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A new study provides a better understanding of how the pandemic virus causes depression, anxiety, and the loss of concentration known as “brain fog” in patients that develop long COVID.

In most individuals, the virus, SARS-CoV-2, is successfully cleared by the immune system, but some struggle with prolonged complications, the cause of which is unknown.

Led by researchers from NYU Grossman School of Medicine, w wordsworth preface to lyrical ballads summary the study, which examined hamsters and human tissue samples, found that, well after the initial viral infection was over, the most profound biological changes occur in the olfactory system, made up of the nasal cavity, the specialized cells lining it, and the adjacent brain region that receives input on odors, the olfactory bulb. While a recent study from the same lab showed how SARS-COV-2 infection hinders the sense of smell by changing the activity of certain olfactory proteins (receptors), the new study reveals how the sustained immune reaction in olfactory tissue affects brain centers that govern emotion and cognition.

Published online June 7in Science Translational Medicine, the study is the first to show that hamsters previously infected with SARS-CoV-2 develop a unique inflammatory response in olfactory tissue, say the study authors. Unlike much of the COVID-19 research published to date, this study benchmarked how the response to SARS-CoV-2 in hamsters compared to influenza A, the virus responsible for the ‘swine flu’ pandemic in 2009. Specifically, the study found that while the two viruses generated a similar response in the lungs, only SARS-CoV-2 triggered a chronic immune response in the olfactory system that was still evident one month post-viral clearance.

This chronic inflammatory state seen with SARS-CoV-2 corresponded with an inrushing of immune cells such as microglia and macrophages, which clean up debris left in the wake of the dead and dying olfactory cell lining. They recycle that material but also trigger additional production of cytokines, pro-inflammatory signaling proteins. This biology was also evident in olfactory tissue taken from autopsies in patients that had recovered from initial COVID-19 infections, but had died of other causes.

“Given the systemic scope of its findings, this study suggests that the molecular mechanism behind many long COVID-19 symptoms stems from this persistent inflammation while describing an animal model close enough to human biology to be useful in the design of future treatments,” says senior study author Benjamin tenOever, PhD, professor in the Departments of Medicine and Microbiology at NYU Langone Health.

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