What could be causing neurological symptoms?
- Clinicians have found that COVID-19 is associated with neurological symptoms.
- Scientists need to do more research to understand how COVID-19 is linked to these neurological symptoms.
- The researchers presented their findings on these links at Neuroscience 2021, the annual conference of the Society for Neuroscience.
Researchers explored how COVID-19 affects a person’s nervous system, causing neurological symptoms.
This week, they presented their findings at Neuroscience 2021. This event is the annual meeting of the Society for Neuroscience, which is the world’s largest society for scientists and clinicians focused on brain and nervous system health issues.
The results indicate how SARS-CoV-2 – the virus that causes COVID-19 – accesses a person’s brain. They also give insight into the effects it has once it has entered that part of the body.
For most people, the main symptoms of COVID-19 are respiratory. According to
These and other less common symptoms can range in severity from mild to life threatening. Some people who get an infection with SARS-CoV-2 may even remain asymptomatic.
In addition to these respiratory symptoms, clinicians and researchers have also observed various neurological symptoms associated with COVID-19.
Researchers have linked COVID-19 to headaches, inflammation of the brain, muscle weakness or pain, and numbness or weakness in a person’s hands, feet or limbs.
However, more research is needed to understand how COVID-19 affects a person’s nervous system.
At Neuroscience 2021, a number of articles detailed the findings exploring how SARS-CoV-2 is likely to affect a person’s brain.
Dr Ashutosh Kumar, Assistant Professor in the Department of Anatomy at the All India Institute of Medical Sciences, Patna, India, presented results that identified a possible receptor that could give SARS-CoV-2 access to the brain of a anybody.
In other parts of the body, SARS-CoV-2 accesses cells by binding to angiotensin-converting enzyme 2 (ACE2) using transmembrane serine protease 2 (TMPRSS2). However, ACE2 and TMPRSS2 are not significantly present in a person’s brain.
Talk with Medical News TodayDr Kumar said: âWe know that COVID-19 patients have significant neuropsychiatric symptoms and [that] virus-induced injury – including evidence of virus replication in brain tissue – has been noted in postmortem studies. However, negligible expression of ACE2 and TMPRSS2 left a key question [un]Answered: How does SARS-CoV-2 get into brain cells?
“Through [the middle] last year, another receptor – the precursor of neuropilin-1 (NRP1), a cell surface protein involved in brain development and the cause of cancers – was found to be able to bind to the protein of furin-cleaved SARS-CoV-2 tip[s]. Uniquely, binding to NRP1 did not require TMPRSS2.
âOut of curiosity, we checked the expressions of NRP1 and furin in post-mortem human brain tissue, which [revealed] that these two molecules are abundant in all key regions of the brain, mainly the olfactory and the hippocampus.
âOlfactory nerves present a route for the virus to enter the brain through the nose, and their infection may also explain loss of smell as a key symptom of COVID-19. Additionally, the involvement of the hippocampus may explain the importance of psychiatric symptoms in COVID-19 patients during and after recovery from acute illness, âsaid Dr. Kumar.
For Dr Kumar, his team’s findings could help identify future drugs to protect or treat neurological symptoms of COVID-19.
âOur findings are important in that they indicate putative drug targets for preventing and treating neuropsychiatric symptoms in COVID-19. The NRP1 and furin binding sites at the SARS-CoV-2 spike protein can be targeted with various approaches, such as with monoclonal antibodies or decoy receptors, âsaid Dr. Kumar.
The results appear in both the Neuroscience Research Journal and Frontiers in immunology.
Professor John H. Morrison, director of the California National Primate Research Center at the University of California at Davis, presented research on a study using rhesus monkeys. These results also suggest that the olfactory system may be the means by which SARS-CoV-2 accesses the brain.
Professor Morrison said MNT: “The monkeys were infected both through the nose and trachea and were sacrificed  days after infection. We were particularly interested in whether elderly type 2 diabetic (T2D) monkeys were more vulnerable to neuroinvasion by the virus than young monkeys, given that aging and T2D are key comorbidities in humans.
âWe studied the brains of four groups: 1) young people [with neither the infection nor diabetes], 2) young [with the infection but without diabetes], 3) aged [with neither the infection nor diabetes], and 4) aged [with both the infection and diabetes]. The main findings are that:
- SARS-CoV-2 proteins and evidence of productive viral infection were present in several areas of the brain 7 days after infection.
