Barnali Ray Basu

Abstract

Worldwide pandemic of COVID-19 has resulted in various physiological manifestations mainly affecting the respiratory system and also the nervous system. Inflammation, a hallmark symptom of diseases links both COVID-19 and neurodegenerative disorders. COVID-19 infection resulted in immune responses like cytokine and chemokine production, and even cytokine storms (in severe cases), which lead to inflammation. Parkinson’s Disease (PD), characterised by motor difficulties is mainly due to ?-synuclein aggregates and the disease is known to have dual instigations. In one way the central inflammation caused due to tissue injury, glial cell dysfunction and proinflammatory molecule production, resulting in Blood Brain Barrier leakage and in another way peripheral inflammation occurs due to altered gut microbiome after pathogen attack, producing inflammatory mediators. Inflammation being a potential threat for onset and progression of PD is the major concern of this article. Immediate effect of COVID-19 might be respiratory ailment and hypoxia might contribute to inflammation but the long-lasting effects are uncertain which might increase neurodegenerative diseases in future. Anti-inflammatory therapeutic interventions have already shown varied results for COVID-19 infections of various stages but its impact on PD is yet to be studied. Here, we have elucidated the role of inflammation in the pathophysiology of PD and developing new therapeutic approach by targeting the inflammatory cascade.   Keywords: COVID- 19, Cytokines, Inflammation, Parkinson’s Disease.

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Abstract

Background: Polycystic ovary syndrome (PCOS), a multifaceted condition, often has salient features like insulin resistance (IR). Abnormal alternation in insulin synthesis and function usually alters PCOS expressivity by deviating molecular and biochemical activity underlying this pathophysiology. Aims: This review intends to unveil the molecular basis of the genetic polymorphism of IR and its correlation with PCOS. It also highlights the existing methods of IR estimation. Material and Methods: Searching of different articles using keywords including PCOS, IR, and polymorphism in various databases was performed to illustrate the review article. Conclusion: POCS, and IR are complex and multifactorial conditions in terms of the contributing factors, their interactions, and expressivity. Further studies on diversified genotype responses to environmental and ethnic variances are required for precise understanding. Key Messages: Insulin resistance (IR) and polycystic ovary syndrome (PCOS) are intricately interacted conditions that abnormally alter functions from genetic to organ system level. Complex gene-environment interactions make it difficult to understand the etiology and manifestation, and so diagnosis and management approaches of the heterogeneous pathophysiology are not foolproof. Further studies on genetic susceptibility related to ethnic distribution are essential for the implementation of personalized treatment of IR and PCOS.   Keywords: Polycystic ovary syndrome, Insulin resistance, Genetic polymorphism.

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