Microglial senescence contributes to female-biased neuroinflammation in the aging mouse hippocampus: implications for Alzheimer's disease.
Sarah R OcañasKevin D PhamJillian E J CoxAlex W KeckSunghwan KoFelix A AmpaduHunter L PorterVictor A AnsereAdam KulpaCollyn M KelloggAdeline H MachalinskiAna J Chucair-ElliottWillard M FreemanPublished in: bioRxiv : the preprint server for biology (2023)
These data suggest that female microglia adopt disease-associated and senescent phenotypes in the aging mouse hippocampus, even in the absence of disease pathology, to a greater extent than males. This sexually divergent microglial phenotype may explain the difference in susceptibility and disease progression in the case of AD pathology. Future studies will need to explore sex differences in microglial heterogeneity in response to AD pathology, and explore how sex-specific regulators (i.e., sex chromosomal or hormonal) elicit these sex effects.
Keyphrases
- inflammatory response
- lipopolysaccharide induced
- lps induced
- neuropathic pain
- traumatic brain injury
- cognitive impairment
- cognitive decline
- cerebral ischemia
- gene expression
- single cell
- machine learning
- transcription factor
- spinal cord injury
- dna methylation
- adipose tissue
- current status
- deep learning
- oxidative stress
- blood brain barrier