Protein Modifications and Interactions in Alzheimer’s Disease

  • M. A. Smith
  • G. Perry
Part of the Ernst Schering Research Foundation Workshop book series (SCHERING FOUND, volume 17)

Abstract

Alzheimer’s disease, an age-related neurodegenerative disease, is characterized by several coincidental features including neuronal loss, neurofibrillary tangles and senile plaques. While the precise mechanism(s) underlying Alzheimer’s disease are incompletely understood, it is apparent that age is essential since the disease rarely strikes prior to age 55. Many other conditions such as emphysema, arthritis, and atherosclerosis also show an age-related penetrance and occur after the normal reproductive life span. This latter aspect is especially important since there is very little evolutionary pressure to maintain normal physiological relationships between biomolecules and preclude the development of these diseases. This lack of evolutionary selection allows altered or novel macromolecular relationships. Our hypothesis is that altered protein interactions and protein modifications could destabilize homeostatic relationships and/or be themselves damaging to the cellular system promoting the pathogenesis of Alzheimer’s disease and other chronic degenerative diseases.

Keywords

Proline Carbonyl Lysine Trypsin Neurol 

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Copyright information

© Springer-Verlag Berlin Heidelberg 1996

Authors and Affiliations

  • M. A. Smith
  • G. Perry

There are no affiliations available

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