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| First Name: | Steven | | Last Name: | Brenner | | Title: | MD | | Advanced Degrees: | Neurology Residency | | Affiliation: | Saint Louis University | | Department: | Neurology and Psychiatry | | Street Address 1: | Monteleone Hall | | Street Address 2: | 1438 South Grand Boulevard | | City: | Saint Louis | | State/Province: | MO | | Zip/Postal Code: | 63104 | Country/Territory: | U.S.A. | | Phone: | (314) 977-6082 | | Fax: | (314) 977-6086 | | Email Address: |  |
Disclosure:
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Member reports no financial or other potential conflicts of interest. [Last Modified: 10 September 2011]
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View all comments by Steven Brenner
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Alzheimer Disease, Aging Process, Stroke and Trauma, Parkinson Disease
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Diagnosis, Epidemiology, Oxidative Stress, Apoptosis/Cell cycle
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I have worked primarily as a clinician but have done work in attempt to develop an animal model of Alzheimers disease, and worked in the last few years in a part time capacity with reference to understanding aluminum toxicty and also cell death studies with reference to neuronal injury and ischemia models.
I have developed an interest in nutritional aspects of the epidemiology of neurodegenerative disease such as Alzheimer's disease and various cultural aspects of neuroepidemiology in different cultures. |
1.Neurogenesis or regeneration of the nervous system.
2.Also basic aspects of aging and if aging as such leads to development of degenerative disease, or if neurodegenerative disease would be likely to occurr even if basic biological mechanisms of aging are understood and overcome.
3. Understanding if Alzheimer's disease is a deficiency disease, such as Parkinsonism with a deficiency of dopamine, or rather is a progressive destructive disease due to loss of basic protective mechanisms from aging.
This probably implies a basic understanding of aging, and what occurrs to cellular protective mechanisms. I have tried to pose the question "Why don't children develop Alzheimer's disease?" in order to focus attention on understanding basic mechanisms of cellular function during childhood, adulthood and senesence. |
an article on insulin like growth factor and its influence on beta amyloid in Nature Medicine.
Sulfatide levels in spinal fluid in Annals of Neurology in the August Issue. |
1. Studying carnosine and homocarnosine levels in brains of demented persons with nuclear medicine spectroscopy. If there was such as deficiency noted on spectroscopic investigations, then by implication oligodendrocytic function would be deficient.
Restoring levels of carnosine and carnosine like substances with carnosine supplements or carnosine precursors might be of some value.
Some anticonvulsants are know to increase the levels of homocarnosine in epileptics and might be benificial for Alzheimer patients especially since some of them develop seizures related to Alzheimer's disease.
2. Effect of multiple nutritional agents in progression of Alzheimer's disease. Recent studies of the effect of Co enzyme Q 10 on progression of Parkinson's disease may have some importance in focusing attention in other neurodegnerative diseases.
3. Effect of melatonin on oxidative stress in Alzheimer's disease.
4. Studying peripheral biological markers of Alzheimer's disease to determine if there are systemic functions which reach beyond the nervous system.
5. Studying the oldest old with reference to basic metabolic function, hormonal status and activity levels to determine if there is some intrinsic resistance to Alzheimer's disease in some persons. This would be an attempt to see if everyone actually has some form of Alzheimer's disease but only a few people develop susceptibility to development of the disease through lack of resistance.
Also studying such patients mitochondrial function might have some indication of oxidative function in such patients. |
My current hypothesis is protective substances from white matter, probably oligodendroglial cells become deficient through injury or deterioration of blood brain barrier and oxidative stress leading to loss of carnosine and sulfatides, with multible deficiencies leading to neuronal stress and probably accelerated production of beta amyloid which is a well recognized neurotoxin. Protective elements would likely include carnosine and carnosine like elements which have antioxident effects, metal chelation effects and also may have some effect on prevention of beta amyloid aggregation
It may be termed a garden hypothesis, in that in the garden the earth supplies the nutrients to the vegetables, by analogy the neurons.
If the moisture is deficient, then the vegetables will wither, and although they may not die, they will not be productive, likewise if minerals are deficient or nutrients deficient then the vegetables will not be productive.
By analogy, the white matter, made up of astrocytes and oligodendrocytes would be the earth. If there are nutritional deficiencies then the neurons could not be expected to be productive of neuortransmitters and synaptic vessicles needed for normal neuronal communication in neuornal tracts and at synapses.
There may not be any one particular nutrient which leads to neuronal deterioration but if any of the necessary nutrients, and energy supplies are deficient then neuronal function would suffer and probably defensive mechanisms against oxidative stress would also be effected. |
Carnosine and homocarnosine levels detected by nuclear magnetic resonance spectroscopy of the brain could help to determine if such compounds are missing in the brain in development of Alzheimers disease.
Carnosine is known to be present in the olfactory system, and Alzheimer's patients frequently lose their smell.
If levels of carnosine or homocarnosine could be boosted in some way and the patients clinical status improved, then it would be confirmatory of the carnosine deficiency hypothesis. |
Oligodendrocyte function probably is very sensitive to dysfunction of the blood brain barrier. If the blood brain barrier was not functioning normally, then glial function and subsequently neuronal function would be impaired.
Beta amyloid is known to cause a vasculopathy in susceptible individuals and could be expected to cause dysruptions of nutrient supply from the vasculature to the neuron. |
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