role of glutamate neurotoxicity in hypoxic-ischemic neuronal death. Annu Rev Neurosci 13: 171-182, 1990.

231.  Olney, J.W. Excitotoxic amino acids and neuropsychiatric disorders. Annu Rev Pharmacol Toxicol 30: 47-71, 1990.

232.  Olney, J.W. Excitotoxicity: an overview. Biol Psychiatry 27: 90A, 1990. (Abstract)

233.  Coyle, J.T. Glutamate receptors and age-related neurodegenerative disorders. Biol Psychiatry 27: 91A, 1990.

234.  Pomara, N., Deptula, D., Singh, R., LeWitt, P.A., and Banay-Schwartz, M. Excitatory amino acid concentrations in CSF of patients with Alzheimer's disease. Biol Psychiatry 27: 91A, 1990.

235.  Zukin, S.R., and Javitt, D.C. The NMDA-PCP theory of schizophrenia: implications of receptor interactions. Biol Psychiatry 27: 91A, 1990.

236.  Olney, J.W. Excitotoxins and neurological diseases. Proceedings of the 11th International Congress of Neuropathology, Kyoto, Japan, September 2-8, 1990.

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