Reviewing data from past pandemics, researchers suggest some of those exposed to COVID-19 could have an increased risk of developing neurological and mental health disorders in the long term. Acute viral infections can result in encephalopathy, psychosis, depression, demyelination disorders, and problems with neuromuscular function.
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Enhancing mitochondrial transportation and cellular energetics could help promote regeneration and function following spinal cord injury.
Dopamine may play a role in activating immune cells to migrate in the early stages of infection.
A global knockout of the thrombin receptor PAR1 accelerates myelin development. The findings could help with the development of treatments for diseases associated with demyelination, like multiple sclerosis.
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Intercepting CCL2 with specific antibodies may provide an early intervention for chronic neuropathic pain.
Lewy body disorders, including Parkinson's disease and Lewy body dementia, comprise of two distinct subtypes. One subtype originates in the peripheral nervous system (PNS) of the gut and spreads to the brain. The other originates in the brain, or enters the brain via the olfactory system, before spreading to the brainstem and PNS.
In aging mice, chronic inflammatory processes lead lymphoma cells which entered the brain to be retained, rather than released directly back into the blood.
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People with functional dizziness do not appear to process sensory-motor impression correctly. Instead, they rely on a stored memory model which no longer matches immediate reality.
HIV can persist in the nervous system, even when the virus is suppressed. Even when the virus is suppressed, neurocognitive problems associated with the infection can persist.
A healthy and diverse microbiome is essential for quickly clearing viral infections in the nervous system to prevent risks associated with multiple sclerosis. Mice with lower gut bacteria had weaker immune responses and were unable to eliminate viruses, leading to worsening paralysis. Those treated with antibiotics before infection had fewer microglia.
Severed axonal segments signal to Schwann cells to begin actin sphere formation and axon disintegration. If the process is disrupted, axon disintegration is slowed and axon fragments impair nerve regeneration.
Schwann cells are much more prolific in generating myelin than previously believed. Knocking out the fbxw7 gene in mouse models, researchers discovered individual Schwann cells began to spread myelin across many axons.