- Clinicians have found that COVID-19 is associated with neurological symptoms.
- Scientists need to do more research to understand how COVID-19 is related to these neurological symptoms.
- Researchers presented their findings on these connections at Neuroscience 2021, the annual conference of the Society for Neuroscience.
Researchers have investigated how COVID-19 affects a person’s nervous system and causes neurological symptoms.
This week they presented their findings at Neuroscience 2021. This event is the annual meeting of the Society for Neuroscience, the largest global association for scientists and clinicians focusing on brain and nervous system health issues.
The findings indicate how SARS-CoV-2 — the virus that causes COVID-19 — gains access to a person’s brain. They also provide insight into the effects it has once it gets into this part of the body.
For most people, the primary symptoms of COVID-19 are breathing problems. According to the
These symptoms and other less common symptoms can range in severity from mild to life-threatening. Some people who get SARS-CoV-2 infection may even remain asymptomatic.
In addition to these respiratory symptoms, clinicians and researchers have also observed several neurological symptoms associated with COVID-19.
Researchers have linked COVID-19 to headaches, brain inflammation, muscle weakness or pain, and numbness or weakness in a person’s hands, feet or limbs.
However, further research is needed to understand how COVID-19 affects a person’s nervous system.
At Neuroscience 2021, a number of articles have detailed findings examining how SARS-CoV-2 is likely to affect a person’s brain.
dr. Ashutosh Kumar, an assistant professor in the Department of Anatomy at the All India Institute of Medical Sciences, Patna, India, presented findings identifying a potential receptor that may allow SARS-CoV-2 access to a person’s brain.
In other parts of the body, SARS-CoV-2 gains access to cells by binding to the protein angiotensin converting enzyme 2 (ACE2) using transmembrane serine protease 2 (TMPRSS2). However, ACE2 and TMPRSS2 are not significantly present in a person’s brain.
Speak with Medical news today, dr. Kumar said: “We know that COVID-19 patients show prominent neuropsychiatric symptoms and [that] virus-induced injuries – including evidence of the virus replicating in brain tissue – have been noted in the postmortem studies. However, a negligible expression of the ACE2 and TMPRSS2 left an important question [un]replied: How does SARS-CoV-2 enter brain cells?”
“Through [the middle] In the past year, another receptor — neuropilin-1 precursor (NRP1), a cell surface protein involved in brain development and causing cancer — was shown to be able to bind to furin-cleaved SARS CoV-2 spike protein[s]. Uniquely, no TMPRSS2 was required for binding to the NRP1.”
“Out of curiosity, we monitored the expressions of NRP1 and furin in postmortem human brain tissue, which” [revealed] that both molecules are abundant in all major brain regions – primarily the olfactory and hippocampus.”
Olfactory nerves provide a way for the virus to get to the brain through the nose, and their infection may also explain the loss of smell as a key symptom in COVID-19. Furthermore, the involvement of the hippocampus may explain the prominence of psychiatric symptoms in COVID-19 patients during and after recovery from acute illness,” said Dr. Kumar.
for dr. Kumar’s findings could help identify future drugs to protect against or treat the neurological symptoms of COVID-19.
“Our findings are important in that they indicate putative drug targets for the prevention and treatment of neuropsychiatric symptoms in COVID-19. The binding sites of NRP1 and furin on the SARS-CoV-2 spike protein can be attacked by various approaches, such as with monoclonal antibodies or decoy receptors,” said Dr. Kumar.
The findings appear in both the Journal of Neuroscience Research and Frontiers in Immunology.
Prof. dr. John H. Morrison, director of the California National Primate Research Center at the University of California, Davis, presented research on a study involving rhesus monkeys. These findings also suggest that the olfactory system could be the way SARS-CoV-2 accesses the brain.
Prof. dr. Morrison told: MNT: “The monkeys were infected and sacrificed through the nose as well as through the trachea  days after infection. We were particularly interested in whether old type 2 diabetic (T2D) monkeys were more vulnerable to neuroinvasion by the virus than young monkeys, as aging and T2D are important co-morbidities in humans.”
