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Basic Science and Pathogenesis.

Maya Koronyo-Hamaoui1,2,3,4, Jonah Doustar1, Yosef Koronyo1

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Alzheimer's disease (AD) involves retinal vascular changes like amyloid plaque buildup and pericyte loss, contributing to cognitive decline. These retinal biomarkers may help predict AD progression and assess cerebral amyloid angiopathy (CAA).

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Area of Science:

  • Neuroscience
  • Ophthalmology
  • Vascular Biology

Background:

  • Alzheimer's disease (AD) pathogenesis involves vascular dysfunction and amyloidosis, impacting cognitive decline.
  • The retina offers a noninvasive window into AD-related vascular pathology due to shared embryonic origins with the brain.
  • Retinal vascular damage in early AD, its link to cerebral amyloid angiopathy (CAA), and cognitive impairment are understudied.

Purpose of the Study:

  • To investigate retinal vascular abnormalities in mild cognitive impairment (MCI) and AD.
  • To explore the relationship between retinal vascular pathology, cerebral amyloid angiopathy (CAA), and cognitive decline.
  • To assess the potential of retinal biomarkers for predicting cognitive impairment and monitoring AD progression.

Main Methods:

  • Histopathological examination of postmortem retinas from MCI/AD patients and controls, focusing on pericyte integrity, amyloid-beta (Aβ) levels, and endothelial tight junction (TJ) proteins.
  • In-vivo retinal imaging using scanning-laser ophthalmoscopy with curcumin-amyloid to assess perivascular amyloid plaques (APs) in live participants.
  • Correlation analysis of retinal findings with MRI measures (hippocampal volume, white matter hyperintensities) and cognitive/neuropsychiatric assessments.

Main Results:

  • Significant pericyte loss and increased vascular Aβ42/40 accumulation were observed in MCI and AD retinas, correlating with CAA severity.
  • Reduced retinal endothelial ZO-1 and claudin-5 levels indicated impaired Aβ clearance, strongly associating with CAA and cognitive decline.
  • In-vivo imaging revealed perivascular APs in retinal arterioles, particularly in secondary and tertiary branches, correlating with cognitive impairment, hippocampal atrophy, and white matter lesions.

Conclusions:

  • Retinal arteriolar Aβ accumulation, pericyte loss, and TJ dysfunction are key contributors to early AD vascular pathology.
  • Retinal vascular biomarkers show promise for predicting cognitive decline and assessing CAA severity in AD.
  • Further validation in larger cohorts could establish retinal biomarkers for AD monitoring and progression assessment.