Browsing by Author "Anindita Banerjee"

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COVID-19 in India: Are biological and environmental factors helping to stem the incidence and severity?
(International Society on Aging and Disease, 2020) Sankha Shubhra Chakrabarti; Upinder Kaur; Anindita Banerjee; Upasana Ganguly; Tuhina Banerjee; Sarama Saha; Gaurav Parashar; Suvarna Prasad; Suddhachitta Chakrabarti; Amit Mittal; Bimal Kumar Agrawal; Ravindra Kumar Rawal; Robert Chunhua Zhao; Indrajeet Singh Gambhir; Rahul Khanna; Ashok K. Shetty; Kunlin Jin; Sasanka Chakrabarti
The ongoing Corona virus (COVID-19) pandemic has witnessed global political responses of unimaginable proportions. Many nations have implemented lockdowns that involve mandating citizens not to leave their residences for non-essential work. The Indian government has taken appropriate and commendable steps to curtail the community spread of COVID-19. While this may be extremely beneficial, this perspective discusses the other reasons why COVID-19 may have a lesser impact on India. We analyze the current pattern of SARS-CoV-2 transmission, testing, and mortality in India with an emphasis on the importance of mortality as a marker of the clinical relevance of COVID-19 disease. We also analyze the environmental and biological factors which may lessen the impact of COVID-19 in India. The importance of cross-immunity, innate immune responses, ACE polymorphism, and viral genetic mutations are discussed. © 2020 Chakrabarti S et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Interaction of α-synuclein and Parkin in iron toxicity on SH-SY5Y cells: Implications in the pathogenesis of Parkinson's disease
(Portland Press Ltd, 2020) Upasana Ganguly; Anindita Banerjee; Sankha Shubhra Chakrabarti; Upinder Kaur; Oishimaya Sen; Roberto Cappai; Sasanka Chakrabarti
The toxicity of accumulated α-synuclein plays a key role in the neurodegeneration of Parkinson's disease (PD). This study has demonstrated that iron in varying concentrations (up to 400 mM) causes an increase in α-synuclein content in SH-SY5Y cells associated with mitochondrial depolarization, decreased cellular ATP content and loss of cell viability during incubation up to 96 h. Knocking-down α-synuclein expression prevents cytotoxic actions of iron, which can also be prevented by cyclosporine A (a blocker of mitochondrial permeability transition pore). These results indicate that iron cytotoxicity is mediated by α-synuclein acting on mitochondria. Likewise siRNA mediated knock-down of Parkin causes an accumulation of α-synuclein accompanied by mitochondrial dysfunction and cell death during 48 h incubation under basal conditions, but these changes are not further aggravated by co-incubation with iron (400 mM). We have also analyzed mitochondrial dysfunction and cell viability in SH-SY5Y cells under double knock-down (α-synuclein and Parkin concurrently) conditions during incubation for 48 h with or without iron. Our results tend to suggest that iron inactivates Parkin in SH-SY5Y cells and thereby inhibits the proteasomal degradation of α-synuclein, and the accumulated α-synuclein causes mitochondrial dysfunction and cell death. These results have implications in the pathogenesis of sporadic PD and also familial type with Parkin mutations. © 2020 The Author(s).
Multi-Target Directed Ligands (MTDLs): Promising Coumarin Hybrids for Alzheimer’s Disease
(Bentham Science Publishers, 2021) Rohit Bhatia; Sankha S. Chakrabarti; Upinder Kaur; Gaurav Parashar; Anindita Banerjee; Ravindra K. Rawal
Alzheimer’s disease (AZD) is an age-associated neurodegenerative disorder and is one of the common health issues around the globe. It is characterized by memory loss and a decline in other cognitive domains, including executive function. The progression of AZD is associated with complex events, and the exact pathogenesis is still unrevealed. Various mechanisms which are thought to be associated with the initiation of AZD include a decreased concentration of acetylcholine (ACh), deposition of amyloid-β (Aβ) peptide, dyshomeostasis of redox metal ions, and prolonged oxidative stress. Due to the simultaneous progression of diverse pathogenetic pathways, no ideal therapeutic agent has been developed to date. The drugs which are available against AZD provide only symptomatic benefits and do not have disease-modifying activity. Therefore, in search of ideal therapeutic candidates, the concept of molecular hybrids has been under keen investigation for the past few years. Hybrid molecules are able to inhibit or activate or modify the physiology of more than one target simultaneously. Coumarin scaffold have shown the excellent potential of ACh esterase inhibition, MAO-B inhibition, and anti-Aβ aggregation. In the present review, we have focused on different reported coumarin hybrids as multi-target-directed agents against AZD. These include hybrids of coumarin with carbazole, benzofuran, dithiocarbamate, quinoline, pargyline, tacrine, N-benzyl pyridinium, donepezil, purine, piperidine, morpholine, aminophenol, benzylamino, halophenylalkylamidic, thiazole, thiourea, hydroxypyridinone, triazole, piperazine, chalcone, etc. Along with the therapeutic potentials of these hybrids, important clinical investigations and the structure-activity relationship have also been discussed in this compilation. © 2021 Bentham Science Publishers.
Serum 24-hydroxycholesterol in probable Alzheimer's dementia: Reexploring the significance of a tentative Alzheimer's disease biomarker
(Blackwell Publishing Ltd, 2019) Debashree Roy; Sankha Shubhra Chakrabarti; Anindita Banerjee; Pallav Sharma; Atanu Biswas; Sasanka Chakrabarti
Objective: This study measured and analyzed the serum levels of 24-hydroxycholesterol in patients with probable Alzheimer's disease (AD) and age-/sex-matched controls. Methods: A case-control study involving 40 AD patients and 40 controls was performed at a tertiary neurological teaching hospital in eastern India. Blood and serum samples were collected for APOE genotyping and 24-hydroxycholesterol levels, respectively. Results: Serum 24-hydroxycholesterol was significantly lower in AD patients compared to controls (median concentration: controls, 47.14 ng/mL (interquartile range, 16.34); AD patients, 32.93 ng/mL (interquartile range, 9.45); P < 0.001) but showed no significant correlation with Mini Mental State Examination (MMSE) score in AD cases (r = −0.169, P = 0.298) or in controls (r = 0.18, P = 0.26). No statistically significant difference was observed between serum 24-hydroxycholesterol levels of the APOE4-positive and -negative subgroups in AD patients (P = 0.79). Findings were consistent and unchanged even when the ratio of serum 24-hydroxycholesterol to serum total cholesterol was considered. Conclusion: The decreased 24-hydroxycholesterol level in peripheral circulation in AD cases observed in the present study may suggest its role in AD pathogenesis. The lack of a clear correlation between serum levels of 24-hydroxycholesterol and MMSE score—a surrogate marker of AD severity—raises the question as to whether 24-hydroxycholesterol level declines with decreasing neuronal mass or whether the steroid continues to play a protective role. © 2019 The Authors. Aging Medicine published by Beijing Hospital and John Wiley & Sons Australia, Ltd.