CD33 and Alzheimer’s Disease

Abstract

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

Keywords

• Alzheimer’s disease,CD33,sialic ac,amyloid,neurodegenerative

CD33 ve Alzheimer Hastalığı

Öz

Hafızadaki bozukluklar ile karakterize Alzheimer hastalığı (AH) yaşlanan nüfustaki artış nedeniyle hızla büyüyen klinik ve halk sağlığı sorunu haline gelmiştir. Amiloid-beta (Aβ) yapısındaki senil plakların birikimi ve nörofibriler yumaklar hastalığın nöropatolojik özellikleri arasındadır. Aβ-peptid kaskad hipotezi, Aβ birikiminin AH için başlatıcı ve majör patojenik olay olduğunu düşündürmektedir. Son yıllarda yapılan genom çapında ilişkilendirme çalışmalarında, hücre-hücre etkileşimine aracılık eden ve Tip 1 transmembran proteini olan farklılaşma kümesi 33 (CD33 (cluster of differentiation 33)),  AH için yeni bir risk faktörü olarak önerilmektedir. Mikroglial hücrelerde ifade edilen CD33 düzeyinin amiloid plak miktarı ve hastalık şiddeti ile ilişkili olduğu bulunmuştur.

Anahtar Kelimeler

• Alzheimer Hastalığı,CD33,sialik asit,amiloid,nörodejeneratif

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