Beta‐Amyloid, Phospho‐Tau and Alpha‐Synuclein Deposits Similar to Those in the Brain Are Not Identified in the Eyes of A lzheimer's and P arkinson's Disease Patients

A lzheimer's disease ( AD ) and P arkinson's disease ( PD ) are the two most common neurodegenerative disorders, and are characterized by deposition of specific proteins in the brain. If similar abnormal protein deposits are present in the eye, it would facilitate noninvasive diagnosis and monitoring of disease progression. We therefore evaluated expression of proteins associated with AD and PD pathology in postmortem eyes and brains in a case‐control study. Eyes from 11 cases of AD , 6 cases of PD or PD with dementia, and 6 age‐matched controls were retrieved from the autopsy archives of T he J ohns H opkins H ospital. Immunostains for β‐amyloid, phospho‐tau and α‐synuclein and C ongo red stains were performed in the same laboratory in both brains and eyes. No amyloid deposits or abnormal tau accumulations were detected in the lens, retina or other structures in the eyes of AD patients. Eyes also lacked definite L ewy bodies or L ewy neurites in either PD or AD cases. Patchy cytoplasmic α‐synuclein positivity was seen in the retina of AD , PD and control cases, but did not correlate with the presence or extent of L ewy body pathology in the brain. Abnormal protein aggregations characteristic of AD and PD are thus not commonly present in the retinas or lens of affected patients when assayed using the same protocols as in the brain. This suggests that β‐amyloid, phospho‐tau and α‐synuclein either do not deposit in the eye in a manner analogous to brain, or are present at lower levels or in different forms.