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Inflammation, Apoptosis, and Alzheimer's Disease

Alzheimer Research Laboratory Department of Neurosciences Case Western Reserve University School of Medicine Cleveland, Ohio

Gary E. Landreth

Alzheimer Research Laboratory Department of Neurosciences Case Western Reserve University School of Medicine Cleveland, Ohio;Alzheimer Research Laboratory, Case Western Reserve University, School of Medicine, 10900 Euclid Ave., Cleveland, OH 44106; gel2{at}po.cwru.edu

The pathophysiology of Alzheimer's disease (AD) involves the deposition of amyloid in the brain and the extensive loss of neurons. The mechanisms subserving neuronal death in the disease remain unclear, although it has been postulated that this is due to apoptosis. There is compelling evidence that inflammatory processes play a role in disease progression and pathology. Amyloid plaque deposition is accompanied by the association of microglia with the senile plaque, and this interaction stimulates these cells to undergo phenotypic activation and the subsequent elaboration of proinflammatory and neurotoxic products. This review focuses on the mechanisms by which neurons are lost in AD and the role microglial proinflammatory products play in neuronal death.

Key Words: Alzheimer's disease • Microglia • Inflammation • Apoptosis

The Neuroscientist, Vol. 8, No. 3, 276-283 (2002)
DOI: 10.1177/1073858402008003013


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