期刊
ANNALS OF INDIAN ACADEMY OF NEUROLOGY
卷 26, 期 2, 页码 127-136出版社
WOLTERS KLUWER MEDKNOW PUBLICATIONS
DOI: 10.4103/aian.aian_767_22
关键词
Neurodegeneration; neuro-inflammation; olfactory nerve; Parkinson's disease; SARS-CoV2; vagus nerve
Since the emergence of COVID-19, evidence has shown that SARS-Cov2 affects not only the lungs but also various cellular pathways related to protein homeostasis, mitochondrial function, stress response, and aging. Survivors of COVID-19 may be at risk for developing neurodegenerative diseases, including Parkinson's disease, due to the virus's ability to invade the central nervous system and induce abnormal protein folding and stress response. However, more robust evidence is needed to confirm this potential link.
Since the first emergence of COVID-19 on the global stage, there has been a wealth of evidence to suggest that SARS-Cov2 is not merely a pulmonary pathogen. This virus is unique in its ability to disrupt cellular pathways related to protein homeostasis, mitochondrial function, stress response, and aging. Such effects raise concerns about the long-term fate of survivors of COVID-19 infection, particularly regarding neurodegenerative diseases. The concept of interaction between environmental factors and alpha-synuclein formation in the olfactory bulb and vagal autonomic terminals with subsequent caudo-cranial migration has received much attention in the context of PD pathogenesis. Anosmia and gastrointestinal symptoms are two well-known symptoms of COVID-19, with evidence of an olfactory bulb and vagal infiltration by SARS-CoV2. This raises the possibility of the spread of the viral particles to the brain along multiple cranial nerve routes. Neurotropism, coupled with the ability of the SARS-Cov2 virion to induce abnormal protein folding and stress responses in the central nervous system, in presence of an inflammatory milieu, reinforced by hypoxia, coagulopathy, and endothelial dysfunction, reverberates the intriguing possibility of activation of a neurodegenerative cascade leading to the development of pathological alpha-synuclein aggregates and thus, triggering the development of PD in survivors of COVID19. This review attempts to summarize and critically appraise existing evidence from basic science research and clinical reports of links between COVID-19 and PD and explores the prospect of a multi-hit pathophysiological process, induced by SARS-Cov2 infection, ultimately converging on perturbed cellular protein homeostasis, which although is intriguing, presently lacks robust evidence for confirmation.
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