“We studied the brains of four groups: 1) young [with neither the infection nor diabetes], 2) young [with the infection but without diabetes], 3) old [with neither the infection nor diabetes], and 4) old [with both the infection and diabetes]. The main findings are that:
- SARS-CoV-2 proteins and evidence of productive viral infection were present in multiple brain regions 7 days post-infection.
- The regions primarily affected were the cortical regions that receive direct olfactory input, suggesting that the virus enters the nose through the olfactory system.
- Neurons were the main cell type to get infected.
- Pathology is also seen in cortical regions receiving input from the primary olfactory regions, demonstrating that the virus can be transmitted through circuits and connections.
- SARS-CoV-2 infection led to neuroinflammation, as well as neurodegeneration.
- Older T2D monkeys have much more widespread and aggressive brain infections.”
For Prof. Morrison, the findings make it clear that COVID-19 is both a neurological and a respiratory disease.
“There is an ongoing debate about whether SARS-CoV-2 can infect neurons,” says Prof. Morrison. “These 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 from the nose.”
“The direct access via [the] olfactory system, productive infection of neurons and transport to multiple brain regions by SARS-CoV-2 is the likely cause of neurological complications in COVID-19, such as anxiety, amnesia and ‘brain fog’. The increased vulnerability of ancient T2D monkeys suggests that such comorbidities in humans may also lead to more extensive neurological complications.”
“So Covid-19 is potentially both a brain disease and a respiratory disease, and prevention and treatment of patients with long-term symptoms of COVID-19 should focus on protecting the brain and [the] heart and lungs. In addition, such treatments should be applied very early after infection, as this occurred in  to dawn.”
For Prof. Morrison, a better understanding of the neurological effects of COVID-19 will likely help researchers understand long-term COVID-19.
“Many of the symptoms associated with ‘long COVID’ are neurological in nature and are likely caused by neuroinvasion and infection of neurons. We do not know whether such symptoms are related to persistent infection of circuitry-connected neurons or by damage that occurred early and lasts longer than the infection,” said Prof. Morrison.
Prof. dr. Morrison noted that the finding that older T2D monkeys had more severe neurological infections was supported by research in humans.
“Clinical studies have shown that [older people] are much more likely to show neurological symptoms. In addition, the virus reaches some areas of the brain that are also very vulnerable to Alzheimer’s disease, but we don’t know whether such an infection makes a patient more vulnerable to Alzheimer’s disease in the future,” said Prof Morrison.
In another study, researchers found that SARS-CoV-2 may also be able to access a person’s brain through nerves that transmit touch and pain.
Jonathan Joyce – a graduate student in Dr. Andrea S. Bertke in the Department of Population Health Sciences at Virginia Tech, Blacksburg, VA — used a mouse model to investigate whether SARS-CoV-2 could infect peripheral nerves. dr. Bertke worked closely with Joyce during the investigation.
Speak with MNT, Joyce said that “[w]While most of the attention that has been paid to assessing the ability of SARS-CoV-2 to enter the nervous system has focused on the central nervous system – the brain, for example – we have found that SARS-CoV-2 neurons of the peripheral nervous system.”
“Previous studies have shown that SARS-CoV-2 can infect nerves in the peripheral nervous system, but they only looked at nerves responsible for smell.”
“We have shown that SARS-CoV-2 is able to infect additional nerves of the peripheral nervous system in the head, neck and body that are responsible for performing automatic bodily – e.g. superior cervical ganglion – functions and transmitting of sensory information, particularly those that transmit touch and pain to the brain and spinal cord – for example, trigeminal ganglion and dorsal root ganglion.”
“We also found that several brain regions affected by COVID-19 can be infected by SARS-CoV-2. It is worth noting that these findings are based on a mouse model of infection and will need to be replicated in other animal models for verification,” Joyce said.
According to Joyce, the value of the research is that it shows that SARS-CoV-2 is not limited to infecting the central nervous system, but can also infect the peripheral nervous system at multiple points.
“Many studies examining how SARS-CoV-2 enters the nervous system focuses on how it enters the brain using neurons in the nose that are responsible for smell,” Joyce said.
“Our findings show that the virus can infect the peripheral nervous system at multiple points, particularly between nerves that transmit touch and pain, and that some of these points have connections to areas of the brain affected by COVID-19.”
“Presence of the virus in these nerves may contribute to the symptoms” [that] people with COVID-19 [experience].”
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