Deepshikha Pande Katare

Bio: Deepshikha Pande Katare is an academic researcher from Amity Institute of Biotechnology. The author has contributed to research in topics: Lung cancer & Medicine. The author has an hindex of 10, co-authored 51 publications receiving 532 citations. Previous affiliations of Deepshikha Pande Katare include Amity University & Hamdard University.

Shared links between type 2 diabetes mellitus and Alzheimer's disease: A review

Abstract: Epidemiological studies have proved that, there are pathophysiological connections between Type 2 Diabetes Mellitus (T2DM) and Alzheimer's disease (AD). Diabetic patients have higher incidences of cognitive impairment and hence they are more at the risk of developing AD. Some of the recent evidences have majorly stated the effects of insulin resistance in the disturbance of various biological processes and signaling pathways. Both hyperglycemia and hypoglycemic conditions contributes in dysfunctioning of cognitive abilities and functions. The present review summarizes the evidences which establish the possible links between the two pathologies on the account of molecular, biochemical and at histopathological level. The information regarding their interactions was collected from different databases and journals. The gathered information will clearly establish the link among the two pathologies and will be helpful in future for the development of drugs for Type 3 Diabetes.

Type 3 Diabetes: Cross Talk between Differentially Regulated Proteins of Type 2 Diabetes Mellitus and Alzheimer’s Disease

Abstract: Type 3 Diabetes (T3D) is a neuroendocrine disorder that represents the progression of Type 2 Diabetes Mellitus (T2DM) to Alzheimer’s disease (AD). T3D contributes in the increase of the total load of Alzheimer’s patients worldwide. The protein network based strategies were used for the analysis of protein interactions and hypothesis was derived describing the possible routes of communications among proteins. The hypothesis provides the insight on the probable mechanism of the disease progression for T3D. The current study also suggests that insulin degrading enzyme (IDE) could be the major player which holds the capacity to shift T2DM to T3D by altering metabolic pathways like regulation of beta-cell development, negative regulation of PI3K/AKT pathways and amyloid beta degradation.

Sesamin attenuates neurotoxicity in mouse model of ischemic brain stroke.

Abstract: Stroke is a severe neurological disorder characterized by the abrupt loss of blood circulation into the brain resulting into wide ranging brain and behavior abnormalities. The present study was designed to evaluate molecular mechanism by which sesamin (SES) induces neuroprotection in mouse model of ischemic stroke. The results of this study demonstrate that SES treatment (30 mg/kg bwt) significantly reduced infarction volume, lipid per-oxidation, cleaved-caspase-3 activation, and increased GSH activity following MCAO in adult male mouse. SES treatment also diminished iNOS and COX-2 protein expression, and significantly restored SOD activity and protein expression level in the ischemic cortex of the MCAO animals. Furthermore, SES treatment also significantly reduced inflammatory and oxidative stress markers including Iba1, Nox-2, Cox-2, peroxynitrite compared to placebo MCAO animals. Superoxide radical production, as studied by DHE staining method, was also significantly reduced in the ischemic cortex of SES treated compared to placebo MCAO animals. Likewise, downstream effects of superoxide free radicals i.e. MAPK/ERK and P38 activation was also significantly attenuated in SES treated compared to placebo MCAO animals. In conclusion, these results suggest that SES induces significant neuroprotection, by ameliorating many signaling pathways activated/deactivated following cerebral ischemia in adult mouse.

A Review on Hepatoprotective and Immunomodulatory Herbal Plants.

