Molecular aspects of medicineSep 17, 2026

How Changes in ACE2 and Fat Metabolism May Link COVID-19 and Brain Degeneration

Updated Sep 18, 2026

Abstract

Angiotensin-converting enzyme 2 (ACE2) is the primary cellular receptor of SARS-CoV-2.

ACE2 regulates blood pressure and inflammation by converting pro-inflammatory angiotensin II into the protective peptide angiotensin (1-7).
The lipid composition of the plasma membrane, particularly cholesterol-rich lipid rafts, influences ACE2 localization and viral access.
Dyslipidaemia, often seen in obesity and metabolic syndrome, is associated with higher susceptibility to severe COVID-19 and may increase systemic inflammation.
Aberrant lipid metabolism is linked to neurodegenerative diseases, which can cause neuroinflammation and synaptic dysfunction.
Similar lipid disturbances and inflammation are observed in patients with Long COVID, potentially worsening neurodegenerative processes.
Therapeutic strategies targeting ACE2 and lipid metabolism are reviewed for their potential to alleviate acute infection and long-term neurological effects.

Simplified

Angiotensin-converting enzyme 2 (ACE2) is the primary cellular receptor of SARS-CoV-2. It is a key regulator of the renin-angiotensin system (RAS) and modulates blood pressure and inflammatory pathways. ACE2 converts pro-inflammatory angiotensin II into the vasoprotective peptide, angiotensin (1-7). This is strongly influenced by the lipid composition of the plasma membrane. Cholesterol-rich lipid rafts play an important role in determining receptor localisation and viral accessibility. Dyslipidaemia, which is common in obesity, diabetes, and metabolic syndrome, has been associated with an increased susceptibility to severe COVID-19 and may amplify systemic inflammation. Aberrant lipid metabolism also contributes to neurodegenerative disorders, including Alzheimer's and Parkinson's diseases, which drive neuroinflammation, synaptic dysfunction, and blood-brain barrier impairment. Notably, similar disturbances and systemic inflammation are increasingly recognised in patients with Long COVID, suggesting overlapping mechanisms that may exacerbate or accelerate neurodegenerative processes. This review explores the interplay between ACE2 regulation, lipid metabolism, and systemic inflammation in COVID-19, with a particular focus on their implications for neurological health. Uniquely, we highlighted the intersection of ACE2 and lipid-related alterations in patients with Long COVID and their potential contribution to the progression of neurodegenerative diseases. In addition, we reviewed therapeutic strategies targeting ACE2, including recombinant soluble ACE2, ACE2-based nanotherapeutics, and lipid-focused interventions, aimed at mitigating acute infection, systemic inflammation, and persistent neurological sequelae. Understanding these mechanisms is essential to prevent long-term neurological consequences of the COVID-19 pandemic.

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How Changes in ACE2 and Fat Metabolism May Link COVID-19 and Brain Degeneration

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