Molecular Neurobiology

, Volume 49, Issue 1, pp 529–535

CD33 in Alzheimer's Disease


DOI: 10.1007/s12035-013-8536-1

Cite this article as:
Jiang, T., Yu, JT., Hu, N. et al. Mol Neurobiol (2014) 49: 529. doi:10.1007/s12035-013-8536-1


The amyloid-beta peptide (Aβ) cascade hypothesis posits that Aβ accumulation is the fundamental initiator of Alzheimer's disease (AD), and mounting evidence suggests that impaired Aβ clearance rather than its overproduction is the major pathogenic event for AD. Recent genetic studies have identified cluster of differentiation 33 (CD33) as a strong genetic locus linked to AD. As a type I transmembrane protein, CD33 belongs to the sialic acid-binding immunoglobulin-like lectins, mediating the cell–cell interaction and inhibiting normal functions of immune cells. In the brain, CD33 is mainly expressed on microglial cells. The level of CD33 was found to be increased in the AD brain, which positively correlated with amyloid plaque burden and disease severity. More importantly, CD33 led to the impairment of microglia-mediated clearance of Aβ, which resulted in the formation of amyloid plaques in the brain. In this article, we review the recent epidemiological findings of CD33 that related with AD and discuss the levels and pathogenic roles of CD33 in this disease. Based on the contributing effects of CD33 in AD pathogenesis, targeting CD33 may provide new opportunities for AD therapeutic strategies.


Alzheimer's disease CD33 Aβ Genetics Microglia Pathogenesis Therapy 

Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  1. 1.Department of Neurology, Qingdao Municipal HospitalNanjing Medical UniversityNanjingChina
  2. 2.Department of Neurology, Qingdao Municipal Hospital, School of MedicineQingdao UniversityQingdaoChina
  3. 3.Department of Neurology, Qingdao Municipal Hospital, College of Medicine and PharmaceuticsOcean University of ChinaQingdaoChina

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