SARS-COV-2 AND NEURODEGENERATIVE DISEASE PROGRESSION: EXPLORING THE LINK BETWEEN VIRAL INFECTION AND NEUROLOGICAL DECLINE

Abstract

Purpose: The COVID-19 pandemic caused by SARS-CoV-2, has highlighted its systemic impact including long-term neurological consequences. Beyond acute symptoms such as encephalopathy and anosmia, evidence increasingly links SARS-CoV-2 infection to accelerated or aggravated neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), Parkinson’s disease (PD), and Alzheimer’s disease (AD). These disorders share pathological hallmarks such as chronic neuroinflammation, misfolded protein aggregation, and progressive neuronal loss. This review aims to elucidate the molecular mechanisms, clinical evidence, and epidemiological trends underlying the intersection between SARS-CoV-2 and neurodegeneration.

Key words: SARS Co V2, Neurodegeneration, Neuroinflamation, Protein aggregation, Alzemier disease, Parkinson disease

Methods: Studies on molecular pathways, neuroimaging results, biomarker studies, and epidemiological data connecting COVID-19 to neurodegenerative diseases were all included in the inclusion criteria. The main processes of interest included mitochondrial malfunction, cytokine-mediated neuroinflammation, hypoxia-induced neuronal death, and disruption of the blood-brain barrier (BBB).

Results: Results show a consistent correlation between SARS-CoV-2 infection and increased risk for cognitive decline and the advancement of neurodegenerative diseases. There were frequent reports of elevated pro-inflammatory cytokines, mitochondrial damage, and BBB permeability. According to MRI studies, COVID-19 survivors exhibit structural changes in their brains, especially in areas related to memory and motor control. After infection, biomarker investigations show elevated levels of tau phosphorylation, α-synuclein aggregation, and neurofilament light chain.

Conclusions: SARS-CoV-2 may exacerbate neurodegenerative processes through intertwined inflammatory, metabolic, and vascular mechanisms. Recognizing these links underscores the urgent need for longitudinal studies, early screening strategies, and targeted neuroprotective interventions. Understanding these pathways will inform future therapeutic and preventive measures to mitigate the neurological burden of COVID-19.