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May 1, 2026

CD33 Isoform Splicing Dysregulation: A Molecular Determinant of Microglial Dysfunction in Alzheimer's Disease Pathology.

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Authors

XLXiao-Yan LiYZYu ZhangZRZhao Ran

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Overview

Review explores CD33 isoforms' roles in microglial dysfunction and therapeutic strategies in Alzheimer's disease, suggesting implications for treatment.

Key Points

  • This review aims to dissect the splicing dysregulation of CD33 isoforms and their impact on microglial dysfunction in Alzheimer's disease.
  • Analysis of CD33 isoforms CD33M and CD33m in relation to microglial activity and neuroinflammation.
  • Examination of genetic polymorphisms and splicing regulation by specific proteins.
  • Evaluation of therapeutic strategies targeting CD33, including immunotherapies and splicing modulators.
  • CD33M isoform is pro-pathogenic, while CD33m is protective, influencing Aβ clearance.
  • CD33 and TREM2 interplay affects DAP12 signaling pathways.
  • Emerging therapies face challenges in brain barrier penetration and specificity.

Cite This Study

Li et al. (2026) studied this question.

synapsesocial.com/papers/69f4443a967e944ac55672ffhttps://doi.org/10.1007/s12035-026-05886-w
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Alzheimer’s disease associated isoforms of human CD33 distinctively modulate microglial cell responses in 5XFAD mice2024 · 31 citations
  2. 2CD33 and clusterin interact biophysically and genetically to modulate Alzheimer risk2026
  3. 3CD33 and Clusterin Interact Biophysically and Genetically to Modulate Alzheimer Risk2025 · 3 citations
  4. 4CD33 and SHP-1/PTPN6 Interaction in Alzheimer’s Disease2024 · 2 citations
  5. 5CD33-CD45 Interaction Reveals a Mechanistic Link to Alzheimer's Disease Susceptibility2025 · 4 citations