Coronavirus increases the deposit of a protein linked to Alzheimer's

A study published in the journal Science Advances analyzed the presence of beta-amyloid deposits, which are linked to Alzheimer's disease, in post-mortem retinas of people with COVID-19 and found them to be larger than in those of people without COVID. In other experiments, the virus protein caused deposits to increase in retinal cells, but when a drug that blocks the virus from entering neurons was used, the accumulation was lower.

The study, led by Sean Miller at Yale University (USA), reinforces the emerging theory that immune responses to infections in the central nervous system , such as those caused by SARS-CoV-2, could trigger the accumulation of amyloid-beta (Aβ), a key marker in the development of Alzheimer's disease.

Although the Aβ protein has been widely linked to Alzheimer's disease, new theories suggest that this protein may play a defensive role in the innate immune system by forming aggregates that trap invading pathogens in the nervous system. Over time, and after repeated infections, this defense mechanism could become pathological.

To investigate this hypothesis, the scientists analyzed ocular tissue from 20 patients diagnosed with Alzheimer's postmortem, observing the presence and distribution of Aβ. They then cultured human retinal organoids from these samples and exposed them to the SARS-CoV-2 virus.

They also studied the eyes of patients who had had COVID-19 but had no history of Alzheimer's. In both cases, they found that the viral infection was associated with immune cell-mediated extracellular accumulation of Aβ.

The team then tested whether a drug could prevent the virus from causing this buildup. By blocking the virus from binding to a protein called Neuropilin-1, they were able to significantly reduce the formation of plaques in the retina.

"Our findings suggest that amyloid-β accumulation may be related to the cognitive symptoms observed after COVID-19, and that NRP1 inhibitors or antiviral drugs may have a therapeutic role to prevent these consequences," the authors conclude.

This study not only offers a possible explanation for the persistent neurological symptoms following SARS-CoV-2 infection, but also reinforces the hypothesis that infections could be a key trigger in the development of Alzheimer's.

However, experts consulted by Science Media Centre , such as Eloy Rodríguez Rodríguez, head of the Neurology Department at the Marqués de Valdecilla University Hospital-IDIVAL , recommend interpreting the results with caution. In his opinion, this is a basic research study with certain important methodological limitations : a small number of samples (only 3-4 people per group), a lack of detailed clinical information on the patients, and exposure to a single viral protein in experimental models.

Rodríguez emphasizes that beta-amyloid could be acting as a natural immune response to any infectious agent, not just SARS-CoV-2. " It would have been interesting to repeat the experiments with other common viruses to compare results ," he notes. Furthermore, he considers it premature to talk about the use of the retina as a diagnostic tool for "long COVID" or a possible post-COVID Alzheimer's "epidemic," and warns that the real effects on population incidence can only be assessed with long-term studies.