Does the temporary inactivation of ACE2 by the SARS-CoV-2 spike protein play a role in Alzheimer-like neurodegeneration?
This review highlights the potential role of ACE2 inactivation by SARS-CoV-2 in post-COVID-19 neurodegenerative processes, suggesting it as a possible biomarker or therapeutic target.
Angiotensin-converting enzyme 2 (ACE2) is a key component of the renin-angiotensin system's counter-regulatory pathway. ACE2 is a multifunctional protein whose location and form determine its catalytic and non-catalytic functions, including amino acid transport, the creation of structural complexes, adhesion, and involvement in signaling pathways. In addition, ACE2 influences neurotransmitter systems in the brain. As the main receptor for SARS-CoV-2, ACE2 has been the subject of increasing research interest. Although ACE2 levels in the brain are low, brain damage from SARS-CoV-2 increases the risk of neurodegenerative diseases. This review aims to clarify an important issue: does the temporary inactivation of ACE2 by the SARS-CoV-2 spike protein play a role in Alzheimer-like neurodegeneration, meaning that the protein may serve as a biomarker or therapeutic target?
Кононова et al. (Mon,) studied this question.
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