Nikhil Prasad Fact checked by:Thailand Medical News Team Nov 19, 2025 7 hours, 11 minutes ago
Medical News: A new scientific review warns that the same ACE2 receptor used by the SARS-CoV-2 virus to enter human cells may also play a far more dangerous long-term role in the brain. Researchers from the Institute of Cell Biophysics at the Federal Research Center Pushchino Scientific Center for Biological Research of the Russian Academy of Sciences, the National Medical Research Center for Obstetrics Gynecology and Perinatology in Moscow, and the Institute of Future Biophysics have pieced together a concerning picture of how ACE2 disruption may trigger Alzheimer-like changes in people recovering from COVID-19.
ACE2 Disruption After COVID-19 May Spark Hidden Brain Decline
How ACE2 Keeps the Brain in Balance
ACE2 is not just a viral entry point. It is a key molecule that helps reduce inflammation, protect nerves, regulate blood flow, and balance critical brain chemicals. Although ACE2 levels in the brain are naturally low, they are concentrated in areas important for memory, smell, mood, and movement. When functioning normally, ACE2 reduces the harmful effects of another molecule called Angiotensin II, which can cause oxidative stress, inflammation, and damage to blood vessels. When ACE2 is reduced or temporarily switched off, these harmful processes intensify. According to this
Medical News report, even mild disruptions may cause long-term consequences.
How COVID19 Interferes with ACE2
The virus binds tightly to ACE2 on brain-related cells, temporarily disabling it. This loss triggers a chain reaction: inflammation increases, oxidative stress rises, and protective molecules like Angiotensin (1–7) decrease. Over time, these changes can weaken the blood-brain barrier, reduce the brain’s ability to clear toxic proteins, and interfere with neurotransmitters responsible for mood and cognition. The study highlights that ACE2 also influences systems such as GABA and glutamate, which are essential for learning, memory, and preventing nerve cell over-excitation.
Key Findings from the Study
Researchers showed that:
– SARS-CoV-2-mediated ACE2 inactivation pushes the brain’s chemical balance toward inflammation.
– ACE2 regulates beta-amyloid breakdown, suggesting its loss could mimic early Alzheimer’s disease pathways.
– Chronic ACE2 imbalance affects blood flow regulation, making nerve cells more vulnerable to injury.
– Long COVID patients with brain fog, memory problems, or mood shifts may be experiencing early neurodegenerative-like changes driven by disturbed ACE2 pathways.
– ACE2 interacts with many signaling routes linked to oxidative stress, cell survival, and inflammation, meaning its impairment affects multiple systems simultaneously.
Conclusion
Although the review does not claim that COVID-19 directly causes Alzheimer’s disease, it
warns that repeated or prolonged ACE2 disruption—especially in older adults or individuals with underlying health risks—may accelerate processes similar to early neurodegeneration. As millions worldwide continue to struggle with long COVID symptoms, understanding ACE2’s role may be crucial for developing future treatments. Protecting ACE2 function could become an important strategy to reduce long-term neurological damage.
The study findings were published in the peer reviewed International Journal of Molecular Sciences
https://www.mdpi.com/1422-0067/26/22/11104
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Read Also:
https://www.thailandmedical.news/articles/coronavirus
https://www.thailandmedical.news/articles/long-covid
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