Stereo-seq of the prefrontal cortex in aging and Alzheimer's disease

Nat Commun. 2025 Jan 8;16(1):482. doi: 10.1038/s41467-024-54715-y.

Abstract

Aging increases the risk for Alzheimer's disease (AD), driving pathological changes like amyloid-β (Aβ) buildup, inflammation, and oxidative stress, especially in the prefrontal cortex (PFC). We present the first subcellular-resolution spatial transcriptome atlas of the human prefrontal cortex (PFC), generated with Stereo-seq from six male AD cases at varying neuropathological stages and six age-matched male controls. Our analyses revealed distinct transcriptional alterations across PFC layers, highlighted disruptions in laminar structure, and exposed AD-related shifts in layer-to-layer and cell-cell interactions. Notably, we identified genes highly upregulated in stressed neurons and nearby glial cells, where AD diminished stress-response interactions that promote Aβ clearance. Further, cell-type-specific co-expression analysis highlighted three neuronal modules linked to neuroprotection, protein dephosphorylation, and Aβ regulation, with all modules downregulated as AD progresses. We identified ZNF460 as a transcription factor regulating these modules, offering a potential therapeutic target. In summary, this spatial transcriptome atlas provides valuable insight into AD's molecular mechanisms.

MeSH terms

  • Aged
  • Aged, 80 and over
  • Aging* / genetics
  • Aging* / metabolism
  • Alzheimer Disease* / genetics
  • Alzheimer Disease* / metabolism
  • Alzheimer Disease* / pathology
  • Amyloid beta-Peptides* / genetics
  • Amyloid beta-Peptides* / metabolism
  • Case-Control Studies
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism
  • Gene Expression Profiling / methods
  • Humans
  • Male
  • Middle Aged
  • Neuroglia / metabolism
  • Neuroglia / pathology
  • Neurons / metabolism
  • Prefrontal Cortex* / metabolism
  • Prefrontal Cortex* / pathology
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • Transcriptome*

Substances

  • Amyloid beta-Peptides
  • Transcription Factors
  • DNA-Binding Proteins