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Book ChapterDOI

Trophic Factors in Brain Aging and Disease

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TLDR
To understand the quantitative alterations in the brain of patients with these disorders, it is necessary to define the extent to which normal individuals demonstrate alteration in the number of neurons, in microscopic pathology, and in neurotransmitter metabolism during the aging process.
Abstract
Success in treating and preventing infection and vascular disease has led to a significant increase in the number of people over the age of 65. This increase in the elderly population has focused attention on normal changes of the aging brain and the chronic disorders that may develop during the aging process. Clearly, such disorders are not inevitable consequences of aging, but they are present to a greater extent in aged individuals. The two common conditions which fall into this category are parkinsonism and Alzheimer’s disease. Both of these devastating diseases of the nervous system are degenerative disorders of unknown origin. In each, multiple etiologies, including viral or immunologic causes, have been implicated but never proven. Both conditions reflect pathologic changes in relatively limited pathways within the central nervous system. In Alzheimer’s disease and, to a much lesser extent, Parkinson’s disease, changes are noted which are known to occur in healthy older individuals. Thus, both conditions may represent accelerated aging of specific neuronal pathways. In order to understand the quantitative alterations in the brain of patients with these disorders, it is necessary to define the extent to which normal individuals demonstrate alterations in the number of neurons, in microscopic pathology, and in neurotransmitter metabolism during the aging process.

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Citations
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Journal ArticleDOI

Brain aging and Alzheimer's disease: "Wear and tear" versus "use it or lose it."

TL;DR: This "use it or lose it" principle might explain why certain neurons degenerate in aging or Alzheimer's disease while others do not, and why recovery of various neuronal systems during aging has been obtained by restoration of the missing stimulus.
Book ChapterDOI

A Rationale for the Use of Melanocortins in Neural Injury

TL;DR: Evidence is presented that MSH-like peptides may be formed locally in response to injury and thus play a biologically significant role in the regulation of nerve regeneration.
Journal ArticleDOI

Neuropathobiology of senile dementia and mechanism of action of nootropic drugs.

Olga Benešová
- 01 Apr 1994 - 
TL;DR: Advances in neuroscience and molecular neurochemistry have substantially increased the knowledge of the neuropathobiology of senile dementia and Alzheimer's disease, including nootropic drugs with different mechanisms of action and heterogenous chemical structures.
Journal ArticleDOI

Future health care applications resulting from progress in the neurosciences: The significance of neural plasticity research

TL;DR: The possibilities and probabilities of future improvements in treatment and prevention for a number of nervous system disorders following from neural plasticity research are considered and the overall health policy implications are discussed.
Book ChapterDOI

Nimodipine and neural plasticity

TL;DR: Brain aging is often considered in terms of a reduced neural plasticity, but it has been shown that dynamic adaptive changes at the synapse may lead to totally different communication patterns, resulting in an altered output of the brain.
References
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Journal ArticleDOI

Alzheimer's disease and senile dementia: loss of neurons in the basal forebrain.

TL;DR: Demonstration of selective degeneration of neurons of the nucleus basalis of Meynert represents the first documentation of a loss of a transmitter-specific neuronal population in a major disorder of higher cortical function and points to a critical subcortical lesion in Alzheimer's patients.
Journal ArticleDOI

Growth of a rat neuroblastoma cell line in serum-free supplemented medium.

TL;DR: The rat neuroblastoma B104 cell line was able to proliferate in the absence of serum in synthetic medium supplemented with insulin, transferrin, progesterone, selenium, and putrescine, and in combination there was a marked synergistic effect on cell number.
Journal ArticleDOI

The nerve-growth factor.

TL;DR: Nerve growth factor is a signaling protein and growth factor implicated in a wide range of development and maintenance functions and has been implicated in immune function, stress response, nerve maintenance, and in neurodegenerative diseases.
Journal ArticleDOI

Scrapie prions aggregate to form amyloid-like birefringent rods

TL;DR: The findings raise the possibility that the amyloid plaques observed in transmissible, degenerative neurological diseases might consist of prions, a polymeric form of the scrapie prion.
Journal ArticleDOI

Reduced somatostatin-like immunoreactivity in cerebral cortex from cases of Alzheimer disease and Alzheimer senile dementa.

TL;DR: Results obtained with a RIA for somatostatin are reported, showing that som atostatin-like immunoreactivity in the cerebral cortex is reduced in tissue from AD/SDAT patients.