# A Cerebral Origin for Retinal Degeneration in the Visual Form of Alzheimer's Disease?

## TL;DR

This study explores retinal degeneration in different forms of Alzheimer's disease, finding that a specific type causes more thinning in a retinal sector linked to visual impairments.

## Contribution

The study identifies sector-specific retinal thinning in PCA-AD linked to visuospatial impairments, suggesting retrograde degeneration along the magnocellular pathway.

## Key findings

- PCA-AD patients showed greater thinning in the inferior temporal retinal sector compared to typical AD.
- The amount of retinal thinning correlated with visuospatial impairment scores.
- The thinning is proposed to reflect retrograde degeneration along the magnocellular pathway.

## Abstract

Alzheimer's disease (ad) manifests commonly as an amnestic syndrome (tad), but also as a rarer focal type, such as posterior cortical atrophy (PCA‐AD), which primarily impairs visuospatial functions. In addition to the brain atrophy, retinal degeneration has been demonstrated, associated with the accumulation of Ab and Tau protein in this tissue, which shares a common origin with the brain. Additionally, retrograde trans‐synaptic degeneration from the brain could affect the retina. We hypothesized that such dying‐back phenomenon would be more important in PCA‐ad than in tad and that this would be reflected on specific optical coherence tomography (OCT) measures. Twenty‐nine AD patients were categorized into 15 typical and 14 PCA forms. Complaints and symptoms were evaluated using a specific screening battery developed to detect PCA (Q‐ACP questionnaire, neuropsychological parietal and non‐parietal scales). Neuroimaging was performed to determine brain atrophy and its lateralization. OCT imaging allowed measuring the volumes of the macular ganglion cell layer (GCL) and the retinal nerve fibre layer (RNFL) of the optic nerve. While the global RNFL thickness and GCL volume were not statistically different, PCA‐ad patients showed more thinning than tAD in the inferior temporal (IT) sector in both eyes. Moreover, the amount of thinning in this sector was correlated with the score on the Q‐ACP questionnaire and on the neuropsychological parietal scales. We propose that the thinning in the IT sector reflects the retrograde damage to the magnocellular pathway, which constitutes a major feed of the dorsal visual stream primarily damaged in PCA.

We compared retinal involvement in typical Alzheimer's disease (tad) and posterior cortical atrophy (PCA‐AD). Although global retinal measures did not differ significantly, we found greater thinning in the inferior temporal (IT) sector in PCA‐ad patients. This thinning was correlated with visuospatial impairments assessed by the Q‐ACP questionnaire and parietal neuropsychological scales. We propose that this sector‐specific thinning reflects enhanced retrograde trans‐synaptic degeneration along the magnocellular pathway, which would correspond to the symptoms of PCA‐ad patients.