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Clinical Manifestations.

Yi Jin Leow1, Justin Jit Hong Ong2, Jia Dong James Wang3

  • 1Lee Kong Chian School of Medicine, Singapore, Singapore, Singapore.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 25, 2025
PubMed
Summary
This summary is machine-generated.

Glial fibrillary acidic protein (GFAP) and cerebral microbleeds (CMBs) impact sleep differently across cognitive stages. Elevated GFAP disrupts sleep in unimpaired individuals, while CMBs worsen sleep in those with cognitive impairment.

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Area of Science:

  • Neuroscience
  • Sleep Medicine
  • Gerontology

Background:

  • Chronic sleep disturbances drive neuroinflammation, astrocytic dysfunction, and neurodegeneration.
  • Glial fibrillary acidic protein (GFAP) is a marker of astrocytic activation linked to sleep-wake disruptions in Alzheimer's disease (AD).
  • Cerebral microbleeds (CMBs), indicative of cerebral small vessel disease (CSVD), also contribute to sleep disturbances, but their interplay with GFAP and sleep across cognitive stages is unclear.

Purpose of the Study:

  • To investigate the associations between plasma GFAP, CMBs, and sleep disturbances in cognitively unimpaired (CU) and cognitively impaired (CI) individuals.
  • To explore how these factors differ across varying stages of cognitive function.

Main Methods:

  • Cross-sectional study of 1,801 community-dwelling participants (mean age 58.7 years).
  • Participants categorized as CU or CI (including mild cognitive impairment and mild AD).
  • Assessed plasma GFAP, APOE ε4 status, sleep quality, and brain imaging for CSVD markers (CMBs). Analyzed associations using ANOVA, correlation, and regression.

Main Results:

  • In CU individuals, higher GFAP correlated with increased odds of poor sleep and longer sleep latency.
  • In CI individuals, higher GFAP was linked to reduced odds of poor sleep and higher sleep efficiency.
  • CMBs were associated with longer sleep latency and increased sleep medication use in the CI group.

Conclusions:

  • GFAP and CMBs have distinct roles in sleep disturbances across cognitive trajectories.
  • In CU individuals, elevated GFAP may disrupt sleep homeostasis via astrocytic activation.
  • In CI individuals, CMBs exacerbate specific sleep issues, underscoring vascular contributions; interventions for sleep disturbances may mitigate neurodegeneration.