Abstract
Alzheimer's disease is a severe neurodegenerative disorder and the most common cause of dementia in the population above 60 years of age. Beta-amyloid accumulation and neurofibrillary tangles formation in the brain precedes the development of Alzheimer's dementia by many years.
As beta-amyloid accumulation inhibition failed as a treatment option, the theories on the Alzheimer's disease pathophysiology are being revised. In this context, research targets the role of inflammation as the possible trigger mechanism and accompanying process of neurodegeneration.
This article summarizes some knowledge of the immune function of brain cells and its potential relation to Alzheimer's disease progression in the light of the immune reaction hypothesis.