Several lines of evidence, including newly discovered genetic mutations, suggest that beta-amyloid (A beta) is directly involved in the neuropathology observed in familial and sporadic forms of Alzheimer's disease (AD). Rather than exerting its neurotoxicity directly, results from our laboratory suggest that fibrillar A beta (fA beta) activates microglia and astrocytes upon injection into the rat brain. The microglia and astrocytes, in turn, form a functional barrier between A beta and surrounding neurons. An increase in inducible nitric oxide synthase (iNOS) immunoreactivity is observed in activated microglia and astrocytes, and specific subpopulations of neurons are lost in fA beta injection areas versus controls. These data, coupled with recent discoveries of the A beta association with the receptor for advanced glycation end products (RAGE) and the class A scavenger receptors (SR), support the hypothesized role of inflammatory mechanisms in AD neurotoxicity.
|Original language||English (US)|
|Volume||52 Suppl 2|
|State||Published - Sep 1997|
ASJC Scopus subject areas
- Geriatrics and Gerontology