During the past 12 years, research on the etiology of Alzheimer disease (AD) has made dramatic advances. Although we still do not have a clear picture of what factor(s) cause AD, growing evidence indicates that the fundamental problem in AD is associated with the death of neurons. The purpose of this article is to re-evaluate in detail how the regulation of intracellular free calcium might play a critical role in cell death and in the expression of AD neuropathology. There is an urgent need to find means to ameliorate the symptoms of AD and ways to slow the progression of the disease process. Unfortunately, AD appears to be a very complex neurochemical puzzle.
|Original language||English (US)|
|Journal||Alzheimer Disease and Associated Disorders|
|Issue number||1 SUPPL.|
|State||Published - 1991|
ASJC Scopus subject areas
- Geriatrics and Gerontology
- Psychiatry and Mental health