Covid brain fog has underlying cause similar to Alzheimer’s disease, study finds

Researchers have identified a protein they suspect is behind the “brain fog” experienced by some Covid patients — and it is also responsible for Alzheimer’s disease.

The finding adds to previous studies indicating that SARS-CoV-2 infection can both increase the risk of Alzheimer’s and worsen the condition among patients with the disease.

The team from Italy conducted experiments both on human nerve cells and mice to explore how the two conditions might be related.

They found that infection with COVID-19 causes so-called tau proteins to accumulate within nerve cells, impairing memory function.

Based on their results, the team are calling for clinicians to be aware of the possible neurological side-effects of Covid.

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The study was undertaken by Dr Cristina Di Primio of the Institute of Neuroscience of the National Research Council of Italy and her colleagues.

The researchers said: “Despite mainly leading to respiratory disease, increasing studies have reported that [Covid] can spread to other organs, including the central nervous system

“COVID-19 patients present indeed with acute neurological manifestations, such as altered smell and taste, as well as with long-term cognitive symptoms, namely fatigue, headache, attention disorders, dyspnea, and cognitive impairment — i.e. brain fog.

“This latter condition is defined as ‘neuro-COVID’ and represents a serious concern for global health as it has also been observed in individuals who experienced mild COVID-19 symptoms.”

In their investigation, the researchers infected both human neuroblastoma cell cultures and mice models with various strains of SARS-CoV-2.

The team found that when the virus infects either the human neuronal cells, or those of the mouse brain, it interacts with so-called tau proteins.

These proteins are ordinarily used by the body to strengthen the tiny tube-like internal structures of nerve cells, or neurons, in the brain.

In Alzheimer’s disease, however, an abnormal form of tau causes the proteins to stick together in certain parts of the brain, accumulating in tangles inside neurons.

These build-ups block the neurons’ transport systems and impedes the ability of nerve cells to communicate with each other — impeding memory function.

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Di Primio and her colleagues found that neuronal infection with Covid causes tau proteins to undergo a process called “hyperphosphorylation” that makes them more likely to form harmful tangles — just as they do in Alzheimer’s disease.

(Hyperphosphorylation is the technical term for when a biochemical gains an excess of phosphoryl group compounds, those made up of both phosphorus and oxygen atoms.

It occurs at sites along the protein dubbed “pathological epitopes”, which serve as binding locations for antibodies — also the same ones involved in Alzheimer’s.)

The team also report detecting a significant increase in tau levels in the insoluble fraction of infected cells — which they explain is another sign of harmful alterations to the protein.

The researchers said: “It is still unclear whether Tau aberrant phosphorylation profile and its consequent aggregation are caused by the virus itself upon infection or/and by an indirect cellular response.”

They explained that — by making the microtubule structure of neurons less stable — the cells could be trying to detach the viruses and prevent them from being transported to a site where they could replicate.

The team concluded: “Our data open up a new molecular mechanism underlying post-COVID neurological manifestations and acknowledge the potential scale of the disease’s long-term course.

“Although vaccination is currently the primary strategy for the management of the SARS-CoV-2 pandemic, patients who already experienced COVID-19 must not be side-lined.

“To limit long-term consequences, it is relevant for clinicians to be aware of the downstream pathophysiological aberrations when dealing with neuro-COVID cases.”

The full findings of the study were published in the journal PNAS Nexus.

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