G-protein coupled estrogen receptor 1, amyloid-β, and tau tangles in older adults

Commun Biol. 2024 May 15;7(1):569. doi: 10.1038/s42003-024-06272-9.

Abstract

Accumulation of amyloid-β (Aβ) and tau tangles are hallmarks of Alzheimer's disease. Aβ is extracellular while tau tangles are typically intracellular, and it is unknown how these two proteinopathies are connected. Here, we use data of 1206 elders and test that RNA expression levels of GPER1, a transmembrane protein, modify the association of Aβ with tau tangles. GPER1 RNA expression is related to more tau tangles (p = 0.001). Moreover, GPER1 expression modifies the association of immunohistochemistry-derived Aβ load with tau tangles (p = 0.044). Similarly, GPER1 expression modifies the association between Aβ proteoforms and tau tangles: total Aβ protein (p = 0.030) and Aβ38 peptide (p = 0.002). Using single nuclei RNA-seq indicates that GPER1 RNA expression in astrocytes modifies the relation of Aβ load with tau tangles (p = 0.002), but not GPER1 in excitatory neurons or endothelial cells. We conclude that GPER1 may be a link between Aβ and tau tangles driven mainly by astrocytic GPER1 expression.

MeSH terms

  • Aged
  • Aged, 80 and over
  • Alzheimer Disease* / genetics
  • Alzheimer Disease* / metabolism
  • Amyloid beta-Peptides* / genetics
  • Amyloid beta-Peptides* / metabolism
  • Astrocytes / metabolism
  • Female
  • Humans
  • Male
  • Neurofibrillary Tangles / metabolism
  • Neurofibrillary Tangles / pathology
  • Receptors, Estrogen* / genetics
  • Receptors, Estrogen* / metabolism
  • Receptors, G-Protein-Coupled* / genetics
  • Receptors, G-Protein-Coupled* / metabolism
  • tau Proteins* / genetics
  • tau Proteins* / metabolism

Substances

  • Amyloid beta-Peptides
  • Receptors, Estrogen
  • Receptors, G-Protein-Coupled
  • tau Proteins
  • GPER1 protein, human