Breaking News! Study Reveals Potential New Form of Brain Neurodegeneration Linked to COVID-19!

Medical News: A groundbreaking study has brought to light the possibility that COVID-19 could be causing a form of neurodegeneration different from Alzheimer’s disease. Researchers from prominent institutions in China and Guizhou Medical University in Guiyang have found that post-COVID-19 patients show unusual signs of brain degeneration, with tau hyperphosphorylation and neuroinflammation, even months after recovery. These findings open the door to new understandings of how COVID-19 might be affecting the brain in ways previously unrecognized.


Study Reveals Potential New Form of Brain Degeneration Linked to COVID-19

COVID-19’s Effect on the Brain
The study, led by Dr Xuetao Qi from Peking University and colleagues from multiple research centers, sheds light on a potentially dangerous consequence of COVID-19 recovery: brain changes that mimic some aspects of Alzheimer's disease but show a distinct pathway. Unlike Alzheimer's, which is primarily driven by amyloid plaques and tau protein tangles, COVID-19 seems to trigger neuroinflammation and hyperphosphorylation of tau proteins without altering amyloid-beta accumulation. This Medical News report will explain the findings of this research in simple terms for easy understanding.
 
The team collected brain samples from people who had died either with acute COVID-19 or months after recovery. Their analysis revealed startling evidence: patients who had recovered from COVID-19 had high levels of tau protein hyperphosphorylation in key brain areas associated with memory and cognition, even though they did not have Alzheimer's disease.
 
The Study’s Key Findings
The research team examined postmortem brain tissues from three different groups: individuals who had no COVID-19 infection, those who died during acute COVID-19, and those who died 4 to 13 months after recovering from the virus. They focused on regions of the brain like the hippocampus and the medial entorhinal cortex, both of which are crucial for memory and are highly vulnerable to degeneration in Alzheimer’s disease.
 
Surprisingly, patients who recovered from COVID-19 showed significant levels of tau hyperphosphorylation, particularly at sites commonly associated with Alzheimer's, such as Thr181, Thr217, and AT8. This tau hyperphosphorylation was absent in those who were not infected with SARS-CoV-2 or who had died during acute infection.
 
What is Tau Hyperphosphorylation?
Tau proteins are important for maintaining the structure of neurons in the brain. In healthy individuals, tau proteins help stabilize the internal scaffolding of nerve cells. However, when tau proteins become hyperphosphorylated, they can no longer perform this function properly. In Alzheimer’s, this leads to the formation of tangles that disrupt brain function, contributing to memory loss and cognitive decline.
 
The researchers observed that, in the brains of COVID-19 survivors, these tau proteins were altered in a way similar to what is seen in Alzheimer’s patients. This suggests that COVID-19 may set off a cascade of changes in the brain that could lead to neurodegeneration over time, even if the person did not have Alzheimer's before the infection.
 
Neuroinflammation and Glia Activation
Another key finding of the study was the presence of neuroinflammation in the brains of those who had recovered from COVID-19. Neuroinflammation refers to the activation of immune cells in the brain, which can lead to further damage if it persists for too long.
 
The researchers found that in COVID-19 survivors, microglia (the brain’s immune cells) were overactive and had an abnormal morphology. The activation of microglia is a known contributor to the development of Alzheimer’s and other neurodegenerative diseases. The study also noted an increase in inflammatory proteins like TNF-α and interleukin-6, which were elevated during both acute and post-acute COVID-19, further supporting the idea that inflammation plays a role in the observed brain changes.
 
No Change in Amyloid-Beta or Neuron Loss
Interestingly, while tau hyperphosphorylation and neuroinflammation were prominent in the brains of COVID-19 survivors, the researchers did not find any significant changes in amyloid-beta, the protein responsible for the hallmark plaques seen in Alzheimer’s. This is a major distinction from Alzheimer’s disease, which is driven by both tau tangles and amyloid plaques.
 
Additionally, the researchers found no evidence of neuron loss in the hippocampus, another feature commonly associated with Alzheimer’s. This suggests that while COVID-19 may induce some Alzheimer’s-like brain changes, it could be doing so through a different mechanism.
 
Impact on the Olfactory System
Given that many COVID-19 patients experience a loss of smell (anosmia) as a symptom, the research team also examined the olfactory system, which is often affected in Alzheimer’s disease. The areas they looked at included the olfactory bulb and other related structures in the brain.
 
The study found no significant changes in tau or amyloid-beta in the olfactory areas of the brain. This indicates that while COVID-19 can cause a loss of smell, this might not be related to the same mechanisms driving the tau hyperphosphorylation seen in the hippocampus and other regions.
 
The Possible Long-Term Effects
The findings of this study raise concerns about the long-term neurological effects of COVID-19. While the full implications are still unknown, it is possible that individuals who have recovered from COVID-19 could be at increased risk of developing a varied form of Alzheimer’s or other forms of neurodegeneration later in life.
 
However, the study also notes that these findings are preliminary, and more research is needed to determine how long these changes persist and what impact they may have on cognitive function over time. The researchers plan to continue their investigations by studying larger groups of patients and examining biomarkers in the blood and cerebrospinal fluid to monitor the progression of these changes.
 
Conclusion
In conclusion, this research highlights the emerging signs of Alzheimer’s-like brain changes in individuals who have recovered from COVID-19. The study demonstrates that COVID-19 can induce tau hyperphosphorylation and neuroinflammation, both of which are important in the development of neurodegenerative diseases. However, unlike Alzheimer’s, COVID-19 does not appear to affect amyloid-beta or cause neuron loss, indicating that this may be a unique form of neurodegeneration triggered by the virus.
 
As the researchers pointed out, more studies are necessary to fully understand the long-term effects of COVID-19 on the brain. Future research will focus on determining whether these changes are reversible or if they lead to a progressive decline in cognitive function.
 
The study findings were published in the peer-reviewed journal: Aging Cell.
https://onlinelibrary.wiley.com/doi/10.1111/acel.14352
 
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