COVID-19 (COVID-19) It may lead to accumulation of proteins similar to those seen in Alzheimer’s disease New research shows that patients – not only in the brain, but also in the eyes.
This may explain why “brain mist,” an umbrella term for memory and cognitive problems, is often reported Covid-19 symptoms.
In a new study led by Yale University, researchers are trying to uncover the clear similarity between COVID brain fog and Alzheimer’s disease. SARS-CoV-2 It can lead to plaques like Alzheimer’s disease, which may explain brain fog after infection.
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“There is growing evidence linking the brain fog with Covid-19, a commonly reported symptom after infection.” say Senior author Brian Haffler, ophthalmologist at Yale University School of Medicine.
“The mechanism of brain fog after Covid-19 is not fully understood, but scientists have discovered it. SARS-CoV-2 It can induce amyloid beta accumulation in the central nervous system. ”
The retina is part of the central nervous system and, as two of the most clinically accessible parts of the system, may provide a window into more than the soul.
Previous research It shows the accumulation of amyloid beta in the retina as well as in the brain of Alzheimer’s patients, suggesting that retinal testing may provide a practical method for the diagnosis and monitoring of large-scale Alzheimer’s disease.
To investigate, researchers used post-mortem human retinal tissue to raise the retina Organoids – Small-scale 3D retinal model derived from humans Stem cells.
They analyzed different cell types found in retinal tissue and measured RNA in the cell nucleus to determine protein production in different cells.
They focused on two proteins: neuropyrin-1 (NRP1) and angiotensin-converting enzyme 2 (ACE2). SARS-CoV-2 It penetrates neurons.
NRP1 appears in neurons and glial cells from the retinal tissue of people with covids and points to possible entry points virus In the human eye.
People with no history of dementia still show an increase in the accumulation of amyloid beta if they have a history of COVID, often producing retinal tissue like Alzheimer’s disease.
Amyloid beta levels also increased after exposure to retinal organoids SARS-CoV-2Spike protein, that’s what helps virus Enter the host cell.
However, when researchers added NRP1 inhibitors to the mix, they were able to counteract the increase in amyloid beta that was otherwise generated in retinal tissue. coronavirus Spike protein.
This suggests that it could target NRP1 and combat neurological complications of Covid, such as commonly labeled brain fog.
“Mechanically, the involvement of NRP1 in amyloid beta aggregation gives specific molecular targets for future investigations,” Haffler said. say.
“Our study showed that exposure SARS-CoV-2particularly spike proteins, can lead to the formation of amyloid beta aggregates in both human retinal tissue and retinal organoids. ”
Haffler said the study also supports the idea that amyloid beta is like a brain bodyguard, not only does it shed light on brain fog.
length i doubt it When it comes to Alzheimer’s disease, these plaques are now widely viewed as indicators of underlying risk.
Amyloid beta is still not well understood, but it is structurally similar to known antimicrobial peptides, and some studies have suggested that it may play an important role in the brain’s immune system.
As Alzheimer’s disease can weaken blood-brain barriers, the accumulation of amyloid beta could indicate a brain attempt to dodge microbial invaders.
“It strengthens the amyloid beta antibacterial hypothesis of Alzheimer’s disease, suggesting that amyloid beta can act as part of the brain’s innate immune response to viral infections,” he said. say.
Other viruses may cause similar accumulation of amyloid beta, the authors point out that more research is needed to investigate.
Hafler and his colleagues are conducting clinical research on their part in the hopes of clarifying whether Covid can increase the risk of long-term Alzheimer’s disease.
“Our ultimate goal is to prevent the long-term neurological effects of COVID-19 and explore NRP1 inhibitors and other modulators. virus– Introducing the interactions between virus-induced amyloid pathology and potential therapeutics to prevent Alzheimer’s disease.” Haffler say.
This study was published in Advances in science.
