Inflammatory pathogenesis in Alzheimer's disease: biological mechanisms and cognitive sequeli

Citation
E. Gahtan et Jb. Overmier, Inflammatory pathogenesis in Alzheimer's disease: biological mechanisms and cognitive sequeli, NEUROSCI B, 23(5), 1999, pp. 615-633
Citations number
196
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
ISSN journal
01497634 → ACNP
Volume
23
Issue
5
Year of publication
1999
Pages
615 - 633
Database
ISI
SICI code
0149-7634(199905)23:5<615:IPIADB>2.0.ZU;2-U
Abstract
Experimental evidence from molecular biology, biochemistry, epidemiology an d behavioral research support the conclusion that brain inflammation contri butes to the pathogenesis of Alzheimer's disease and other types of human d ementias. Aspects of neuroimmunology relating to the pathogenesis of Alzhei mer's disease are briefly reviewed. The effects of brain inflammation, medi ated through cytokines and other secretory products of activated glial cell s, on neurotransmission (specifically, nitric oxide, glutamate, and acetylc holine), amyloidogenesis, proteolysis, and oxidative stress are discussed w ithin the context of the pathogenesis of learning and memory dysfunction in Alzheimer's disease. Alzheimer's disease is proposed to be an etiologicall y heterogeneous syndrome with the common elements of amyloid deposition and inflammatory neuronal damage. (C) 1999 Elsevier Science Ltd. All rights re served.