Post by Nadica (She/Her) on Jun 14, 2024 8:27:09 GMT
Long COVID Looks Like Acute Infection in the Brain: Research finds immune pathway for the 50 percent who recover from long COVID. - Published June 12, 2024
KEY POINTS
Long COVID has the biological signature of an acute infection in the brain, according to a new research study. For patients with difficulty thinking or concentrating due to Long COVID, which has lasted over four years in some, this may be caused by ongoing COVID-19 infection. In addition, 50 percent of people with Long COVID brain fog do not get better, but in the 50 percent that do, the critical immune system pathway involves interferon.
A research team from Rutgers has isolated the molecular makeup of the immune system’s response to Long COVID in the brain by extensively testing cerebral spinal fluid (CSF). By mapping the proteomics of the CSF in Long COVID patients, the team has made an important step toward resolving an ongoing debate about the cause of Long COVID. Long COVID looks like an acute infection. It does not fit the pattern of a post-infectious autoimmune process or Alzheimer’s disease. Further, brain fog is not caused by anxiety or depression and is not “all in the patient’s head.”
Since evidence is growing that about 24 million Americans have had some form of Long COVID, and that we can develop long COVID even after several infections, these findings are important for all of us.
Clinical and CSF single-cell profiling of post-COVID-19 cognitive impairment - Published March 13, 2024
Highlights
•Improvement from post-COVID-19 cognitive impairment (CI) is slow
•Post-COVID-19 CI is molecularly distinct from Alzheimer’s disease
•Post-COVID-19 CI is associated with CSF monocyte recruitment and gene alterations
•Improvement from post-COVID-19 CI is linked to greater CSF interferon responses
Summary
Natural history and mechanisms for persistent cognitive symptoms (“brain fog”) following acute and often mild COVID-19 are unknown. In a large prospective cohort of people who underwent testing a median of 9 months after acute COVID-19 in the New York City/New Jersey area, we found that cognitive dysfunction is common; is not influenced by mood, fatigue, or sleepiness; and is correlated with MRI changes in very few people. In a subgroup that underwent cerebrospinal fluid analysis, there are no changes related to Alzheimer’s disease or neurodegeneration. Single-cell gene expression analysis in the cerebrospinal fluid shows findings consistent with monocyte recruitment, chemokine signaling, cellular stress, and suppressed interferon response—especially in myeloid cells. Longitudinal analysis shows slow recovery accompanied by key alterations in inflammatory genes and increased protein levels of CXCL8, CCL3L1, and sTREM2. These findings suggest that the prognosis for brain fog following COVID-19 correlates with myeloid-related chemokine and interferon-responsive genes.
KEY POINTS
- Long COVID patients with brain fog have the biological signature of an acute infection in the brain.
- 50 percent of people with cognitive impairment from Long COVID improve after two years, but very slowly.
- An effective interferon lambda response in the brain helps recovery from Long COVID cognitive impairment.
- Researchers call for a clinical trial on the use of interferon lambda to treat Long COVID brain fog.
- Long COVID brain fog is an inflammatory condition and is not "all in your head."
Long COVID has the biological signature of an acute infection in the brain, according to a new research study. For patients with difficulty thinking or concentrating due to Long COVID, which has lasted over four years in some, this may be caused by ongoing COVID-19 infection. In addition, 50 percent of people with Long COVID brain fog do not get better, but in the 50 percent that do, the critical immune system pathway involves interferon.
A research team from Rutgers has isolated the molecular makeup of the immune system’s response to Long COVID in the brain by extensively testing cerebral spinal fluid (CSF). By mapping the proteomics of the CSF in Long COVID patients, the team has made an important step toward resolving an ongoing debate about the cause of Long COVID. Long COVID looks like an acute infection. It does not fit the pattern of a post-infectious autoimmune process or Alzheimer’s disease. Further, brain fog is not caused by anxiety or depression and is not “all in the patient’s head.”
Since evidence is growing that about 24 million Americans have had some form of Long COVID, and that we can develop long COVID even after several infections, these findings are important for all of us.
Clinical and CSF single-cell profiling of post-COVID-19 cognitive impairment - Published March 13, 2024
Highlights
•Improvement from post-COVID-19 cognitive impairment (CI) is slow
•Post-COVID-19 CI is molecularly distinct from Alzheimer’s disease
•Post-COVID-19 CI is associated with CSF monocyte recruitment and gene alterations
•Improvement from post-COVID-19 CI is linked to greater CSF interferon responses
Summary
Natural history and mechanisms for persistent cognitive symptoms (“brain fog”) following acute and often mild COVID-19 are unknown. In a large prospective cohort of people who underwent testing a median of 9 months after acute COVID-19 in the New York City/New Jersey area, we found that cognitive dysfunction is common; is not influenced by mood, fatigue, or sleepiness; and is correlated with MRI changes in very few people. In a subgroup that underwent cerebrospinal fluid analysis, there are no changes related to Alzheimer’s disease or neurodegeneration. Single-cell gene expression analysis in the cerebrospinal fluid shows findings consistent with monocyte recruitment, chemokine signaling, cellular stress, and suppressed interferon response—especially in myeloid cells. Longitudinal analysis shows slow recovery accompanied by key alterations in inflammatory genes and increased protein levels of CXCL8, CCL3L1, and sTREM2. These findings suggest that the prognosis for brain fog following COVID-19 correlates with myeloid-related chemokine and interferon-responsive genes.