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Drug Development.

Peng Wang1, Ido Weiss1, Pan Zheng1

  • 1OncoC4, Inc., Rockville, MD, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 25, 2025
PubMed
Summary
This summary is machine-generated.

This study demonstrates that increased SIGLEC10 expression in microglia causally contributes to Alzheimer's Disease (AD) pathogenesis. Targeting SIGLEC10 with an antibody significantly reduced key AD pathologies, including neurofibrillary tangles and amyloid plaques.

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Area of Science:

  • Neuroscience
  • Genetics
  • Immunology

Background:

  • Genome-wide association studies link Siglec genes to late-onset Alzheimer's Disease (AD).
  • SIGLEC10 is highly expressed in brain microglia and elevated in AD.
  • Previous research lacked data on a causative link between SIGLEC10 and AD pathogenesis.

Purpose of the Study:

  • To investigate the role of SIGLEC10 in Alzheimer's Disease (AD) pathogenesis.
  • To establish a causative relationship between SIGLEC10 expression and AD hallmarks.

Main Methods:

  • Created transgenic mice expressing human SIGLEC10 and crossed them with SiglecG-deficient mice.
  • Assessed amyloid-beta (Aβ) plaques and phosphorylated Tau neurofibrillary tangles (NFTs) using immunohistochemistry.
  • Administered anti-SIGLEC10 antibody to confirm its contribution to pathology.

Main Results:

  • Transgenic mice showed increased NFTs and Aβ plaques by 9-13 months.
  • Microglia exclusively expressed human SIGLEC10 in the brain.
  • Anti-SIGLEC10 antibody treatment significantly reduced both NFT and Aβ plaque accumulation.

Conclusions:

  • Transgenic expression of SIGLEC10 in microglia exacerbates both NFT and Aβ plaque hallmarks of AD.
  • Anti-SIGLEC10 treatment effectively reduced these pathologies in a mouse model.
  • This study establishes a causal link between SIGLEC10 and late-onset AD pathogenesis.