Citations

AbstractINTRODUCTIONGiven the close interactions between the retina and the brain, retinal amyloid imaging may serve as a diagnostic and prognostic tool for Alzheimer's disease and related dementias. This retrospective study investigated multivariable associations between retinal perivascular amyloid and cognitive domains.METHODSIntegrated analysis of retinal perivascular amyloid imaging, neuropsychological assessment, and brain magnetic resonance imaging in adults with and without cognitive impairment (N = 26; mean age: 65 ± 7 years; 50% female). Correlations between perivascular amyloid plaque burden and cognitive domains were evaluated with linear regression and interactions with hippocampal volumetry were explored.RESULTSHigher perivascular and periarteriolar amyloid plaque count in the secondary small and tertiary branches were associated with poorer verbal and visual memory in this cohort (p = 0.005–0.009). Higher perivascular amyloid burden interacted with hippocampal atrophy to worsen visual memory (p = 0.033).DISCUSSIONRetinal perivascular amyloid may serve as a non‐invasive marker for cognitive impairment and may shed insight into pathological changes in the brain.Highlights In vivo retinal perivascular amyloid plaque counts are associated with poorer memory. Retinal perivascular amyloid interacted with hippocampal atrophy to worsen memory. Retinal amyloid imaging is a potential biomarker for neurodegenerative diseases.

Introduction: Although primarily supplied by the vertebrobasilar system, the hippocampus is partially supplied by ipsilateral carotid artery branches through the anterior choroidal artery or a prominent posterior communicating artery. We report a patient with acute hippocampus infarction likely due to symptomatic ipsilateral tandem carotid stenosis and discuss acute vascular-mediated hippocampal injury. Case Report: An 80-year-old female with obesity, dyslipidemia, hypertension, alcohol use disorder, history of breast cancer on letrozole, and traumatic brain injury was brought into our emergency department for 24 hours of confusion. On examination, she exhibited limited registration, recall, and executive dysfunction with otherwise normal language, visuo-spatial orientation, and praxis. Brain MRI showed a small area of diffusion restriction in the anterior right hippocampus with matched FLAIR hyperintensity, consistent with acute infarction. Computed tomography angiogram head and neck showed 90% stenosis of the proximal right internal carotid artery (ICA), <50% narrowing of the proximal left ICA, and moderate bilateral narrowing of the paraclinoid ICAs, all due to calcific atheromatous plaques. The etiology of the hippocampal infarction was suspected embolism from the ipsilateral severe carotid stenosis. Planning for right cervical carotid revascularization ensued. Conclusion: This case highlights the dual hippocampal vascular supply and that hippocampal embolic infarcts could be a sign of a symptomatic severe carotid artery stenosis that may require urgent revascularization for stroke secondary prevention.