AI Article Synopsis

  • - The study investigates the role of neuroinflammation in Alzheimer's disease (AD), specifically looking at retinal glial activation in mouse models and human biopsies, hypothesizing increased retinal gliosis in preclinical AD patients compared to controls.
  • - Using optical coherence tomography (OCT), researchers analyzed images from 76 participants, including 22 with preclinical AD and 20 healthy controls, focusing on the surface area of retinal gliosis and retinal nerve fiber layer (RNFL) thickness.
  • - Results indicated significantly greater retinal gliosis in the preclinical AD group compared to controls, suggesting that this retinal change could serve as a potential biomarker for neuroinflammation associated with Alzheimer's disease.

Article Abstract

Purpose: Neuroinflammation plays a significant role in the pathology of Alzheimer's disease (AD). Mouse models of AD and postmortem biopsy of patients with AD reveal retinal glial activation comparable to central nervous system immunoreactivity. We hypothesized that the surface area of putative retinal gliosis observed in vivo using en face optical coherence tomography (OCT) imaging will be larger in patients with preclinical AD versus controls.

Methods: The Spectralis II instrument was used to acquire macular centered 20 × 20 and 30 × 25-degrees spectral domain OCT images of 76 participants (132 eyes). A cohort of 22 patients with preclinical AD (40 eyes, mean age = 69 years, range = 60-80 years) and 20 control participants (32 eyes, mean age = 66 years, range = 58-82 years, P = 0.11) were included for the assessment of difference in surface area of putative retinal gliosis and retinal nerve fiber layer (RNFL) thickness. The surface area of putative retinal gliosis and RNFL thickness for the nine sectors of the Early Treatment Diabetic Retinopathy Study (ETDRS) map were compared between groups using generalized linear mixed models.

Results: The surface area of putative retinal gliosis was significantly greater in the preclinical AD group (0.97 ± 0.55 mm2) compared to controls (0.68 ± 0.40 mm2); F(1,70) = 4.41, P = 0.039; Cohen's d = 0.61. There was no significant difference between groups for RNFL thickness in the 9 ETDRS sectors, P > 0.05.

Conclusions: Our analysis shows greater putative retinal gliosis in preclinical AD compared to controls. This demonstrates putative retinal gliosis as a potential biomarker for AD-related neuroinflammation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11077916PMC
http://dx.doi.org/10.1167/iovs.65.5.5DOI Listing

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