Abstract: The liver is the most important organ that plays an important role in maintaining various physiological processes in the body. Hepatitis is an inflammation of the liver and is characterized by the presence of inflammatory cells in the tissue of the organ. There are five main viruses, referred to as types A, B, C, D, and E. These five types are of the greatest concern because of the burden of illness and death. Liver injury or liver dysfunction is a major health problem that challenges not only health care professionals but also the drug regulatory agencies and the pharmaceutical industry. Herbal medicines have been used in the treatment of liver disease for a long time. The immune system is the part of body that diagnoses the pathogen by using a specific receptor to reveal immediate response by the activation of immune components cells, chemokines, and cytokines, and also the release of the inflammatory mediator. They potentiate and modulate the immune system. The plant-derived phytoconstituents (polysaccharides, proteins and flavanoids, lignans, rotenoids, etc.) stimulate the immune system and maintained hepatic diseases. There are a number of hepatoprotective and immunomodulatory herbs that have been reported. The present review is aimed at compiling data on promising phytochemicals from hepatoprotective and immunomodulatory herbs.

Ferroptosis: past, present and future

Abstract: Ferroptosis is a new type of cell death that was discovered in recent years and is usually accompanied by a large amount of iron accumulation and lipid peroxidation during the cell death process; the occurrence of ferroptosis is iron-dependent. Ferroptosis-inducing factors can directly or indirectly affect glutathione peroxidase through different pathways, resulting in a decrease in antioxidant capacity and accumulation of lipid reactive oxygen species (ROS) in cells, ultimately leading to oxidative cell death. Recent studies have shown that ferroptosis is closely related to the pathophysiological processes of many diseases, such as tumors, nervous system diseases, ischemia-reperfusion injury, kidney injury, and blood diseases. How to intervene in the occurrence and development of related diseases by regulating cell ferroptosis has become a hotspot and focus of etiological research and treatment, but the functional changes and specific molecular mechanisms of ferroptosis still need to be further explored. This paper systematically summarizes the latest progress in ferroptosis research, with a focus on providing references for further understanding of its pathogenesis and for proposing new targets for the treatment of related diseases.

The Role of Reactive Oxygen Species in the Pathogenesis of Alzheimer’s Disease, Parkinson’s Disease, and Huntington’s Disease: A Mini Review

Abstract: Neurodegenerative diseases affect not only the life quality of aging populations, but also their life spans. All forms of neurodegenerative diseases have a massive impact on the elderly. The major threat of these brain diseases includes progressive loss of memory, Alzheimer’s disease (AD), impairments in the movement, Parkinson’s disease (PD), and the inability to walk, talk, and think, Huntington’s disease (HD). Oxidative stress and mitochondrial dysfunction are highlighted as a central feature of brain degenerative diseases. Oxidative stress, a condition that occurs due to imbalance in oxidant and antioxidant status, has been known to play a vital role in the pathophysiology of neurodegenerative diseases including AD, PD, and HD. A large number of studies have utilized oxidative stress biomarkers to investigate the severity of these neurodegenerative diseases and medications are available, but these only treat the symptoms. In traditional medicine, a large number of medicinal plants have been used to treat the symptoms of these neurodegenerative diseases. Extensive studies scientifically validated the beneficial effect of natural products against neurodegenerative diseases using suitable animal models. This short review focuses the role of oxidative stress in the pathogenesis of AD, PD, and HD and the protective efficacy of natural products against these diseases.

Brain insulin resistance in Alzheimer's disease and related disorders: mechanisms and therapeutic approaches.

Abstract: Insulin is a peptide secreted by the pancreas and plays an important role in the regulation of glucose metabolism in peripheral tissues. Although the role of insulin in the periphery is well understood, less is known about its multifactorial role in the brain. However, emerging evidence from human and animal studies indicate that insulin influences cerebral bioenergetics, enhances synaptic viability and dendritic spine formation, and increases turnover of neurotransmitters, such as dopamine. Insulin also has a role in proteostasis, influencing clearance of the amyloid β peptide and phosphorylation of tau, which are hallmarks of Alzheimer's disease. Insulin also modulates vascular function through effects on vasoreactivity, lipid metabolism, and inflammation. Through these multiple pathways, insulin dysregulation could contribute to neurodegeneration. Thus, new approaches to restore cerebral insulin function that could offer therapeutic benefit to adults with Alzheimer's disease, vascular cognitive impairment, or related disorders are being investigated.