An abnormal form of the tau protein found to accumulate in the brains of Alzheimer's disease patients also accumulates in the eyes of patients with the condition, according to new findings from Cedars-Sinai investigators.

The study, reported in the journal Acta Neuropathologica Communications, presents the first evidence that abnormal tau accumulates in specialised nerve cells in the eyes of patients with Alzheimer's disease and links this accumulation to deterioration of brain function.

"We discovered that abnormal tau proteins accumulate in retinal ganglion cells, which are key nerve cells in the eye that send information to the brain," said Maya Koronyo-Hamaoui, Ph.D., professor of Neurosurgery and Biomedical Sciences at Cedars-Sinai and senior author of the study.

"We also identified a correlation between early accumulation of abnormal tau and the damage and death of retinal ganglion cells in people showing symptoms of mild cognitive impairment and Alzheimer's disease."

People with mild cognitive impairment and Alzheimer's disease had 46%–57% fewer retinal ganglion cells than people with normal cognition, and their retinal ganglion cells were misshapen and prone to die.

Harmful tau proteins were two to three times more common in the retinal ganglion cells of these people, and the amount of tau-related damage in the retina was linked to Alzheimer's-related damage to the brain and a decline in cognitive function, Koronyo-Hamaoui said.

More information: Miyah R. Davis et al, Retinal ganglion cell vulnerability to pathogenic tau in Alzheimer's disease, Acta Neuropathologica Communications (2025). DOI: 10.1186/s40478-025-01935-y