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Pathological Changes in Microvascular Morphology, Density, Size and Responses Following Comorbid Cerebral Injury

Zareen Amtul1, Jun Yang2, Ting-Yim Lee2

  • 1Department of Anatomy and Cell Biology, University of Western Ontario, London, ON, Canada.

Frontiers in Aging Neuroscience
|April 12, 2019
PubMed

Insights

Alzheimer's disease (AD) and ischemia share common pathological pathways involving brain microcirculation. This study reveals that neural microvasculature deterioration underlies both conditions, suggesting vascular remodeling as a potential therapeutic strategy.

Area of Science:

  • Neuroscience
  • Cerebrovascular Biology
  • Pathology

Background:

  • Alzheimer's disease (AD) and ischemia exhibit shared pathologies including neuroinflammation, amyloid-beta (Aβ) deposition, and blood-brain barrier (BBB) dysfunction.
  • The role of microvascular homeostasis as a common etiological factor and pathogenic substrate in both AD and ischemic conditions remains underexplored.

Purpose of the Study:

  • To investigate the impact of combined β-amyloid (Aβ) toxicity and endothelin-1 (ET1) induced ischemia on cerebral microvascular pathology.
  • To analyze temporal changes in microvascular structure, protein expression, and associated pathological features post-injury.

Main Methods:

  • Utilized a rat model combining Aβ toxicity and ET1-induced ischemia.
  • Employed temporal histopathology to examine cerebral vasculature at days 1, 7, and 28 post-injury.
  • Assessed microvascular anatomy, texture, diameter, density, protein expression, vessel-matrix connections, water exchange, and basement membrane profiles.

Main Results:

  • Combined Aβ and ET1 pathologies induced significant alterations in microvascular anatomy, texture, diameter, and density within the striatal lesion epicenter.
  • Disturbances in vessel-matrix connections, inter-compartmental water exchange, and basement membrane profiles were observed in the combined pathology group.
  • Temporal analysis revealed progressive changes in microvascular integrity and protein expression following the induced injuries.

Conclusions:

  • The neural microvascular network is structurally vulnerable and plays a critical role in the overlapping pathologies of ischemia and Alzheimer's disease.
  • Cerebral microvascular deterioration serves as an underlying vascular etiology common to both AD and ischemic conditions.
  • Targeting vascular remodeling presents a promising therapeutic avenue for conditions involving neurovascular dysfunction.
Keywords:
basement membranebeta-amyloidischemiamicrovesselsvascular anatomy

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