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

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.