Tlr7 drives sex differences in age- and Alzheimer's disease-related demyelination

Science. 2024 Nov 29;386(6725):eadk7844. doi: 10.1126/science.adk7844. Epub 2024 Nov 29.

Abstract

Alzheimer's disease (AD) and other age-related disorders associated with demyelination exhibit sex differences. In this work, we used single-nuclei transcriptomics to dissect the contributions of sex chromosomes and gonads in demyelination and AD. In a mouse model of demyelination, we identified the roles of sex chromosomes and gonads in modifying microglia and oligodendrocyte responses before and after myelin loss. In an AD-related mouse model expressing APOE4, XY sex chromosomes heightened interferon (IFN) response and tau-induced demyelination. The X-linked gene, Toll-like receptor 7 (Tlr7), regulated sex-specific IFN response to myelin. Deletion of Tlr7 dampened sex differences while protecting against demyelination. Administering TLR7 inhibitor mitigated tau-induced motor impairment and demyelination in male mice, indicating that Tlr7 plays a role in the male-biased type I Interferon IFN response in aging- and AD-related demyelination.

MeSH terms

  • Aging
  • Alzheimer Disease* / genetics
  • Alzheimer Disease* / metabolism
  • Animals
  • Apolipoprotein E4 / genetics
  • Demyelinating Diseases* / genetics
  • Demyelinating Diseases* / metabolism
  • Disease Models, Animal
  • Female
  • Genes, X-Linked*
  • Humans
  • Interferon Type I / metabolism
  • Male
  • Membrane Glycoproteins* / genetics
  • Membrane Glycoproteins* / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Microglia* / metabolism
  • Myelin Sheath* / metabolism
  • Oligodendroglia / metabolism
  • Sex Characteristics*
  • Sex Chromosomes* / genetics
  • Toll-Like Receptor 7* / antagonists & inhibitors
  • Toll-Like Receptor 7* / genetics
  • Toll-Like Receptor 7* / metabolism
  • tau Proteins / metabolism

Substances

  • Interferon Type I
  • Membrane Glycoproteins
  • tau Proteins
  • Tlr7 protein, mouse
  • Toll-Like Receptor 7
  • Apolipoprotein E4