E. Gahtan et Jb. Overmier, Inflammatory pathogenesis in Alzheimer's disease: biological mechanisms and cognitive sequeli, NEUROSCI B, 23(5), 1999, pp. 615-633
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.