We enrolled 48 patients, 25 patients with posterior cortical atrophy (PCA) and 23 with typical Alzheimer’s disease (tAD), in addition to 70 cognitively healthy controls. Consistent with the hypothesis of trans-synaptic retrograde neurodegeneration, we hypothesized that particular reductions in retinal thickness would be observed in PCA relative to both tAD and control participants, and in tAD relative to control participants. We assessed retinal thickness measured with optical coherence tomography in PCA, typical AD (tAD) and control participants. Consequently, PCA represents a patient group uniquely positioned to evaluate the hypothesis of retrograde atrophy from cortical visual areas following neurodegeneration. PCA preferentially affects parietal-occipital and occipito-temporal lobes, key areas for visual processing that receive input from retino-cortical projections mainly through the lateral geniculate nucleus and optical radiations. PCA is a neurodegenerative syndrome presenting with progressive cortico-visual problems in contrast to relatively well-preserved memory, language and insight. Retinal thinning is of particular interest in posterior cortical atrophy (PCA), the canonical ‘visual dementia’, and the most common atypical presentation of AD. However, conflicting study findings of retinal thinning in AD have prompted recommendations for investigations comprising well-characterized participants, controlling for confounding factors and comparing purported ocular biomarkers with established AD biomarkers. Retinal thinning has been proposed as a promising non-invasive imaging biomarker, purportedly mirroring cortical atrophy owing to trans-synaptic retrograde neurodegeneration, and/or reflecting parallel processes in both retinal and cortical neurons. Ocular manifestations of AD may include retinal thinning, vascular changes and amyloid-beta and tau retinal deposition. The retina, sharing its embryological origin with the brain, may reflect AD hallmark pathology. There is an urgent need for non-invasive Alzheimer’s disease (AD) biomarkers. Findings from this well-characterized sample, including cases with PCA, do not support the hypothesis that retinal neurodegeneration, measured using conventional OCT, is a useful biomarker for AD or PCA. ![]() Retinal thickness did not discriminate tAD and PCA from controls or from one another despite unequivocal differences on standard clinical, neuro-imaging and CSF measures. Similarly, subgroup analysis with MRI biomarkers (PCA = 18, tAD = 17, controls = 31) showing neurodegeneration, and CSF biomarkers (PCA = 18, tAD = 14, controls = 13) supporting underlying AD pathology did not provide evidence of overall between-group differences in pRNFL or mRT measures (all p > 0.3). ![]() Subgroup analyses were performed in participants with available MRI and CSF measures, providing evidence of neurodegeneration and underlying AD pathology respectively. Participants did not show evidence of any significant ophthalmological conditions. All participants underwent optical coherence tomography (OCT) imaging, including measurement of peripapillary retinal nerve fiber layer (pRNFL) thickness and total macular thickness (mRT). Retinal thickness measures were acquired from 48 patient participants ( N = 25 PCA N = 23 tAD) fulfilling consensus diagnostic criteria and 70 age-matched controls. We therefore evaluated retinal thickness as non-invasive biomarker of neurodegeneration in well-characterized participants with posterior cortical atrophy (PCA) and typical Alzheimer’s disease (tAD). Changes in the visual pathway are of particular interest in posterior cortical atrophy (PCA), the most common atypical AD phenotype predominantly affecting the parietal-occipital cortices. Retinal thinning is hypothesized to be a result of retrograde atrophy and/or parallel neurodegenerative processes. Retinal thickness can be measured non-invasively with optical coherence tomography (OCT) and may offer compelling potential as a biomarker for Alzheimer’s disease (AD).
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