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Basic Science and Pathogenesis.

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Summary
This summary is machine-generated.

This study maps human brain gene expression across the lifespan, revealing age-related changes in neurons and glia. It identifies common aging mechanisms and disease gene links, offering insights into brain development and neurodegeneration.

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Area of Science:

  • Neuroscience
  • Genomics
  • Aging Research

Background:

  • Understanding human brain development and aging is key to neurodegenerative diseases.
  • Previous studies lacked lifespan-spanning, cell-specific transcriptomic data.
  • A harmonized, cell-specific aging trajectory of the human brain transcriptome is needed.

Purpose of the Study:

  • To create a comprehensive atlas of human brain gene expression across the entire lifespan.
  • To identify cell-specific aging trajectories in the prefrontal cortex (PFC).
  • To reveal common molecular mechanisms underlying brain aging and disease associations.

Main Methods:

  • Single-nucleus RNA sequencing of 284 human postmortem PFC samples (0-97 years).
  • Analysis of age-related gene expression changes in 26 cell subclasses across four age groups.
  • Integration of transcriptomic changes with lifespan aging trajectories and disease associations.

Main Results:

  • Age-related gene expression changes occurred in neuronal (2.9%) and glial (1.7%) subclasses during development, stabilizing post-20 and resurging post-60, mainly in glia.
  • Aging increases cellular stressors (DNA damage, oxidative stress, inflammation), converging transcriptome signatures across cell types.
  • Psychiatric disorder genes show sustained neuronal expression; neurodegenerative disease genes are highly expressed in microglia and oligodendrocytes during aging.

Conclusions:

  • The study provides a lifespan aging atlas for every gene across 26 PFC cell subclasses.
  • Valuable insights into common aging mechanisms manifesting across diverse brain cell types are presented.
  • This resource aids understanding of neurodevelopmental vulnerability and aging-related disease pathways.