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Basic Science and Pathogenesis.

Jun Lin1, Jiong Shi2,3

  • 1University of Science and Technology of China, Hefei, Hefei, China.

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

Immune cell differences in cerebrospinal fluid (CSF) distinguish sporadic late-onset Alzheimer's disease (sLOAD) from early-onset Alzheimer's disease (sEOAD). sLOAD shows more T cell expansion, suggesting a greater role for antigen-specific T cells in its progression.

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Area of Science:

  • Neuroimmunology
  • Gerontology
  • Genomics

Background:

  • Immune cell profiles in cerebrospinal fluid (CSF) may differ between sporadic late-onset Alzheimer's disease (sLOAD) and sporadic early-onset Alzheimer's disease (sEOAD).
  • CSF immune cells offer insights into brain immune dysregulation in Alzheimer's disease (AD) patients.

Purpose of the Study:

  • To investigate and elucidate potential differences in immune cell transcriptional signatures between sLOAD and sEOAD.
  • To analyze immune cell composition and function in the CSF of AD patients compared to controls.

Main Methods:

  • Collected CSF samples from sLOAD patients, sEOAD patients, and age-matched controls.
  • Utilized single-cell RNA sequencing (scRNA-seq) and single-cell TCR sequencing (scTCR-seq) on over 52,000 single cells.
  • Performed comprehensive bioinformatics analysis to compare immune cell populations and their gene expression.

Main Results:

  • Observed a decreased proportion of T cells and an increased proportion of microglia-like macrophages in AD patients' CSF.
  • Microglia-like macrophages in AD patients exhibited upregulated inflammation-related genes.
  • Found a higher proportion of clonally expanded CSF T cells in sLOAD patients, indicating a significant role for antigen-specific T cells.

Conclusions:

  • Highlighted distinct transcriptional signatures of immune cells in the CSF of sLOAD and sEOAD.
  • Proposed future integrated analysis of CSF and brain single-cell data to explore immune cell interactions in AD pathogenesis.