Understanding neurodegenerative disease brain anoxia


And neurodegenerative disease

There is a relatively new area of research for which the food industry, to

Date, has had no comment, contradiction or excuse. These are studies which link

MSG to neurodegenerative disease.

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

brain anoxia

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.

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

brain anoxia

Excitotoxicity at both ends of the age spectrum.(231)

All forms of MSG are exogenous sources of glutamic acid, i.E., coming from

Outside of the body. There are over 40 ingredients that contain MSG without

Giving consumers a clue to its presence. In addition, MSG can be produced when protease enzymes or reaction

Flavors are used in the manufacture of 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;

brain anoxia

Amyotrophic lateral sclerosis, parkinsonism, alzheimer’s dementia; huntington’s

Disease; and wernicke/ korsakoff

Syndrome(231). These conditions are referred to as part of the glutamate



Following excerpt from the march 15, 2004 american

Family physician illustrates the relationship between glutamate and

Alzheimer’s disease.

Memantine ( namenda)

For moderate to severe alzheimer’s disease

Adrienne Z. Ables, pharn.D .,

Spartanburg, south carolina


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.Brain anoxia 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.


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,


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.Brain anoxia

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,


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,


236. Olney, J.W. Excitotoxins and neurological diseases. Proceedings

Of the 11th international congress of neuropathology, kyoto, japan, september

2-8, 1990.