The impact of COVID-19 on the brain at the cellular level has been crucially shown by recent studies employing brain organoids, a miniature replica of brain tissue generated in laboratories.
These findings broaden our understanding of how the virus affects the nervous system and offer potential explanations for persistent neurological symptoms experienced by some long COVID-19 patients.
Scientists infected brain organoids with the SARS-CoV-2 virus, discovering that it not only spreads within neurons but also accelerates the destruction of synapses, essential connections between neurons. This synaptic loss may contribute to conditions like “brain fog,” characterized by disorientation, memory loss, chronic headaches, and numbness, affecting nearly 40% of long COVID patients.
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The Long-Term Neurological Effects of COVID-19
Long after the initial infection, COVID-19 patients experience a range of neural and behavioral problems. Some patients, according to neurologist Ayush Batra, exhibit symptoms of brain fog lasting upwards of a year. These lingering effects underscore the need to explore the virus’s persistence and impact on various body organs.
The brain is a complex network of nerve cells communicating through synapses, crucial for memory, movement control, and emotional responses.
Synapses constantly remodel through a process known as synaptic pruning, which is essential for learning, memory encoding, and recovery from injuries. Excessive pruning, however, may lead to neurological disorders such as schizophrenia and neurodegenerative diseases.
Brain organoid studies revealed that SARS-CoV-2 activates microglia—the brain’s immune cells—resulting in increased synaptic pruning. Excessive elimination of synapses, observed in the study, may adversely impact a person’s ability to form new memories and explain the sluggish brain functions seen in long COVID-19 patients with brain fog.
A follow-up study suggests that the C4A protein, involved in removing microbes and infected cells, may tag synapses for removal.
While not directly linking C4A to brain fog, this research hints at genetic factors influencing synaptic pruning after infection-induced inflammation.
Evidence suggests that even mild COVID-19 can lead to a loss of gray matter—the brain’s outer layer responsible for movement control, memory, and emotions.
Studies indicate that the virus may accelerate cognitive decline equivalent to ten years of normal aging, especially in severe cases or prolonged COVID-19.
The study shows that the genes activated by hyperactive microglia in brain organoids after SARS-CoV-2 infection mimic those seen in neurodegenerative disorders. This finding may explain the higher risk of developing neurological or psychiatric conditions post-COVID-19 disease.
Brain organoid studies offer a unique window into understanding how COVID-19 affects the brain at a cellular level.
Insights into synaptic destruction, genetic factors, and hyperactive microglia contribute to understanding long-term neurological symptoms in COVID-19 patients.
Continued research in this area is vital for developing targeted interventions and improving the long-term outcomes for individuals affected by the virus.
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