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

Experimental evidence from molecular biology, biochemistry, epidemiology and behavioral research support the conclusion that brain inflammation contributes to the pathogenesis of Alzheimer's disease and other types of human dementias. Aspects of neuroimmunology relating to the pathogenesis of Alzheimer's disease are briefly reviewed. The effects of brain inflammation, mediated through cytokines and other secretory products of activated glial cells, on neurotransmission (specifically, nitric oxide, glutamate, and acetylcholine), amyloidogenesis, proteolysis, and oxidative stress are discussed within the context of the pathogenesis of learning and memory dysfunction in Alzheimer's disease. Alzheimer's disease is proposed to be an etiologically heterogeneous syndrome with the common elements of amyloid deposition and inflammatory neuronal damage.