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Virus may Stick Around in Your brain

n McNamara, D. (2023, April 13). https://www.medscape.com/ viewarticle/990741

For those experiencing “brain fog” after COVID-19, scientists now have a possible explanation—and it might not bring much comfort. Researchers found that part of the virus, the spike protein, remains in the brain long after viral infection. Researchers in Germany discovered the spike protein from the virus in brain tissue of animals and people after death. The finding suggests these virus fragments build up, stick around, and trigger inflammation that causes long COVID symptoms.

About 15% of COVID patients continue to have long-term effects of the infection despite their recovery, said senior study author Ali Ertürk, PhD, director of the Institute for Tissue Engineering and Regenerative Medicine at the Helmholtz Center Munich in Germany. Reported neurological problems include brain fog, brain tissue loss, a decline in thinking abilities, and problems with memory, he said. “These symptoms clearly suggest damages and long-term changes caused by SARS-CoV-2 in the brain, the exact molecular mechanisms of which are still poorly understood,” Ertürk said. Delivered by circulating blood, the spike protein can stay inside small openings in the bone marrow of the skull called niches. It can also reside in the meninges, thin layers of cells that act as a buffer between the skull and the brain. From there, one theory goes, the spike protein uses channels to enter the brain itself.

The hope is researchers can develop treatments that block one or more steps in this process and help people avoid long COVID brain issues. The spike protein may accumulate in structures outside the brain and cause ongoing inflammation. The clustering of spike proteins would trigger an immune response from this niche reservoir of immune cells that cause the inflammation associated with long COVID and the symptoms such as brain fog, researcher Topol said. Problems with thinking and memory after COVID infection are relatively common. One research team found 22% of people with long COVID specifically reported this issue, on average, across 43 published studies. Even people who had mild COVID illness can develop brain fog later, Ertürk and colleagues note.

So why are researchers blaming the spike protein and not the whole COVID virus? As part of the study, they found SARS-CoV-2 virus RNA in some people after death and not in others, suggesting the virus does not need to be there to trigger brain fog. They also injected the spike protein directly into the brains of mice and showed it can cause cells to die. Researchers also found no SARS-CoV-2 virus in the brain parenchyma, the functional tissue in the brain containing nerve cells and non-nerve cells, but they did detect the spike protein there. Researchers found COVID can change how proteins act in and around the brain. Some of these proteins are linked to Parkinson’s disease and Alzheimer’s disease, but have never before been linked to the virus. Another unexpected finding was how close the findings were in mice and humans. There was a “remarkable similarity of distribution of the viral spike protein and dysregulated proteins identified in the mouse and human samples,” Ertürk said. Tests for protein changes in the skull or meninges would be invasive but possible compared to sampling the parenchyma inside the brain. Even less invasive would be testing blood samples for altered proteins that could identify people most at risk of developing brain complications after COVID illness. It will take more brain science to get there. “Designing treatment strategies for these neurological symptoms requires an in-depth knowledge of molecules dysregulated by the virus in the brain tissues,” Ertürk said.

n Individual response to bP meds Shows “Substantial” Variation

n Hughes, S. (2023, April 13). https://www.medscape.com/ viewarticle/990739

A new study has shown a substantial variation in the blood pressure response to various antihypertensive medications between individuals. Some people may be better treated with one antihypertensive drug rather than another. This raises the possibility of future personalized therapy. The study’s lead author, Johan Sundström, MD, Uppsala University Hospital, Sweden described findings where “using the optimal antihypertensive drug for a particular patient resulted in an average of a 4.4 mm Hg greater reduction of blood pressure compared with a random choice of the other drugs. That is quite a substantial difference, and could be equivalent to adding in another drug.”

Authors note that despite global access to multiple classes of highly effective blood pressure-lowering drugs, only 1 in 4 women and 1 in 5 men with hypertension reach treatment targets. While most hypertension guidelines advocate combination pharmacotherapy, many patients in routine care continue to be treated with monotherapy, with adverse effects and nonadherence being important clinical problems. “One drug often does not give enough blood pressure reduction, but patients are often reluctant to up-titrate to two drugs,” Sundström said. “While we know that the four recommended classes of antihypertensives lower blood pressure equally well on average, we don’t know if their efficacy is the same in individual patients. “We wondered whether there could be different optimal drugs for different people, and if we could identify the optimal drug for each person then maybe more patients could get to target levels with just one drug,” he said.

The researchers conducted a randomized, double-blind, repeated crossover trial at an outpatient research clinic in Sweden, studying 280 men and women with grade 1 hypertension at low risk for cardiovascular