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Basic Science and Pathogenesis.

Xu-Qiao Chen1, Xinxin Zuo1, Hien T Zhao2

  • 1University of California San Diego, La Jolla, CA, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 23, 2025
PubMed
Summary
This summary is machine-generated.

Down syndrome (DS) accelerates Alzheimer's disease (AD) risk via endolysosomal network (ELN) and autophagy dysfunction. Targeting APP or Rab5 normalizes ELN function and mitigates DS-AD pathologies.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Genetics

Background:

  • Down syndrome (DS) significantly elevates Alzheimer's disease (AD) risk.
  • Endolysosomal network (ELN) and autophagy pathway dysfunctions are central to DS-AD pathogenesis.
  • RAB5 hyperactivation's role in DS-AD is not fully understood.

Purpose of the Study:

  • Investigate the impact of APP gene dosage on ELN and autophagy in DS.
  • Clarify the role of RAB5 hyperactivation in DS-AD.
  • Evaluate therapeutic potential of targeting APP or Rab5.

Main Methods:

  • Examined postmortem brain samples from DS, DS-AD individuals, and Dp16 DS mouse models.
  • Assessed RAB5, RAB7, RAB11 activation, their GEFs, cathepsins, and autophagy markers.
  • Treated Dp16 mice with APP- and Rab5-specific antisense oligonucleotides (ASOs).

Main Results:

  • DS and Dp16 brains showed ELN dysfunction with RAB5 hyperactivation, increased RAB7/11 activity, elevated GEFs, and cathepsins, all APP dose-dependent.
  • Impaired autophagy was linked to reduced TSC1/2 and mTOR hyperphosphorylation.
  • ASO treatment in Dp16 mice normalized ELN function, improved autophagy, and reduced DS-AD pathologies.

Conclusions:

  • APP dose-driven RAB5 hyperactivation disrupts ELN and autophagy in DS.
  • Targeting APP or Rab5 shows promise for restoring cellular function in DS-AD.
  • This study highlights APP's role in DS-AD pathogenesis and potential therapeutic avenues.