Cellular communities reveal trajectories of brain ageing and Alzheimer's disease

Nature. 2024 Sep;633(8030):634-645. doi: 10.1038/s41586-024-07871-6. Epub 2024 Aug 28.

Abstract

Alzheimer's disease (AD) has recently been associated with diverse cell states1-11, yet when and how these states affect the onset of AD remains unclear. Here we used a data-driven approach to reconstruct the dynamics of the brain's cellular environment and identified a trajectory leading to AD that is distinct from other ageing-related effects. First, we built a comprehensive cell atlas of the aged prefrontal cortex from 1.65 million single-nucleus RNA-sequencing profiles sampled from 437 older individuals, and identified specific glial and neuronal subpopulations associated with AD-related traits. Causal modelling then prioritized two distinct lipid-associated microglial subpopulations-one drives amyloid-β proteinopathy while the other mediates the effect of amyloid-β on tau proteinopathy-as well as an astrocyte subpopulation that mediates the effect of tau on cognitive decline. To model the dynamics of cellular environments, we devised the BEYOND methodology, which identified two distinct trajectories of brain ageing, each defined by coordinated progressive changes in certain cellular communities that lead to (1) AD dementia or (2) alternative brain ageing. Thus, we provide a cellular foundation for a new perspective on AD pathophysiology that informs personalized therapeutic development, targeting different cellular communities for individuals on the path to AD or to alternative brain ageing.

MeSH terms

  • Aged
  • Aged, 80 and over
  • Aging* / genetics
  • Aging* / metabolism
  • Aging* / pathology
  • Alzheimer Disease* / genetics
  • Alzheimer Disease* / metabolism
  • Alzheimer Disease* / pathology
  • Amyloid beta-Peptides / metabolism
  • Animals
  • Astrocytes / metabolism
  • Astrocytes / pathology
  • Atlases as Topic
  • Cell Biology*
  • Cognitive Dysfunction / genetics
  • Cognitive Dysfunction / metabolism
  • Cognitive Dysfunction / pathology
  • Female
  • Humans
  • Male
  • Microglia / metabolism
  • Microglia / pathology
  • Neurons / metabolism
  • Neurons / pathology
  • Prefrontal Cortex* / cytology
  • Prefrontal Cortex* / metabolism
  • Prefrontal Cortex* / pathology
  • Single-Cell Gene Expression Analysis
  • Tauopathies / genetics
  • Tauopathies / metabolism
  • Tauopathies / pathology
  • tau Proteins / metabolism

Substances

  • Amyloid beta-Peptides
  • tau Proteins