COVID-19 May Trigger Alzheimer's-Like Protein Buildup In Brain And Eyes, Study Finds

New research suggests that COVID-19 can lead to protein build-up similar to that seen in Alzheimer's patients, not just in the brain but also in the eyes. Elevated amyloid beta levels were found in the retinal tissue of people who had COVID-19, similar to Alzheimer's-like retinal conditions. Notably, Amyloid beta buildup is associated with Alzheimer's disease.

Researchers analysed two proteins, neuropilin-1 (NRP1) and angiotensin-converting enzyme 2 (ACE2). The NRP1 protein may serve as an entry point for viruses into human eyes and brains. Researchers found that introducing an NRP1 inhibitor countered the amyloid beta increase caused by COVID-19's spike protein.

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The study, led by Yale University and published in Science Advances, sheds light on COVID-19 brain fog, which was a commonly reported symptom following infection. The researchers believe that amyloid beta may act as a bodyguard for the brain, indicating underlying danger.

"There is growing evidence linking COVID-19 and brain fog, a commonly reported symptom following infection," senior author Brian Hafler, ophthalmologist at Yale School of Medicine, said as quoted by Science Alert.

"While the mechanisms of brain fog after COVID-19 are not fully understood, scientists have found that SARS-CoV-2 can induce amyloid beta accumulation in the central nervous system."

The research team is conducting clinical studies to determine if COVID-19 increases the long-term risk of developing Alzheimer's disease, to explore NRP1 inhibitors as potential therapeutics.

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The involvement of NRP1 in amyloid beta aggregation provides a specific molecular target for future investigation. Other viruses may trigger similar amyloid beta buildups, as there's a need for further research.

This study contributes to understanding the complex relationship between COVID-19 and neurological health. "Our study showed that exposure to SARS-CoV-2, in particular spike protein, can lead to the formation of amyloid beta aggregates in both human retinal tissue and retinal organoids," Hafler says.