Özet:

Alzheimer’s disease (AD), which is mainly characterized by impaired memory, is a rapidly growing clinical and public health issue due tothe aging population. The neuropathological hallmarks of the disease include accumulation of senile plaques, composed of amyloid-beta, andneurofibrillary tangles. The amyloid-beta peptide (Aβ) cascade hypothesis suggests Aβ accumulation is the fundamental initiator and majorpathogenic event for AD. Recent genome-wide association studies have illuminated cluster of differentiation 33 (CD33) is a new geneticrisk factor for AD. CD33 as a type 1 transmembrane protein is mediating the cell–cell interaction. In the brain, CD33 is mainly expressed onmicroglial cells. In AD brain, the CD33 level is found to be positively correlated with amyloid plaque burden and disease severity.

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