- The main areas affected were the cortical regions that receive a direct olfactory supply, suggesting that the virus enters through the olfactory system in the nose.
- Neurons were the main type of infected cells.
- Pathology is also observed in cortical regions which receive information from primary olfactory regions, demonstrating that the virus can be transmitted through circuits and connections.
- Infection with SARS-CoV-2 resulted in neuroinflammation, as well as neurodegeneration.
- Older T2DM monkeys have a much more widespread and aggressive brain infection. “
For Professor Morrison, the results clearly show that COVID-19 is a neurological as well as a respiratory disease.
“There has been an ongoing debate as to whether or not SARS-CoV-2 can infect neurons,” Professor Morrison said. âThese findings unequivocally demonstrate that neurons can be infected in our monkey model of COVID-19 and that the virus appears to enter the brain through olfactory connections in the nose. “
“Direct entry through [the] The olfactory system, productive infection of neurons, and transport to multiple regions of the brain by SARS-CoV-2 are the likely cause of neurological complications in COVID-19, such as anxiety, memory loss, and ” brain fog â. The increased vulnerability of older T2DM monkeys suggests that such comorbidities in humans may also lead to more widespread neurological complications.
“Thus, COVID-19 is potentially a brain disorder as well as a respiratory disease, and the prevention and treatment of patients with long-term symptoms of COVID-19 should aim to protect the brain as well as [the] heart and lungs. In addition, these treatments should be applied very soon after infection as this has occurred in  days.”
For Professor Morrison, a better understanding of the neurological effects of COVID-19 is likely to help researchers understand the long COVID.
“Many of the symptoms associated with ‘long COVID’ are neurological in nature and likely to be caused by neuroinvasion and infection of neurons. We do not know whether such symptoms are related to continued infection of circuit-linked neurons or neurons. by damage that occurred early and survives infection, âsaid Professor Morrison.
Professor Morrison noted that the finding that older T2DM monkeys had more severe neurological infections was supported by research in humans.
âClinical studies have shown that [older people] are much more likely to have neurological symptoms. In addition, the virus also reaches certain regions of the brain that are very vulnerable to Alzheimer’s disease, but we do not know if such an infection makes a patient more vulnerable to Alzheimer’s disease in the future, âsaid the professor. Morrison.
In another study, researchers found that SARS-CoV-2 is also likely to access a person’s brain through the nerves that transmit touch and pain.
Jonathan Joyce – a graduate student in the lab of Dr. Andrea S. Bertke of the Department of Population Health Sciences at Virginia Tech, Blacksburg, VA – used a mouse model to determine if SARS-CoV-2 could infect peripheral nerves . Dr Bertke worked closely with Joyce throughout the study.
Talk with MNT, Joyce said that “[w]While most of the attention paid to assessing the ability of SARS-CoV-2 to invade the nervous system has focused on the central nervous system – for example, the brain – we have found that SARS -CoV-2 can infect neurons of the peripheral nervous system. “
“Previous studies have shown that SARS-CoV-2 can infect nerves in the peripheral nervous system, but they have only looked at the nerves responsible for smell.”
âWe have shown that SARS-CoV-2 is able to infect additional nerves of the peripheral nervous system in the head, neck and body responsible for the automatic performance of bodily functions – for example, the upper cervical ganglia – and the transmission of sensory information, particularly those that transmit touch and pain, to the brain and spinal cord – for example, the trigeminal ganglion and the dorsal root ganglion.
âWe have also found that various regions of the brain impacted by COVID-19 are susceptible to infection with SARS-CoV-2. It should be noted that these results are based on a mouse infection model and will need to be repeated in other animal models for verification, âJoyce said.
According to Joyce, the value of the research is that it shows that SARS-CoV-2 does not only infect the central nervous system but can also infect the peripheral nervous system in several places.
âMany studies that investigate how SARS-CoV-2 enters the nervous system focus on how it enters the brain using the neurons in the nose responsible for smell,â Joyce said.
âOur results show that the virus can infect the peripheral nervous system in several places, especially among the nerves that transmit touch and pain, and that some of these points have connections with regions of the brain affected by COVID-19. “
“The presence of the virus in these nerves can contribute to the symptoms [that] people with COVID-19 [experience]. “
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