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Comorbidity sequence, sex, and APOE-genotype forecast Alzheimer's disease diagnosis.

Frontiers in medicine·2026
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APOE4 accelerates menopause-associated brain metabolic shift and disrupts bioenergetic adaptation.

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Anti-inflammatory and immunomodulatory therapies are associated with reduced risk of age-associated neurodegenerative diseases: impact of sex and treatment duration.

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Related Experiment Video

Updated: Jan 7, 2026

Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses
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Basic Science and Pathogenesis.

Mikaila Ann Bantugan1, Roberta Diaz Brinton1

  • 1University of Arizona, Tucson, AZ, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 25, 2025
PubMed
Summary

Female mice with the APOE4 gene variant show increased neuroinflammation and mitochondrial dysfunction via the cGAS-STING pathway, suggesting a higher Alzheimer

Area of Science:

  • Neuroscience
  • Genetics
  • Immunology

Background:

  • Mitochondrial dysfunction and neuroinflammation are early signs of Alzheimer's disease (AD).
  • The cGAS-STING pathway, involved in innate immunity, plays a role in AD pathogenesis.
  • APOE4 genotype and female sex may worsen mitochondrial dysfunction and neuroinflammation through cGAS-STING signaling.

Purpose of the Study:

  • To investigate sex- and APOE-specific associations with mitochondrial dysfunction and neuroinflammation.
  • To examine the role of the cGAS-STING pathway in these processes within a genetic risk model of AD.

Main Methods:

  • Used 18-month-old humanized APP and APOE3/3 or APOE4/4 mice.
  • Employed bulk RNA sequencing (RNA-seq) on hippocampal tissue.
  • Utilized Gene Set Enrichment Analysis, Ingenuity Pathway Analysis, immunohistochemistry, and western blotting to assess pathways and signaling.

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Main Results:

  • Female hAPP/hAPOE4 mice exhibited higher neuroinflammation, cGAS-STING signaling, and mitochondrial dysfunction compared to males.
  • Sex differences were less pronounced in hAPP/hAPOE3 mice.
  • A significant sex-APOE genotype interaction affected neuroinflammation, mitochondrial dysfunction, and cGAS-STING signaling.

Conclusions:

  • Consistent sex differences in neuroinflammation and mitochondrial pathways were observed.
  • APOE genotype influenced neuroinflammatory signatures, especially in females.
  • Elevated cGAS-STING signaling in female hAPP/hAPOE4 mice may increase AD risk in women, underscoring the need to consider sex and genotype in AD research.