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Basic Science and Pathogenesis.

Xiaoxuan Song1,2, Teodoro De Vecchi1,2, Jeannine Widmann1,2

  • 1Ludwig Maximilian University of Munich, Munich, Bavaria, Germany.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 24, 2025
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Summary
This summary is machine-generated.

Alpha-synuclein co-pathology in Alzheimer's Disease (AD) involves higher phosphorylated tau levels. This suggests alpha-synuclein and tau synergistically drive dementia pathology.

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Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Alzheimer's Disease (AD) cognitive decline mechanism with alpha-synuclein co-pathology is unclear.
  • Mouse studies suggest tau and alpha-synuclein interactions, but human genomic relevance is unknown.

Purpose of the Study:

  • Investigate the genome-centered molecular basis of accelerated cognitive decline in AD with alpha-synuclein co-pathology.
  • Determine the synergistic effects of alpha-synuclein and tau in human AD.

Main Methods:

  • Whole genome sequencing and polygenic risk scores in 137 AD cases.
  • Single-nucleus RNA sequencing and Western Blot on post-mortem tissue, validated in the MSBB cohort.
  • Cellular and molecular analysis using isogenic induced pluripotent stem cells (iPSCs)-derived neurons.

Main Results:

  • AD brains with alpha-synuclein co-pathology showed higher Parkinson's Disease polygenic risk scores, linked to SNCA expression variants.
  • Elevated MAPT and phosphorylated tau expression observed in alpha-synuclein co-pathology cases.
  • iPSC-derived neurons with SNCA triplication exhibited increased pathological tau and alpha-synuclein, with activated GSK3β and dysregulated signaling pathways.

Conclusions:

  • Alpha-synuclein co-pathology in AD is associated with increased phosphorylated tau in patients and iPSC models.
  • Findings provide molecular insights into how alpha-synuclein and tau synergistically contribute to dementia pathology.