ACE2-Associated Vascular and Immune Mechanisms Underlying COVID-19 Neurological Injury

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According to recent research,

Receptor-mediated mechanisms underlying neurological complications in COVID-19: from viral entry to neuroinflammation https://link.springer.com/article/10.1007/s13205-026-04749-4

Neurological problems caused by COVID-19 can occur during the infection or continue afterward as long-term symptoms. Scientists still do not fully understand exactly how these problems develop. However, research from clinical studies, brain imaging, tissue analysis, and molecular biology suggests that the virus usually does not directly infect large parts of the brain. Instead, most neurological damage appears to happen through immune reactions and blood-vessel problems triggered by the virus.

The virus mainly enters cells through a receptor called ACE2. Another molecule, neuropilin-1 (NRP1), may help the virus reach areas such as the olfactory system and nearby blood vessels. Other receptors, including CD147 and DPP4, probably do not act as main entry points for the virus in the brain. Rather, they may influence the disease indirectly by contributing to blood-vessel dysfunction and immune activation.

The body’s immune sensors, especially Toll-like receptors (TLR2, TLR4, and TLR7), can strongly activate inflammation when they detect viral components. This inflammatory response can damage the blood–brain barrier, injure small blood vessels, and keep brain immune cells (microglia) activated for long periods.

Heightened inflammation may indirectly promote disease progression by driving vascular dysfunction and immune activation, thereby potentially contributing to the development of antiphospholipid syndrome (APS). 

Evidence from cerebrospinal fluid tests and brain imaging supports a model in which neurological symptoms arise from two mechanisms: a small amount of direct viral presence in the nervous system combined with a larger immune-mediated injury.

Treatments that target viral entry pathways or reduce brain inflammation are still mostly experimental. Future therapies will likely need to be tailored to the stage of the disease and guided by biological markers, helping doctors manage both the acute neurological effects of COVID-19 and long-term complications.

 

© 2000-2030 Sieglinde W. Alexander. All writings by Sieglinde W. Alexander have a fife year copy right. Library of Congress Card Number: LCN 00-192742 ISBN: 0-9703195-0-9 

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