Nikhil Prasad Fact checked by:Thailand Medical News Team Sep 19, 2026 47 minutes ago
A newly published scientific review is drawing attention to a potentially important biological connection between COVID-19, disrupted fat metabolism, and long-term neurological damage. Researchers argue that changes involving the SARS-CoV-2 receptor ACE2 and cellular lipids could help explain why neurological problems persist in some people with Long COVID and may overlap with pathways involved in Alzheimer’s and Parkinson’s diseases.
Scientists highlight an ACE2-lipid pathway that could connect Long COVID inflammation with lasting
neurological damage and neurodegenerative processes
The researchers are from the Center for Neuroscience and Cell Biology, Center for Innovative Biomedicine and Biotechnology; Department of Life Sciences; and PhD in Biosciences program at the University of Coimbra; CoLAB4Ageing in Portugal; and the Faculty of Chemistry and Biological and Chemical Research Centre at the University of Warsaw in Poland.
ACE2 Does More Than Let the Virus Enter
ACE2 is best known as the cellular receptor SARS-CoV-2 uses for entry, but it also helps control inflammation and blood pressure. It converts pro-inflammatory angiotensin II into angiotensin-(1–7), which has protective vascular effects. When SARS-CoV-2 binds ACE2, the receptor can be internalized, potentially weakening this protective pathway and promoting inflammation.
Crucially, ACE2 does not operate independently of surrounding fats. Cholesterol-rich membrane regions called lipid rafts can influence ACE2 accessibility and facilitate interactions between viral spike proteins and host cells. The review describes evidence that disrupting cholesterol-rich domains can reduce SARS-CoV-2 infection in experimental systems.
COVID-19 Hijacks the Cell’s Fat Machinery
SARS-CoV-2 also exploits cellular lipids after entry. The virus depends on host metabolism to build membranes needed for replication and promotes lipid droplets containing triglycerides. Researchers found alterations involving triglycerides, phosphatidylinositols, ceramides, and other lipid classes across viral variants.
This matters because abnormal lipid metabolism is also implicated in neurodegeneration. In this
Thailand Medical News report, the particularly striking connection is the blood-brain barrier—the protective interface separating circulating blood from brain tissue.
A meta-analysis cited by the authors involving more than four million COVID-19 patients found long-term fatigue in 43.3%, memory disorders in 27.8%, cognitive impairment in 27.1%, sleep disorders in 24.4%, and concentration problems and headaches in 20.3%.
Alzheimer’s and Parkinson’s Connections
The review describes overlapping mechanisms involving chronic inflammation, ACE2 imbalance, blood-brain barrier disruption, and abnormal lipid metabolism. Alzheimer’s research has linked these pathways with amyloid biology, while experimental Parkinson’s studies suggest SARS-CoV-2 proteins can promote neuroinflammation and c
hanges involving alpha-synuclein.
Potential treatments include recombinant soluble ACE2, ACE2-based nanoparticles, statins, cyclodextrins, and omega-3 fatty acids. However, these approaches remain at different experimental and clinical stages, and the review does not establish that they prevent neurodegenerative disease.
Conclusions
The evidence suggests COVID-19 and neurodegeneration may share interconnected ACE2, lipid, inflammatory, and vascular pathways. Determining whether SARS-CoV-2 actually accelerates neurodegenerative disease will require longer-term human studies, while ACE2- and lipid-targeted therapies warrant further clinical investigation.
The study findings were published in the peer reviewed journal: Molecular Aspects of Medicine.
https://www.sciencedirect.com/science/article/pii/S0098299726000750
Read Also:
https://www.thailandmedical.news/articles/coronavirus
https://www.thailandmedical.news/articles/long-covid
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