Rohit R Doke

Abstract

The most prevalent gynecologic disease is cancer of the endometrium, In the US, it is the fourth most prevalent malignancy in women after breast, lung, and colorectal malignancies. Despite a steady prevalence of sickness, during the past 20 years, the death rate has climbed by more than 100%. The risk factors of endometrial cancer includes unopposed estrogen therapy, early menarche, late menopause, tamoxifen therapy, nulliparity, infertility or inability to ovulate, and polycystic ovarian syndrome. Ageing, obesity, hypertension, diabetes mellitus, and genetic nonpolyposis colorectal cancer are additional risk factors. This article presents an overview of endometrial carcinoma's epidemiology, prevention, diagnosis, therapy, and prognosis. Chemotherapy, radiation, surgery, and radiation therapy are all forms of treatment. Nonsurgical treatments can be used to treat endometrial hyperplasia with a low to moderate risk. The likelihood of survival is often determined by the disease stage and histology, with the majority of patients at stages I and II having a good prognosis. Endometrial cancer may be prevented in part by managing risk factors such obesity, diabetes, and hypertension.   Keywords: Chemotherapy, Management of EC, Pathophysiology, Surgical treatment

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Abstract

The incidence of central nervous system (CNS) diseases is expected to rise significantly due to increasing lifespan and changing population demographics. Among CNS diseases, neurodegenerative diseases (ND’s) entail a significant challenge since they frequently involve neuronal loss and age-related progressive deterioration in brain function. Although the mechanisms and pathogenesis of neuronal disorders including Parkinson's disease (PD), Alzheimer's disease, and Huntington's disease (HD) have been extensively studied, effective treatment strategies remain limited. Drug delivery to the CNS is particularly challenging and poses a significant obstacle in the management of neurodegeneration. The present review focuses on the challenges associated with neuronal disorders, especially concerning the delivery of macro molecules containing proteins and nucleic acid. Additionally, we highlight opportunities to enhance therapeutic delivery for the treatment of ND’s. As our understanding of the biological aspects of ND’s continues to grow, there is a growing potential for therapeutic interventions. Therefore, these delivery strategies play a vital role for the future transition of CNS therapies from research labs to clinical practices. Keywords: Parkinson's Disease, Alzheimer's Disease, Huntington's Disease, barriers to CNS delivery, strategies to enhance CNS delivery, Nose to brain drug delivery

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Abstract

Parkinson's disease (PD) is a common neurodegenerative condition marked by the degeneration of dopaminergic neurons and the amassing of ?-synuclein protein in Lewy bodies. Chaperone-mediated autophagy (CMA), a selective form of autophagy, has been implicated in the development of PD. Mutant GBA1, ?-synuclein, UCHL1, VPS35, and LRRK2 are affected proteins in PD that impair the CMA process. CMA Dysfunction cause accumulation of PD-associated proteins such as ?-synuclein and many other, including DJ-1, MEF2D, PARK7,etc resulting in mitochondrial dysfunctioning and apoptosis. The impact of gene mutations associated with PD on CMA has been observed, along with dysregulation of miRNAs targeting CMA components. Toxicant-induced PD models demonstrate that impaired CMA increases ?-synuclein aggregates and neurotoxicity. Understanding the molecular mechanisms of CMA has identified potential therapeutic targets, including increasing LAMP2A levels. Several compounds and substances have shown promise in enhancing CMA and reducing ?- synuclein aggregates, such as 6-aminonicotinamide, geldanamycin, metformin, and natural compounds like trehalose and caffeine. Pharmacological modulation of CMA, such as through retinoic acid derivatives, has demonstrated positive effects on reducing protein aggregates in neurodegenerative diseases. However, the specific effects of inhibiting CMA on macroautophagy remain uncertain. Overcoming challenges in studying CMA, such as developing suitable models and monitoring methods, is crucial for advancing our understanding of CMA's role in neurodegenerative diseases and developing effective therapeutic strategies. Overall, CMA emerges as a key player in the pathogenesis of PD, and targeting this selective autophagy pathway holds promise for developing novel therapies to combat neurodegenerative disorders. Keywords: Autophagy, Chaperone, ­synuclein, LAMP2A, Chaperone­mediated autophagy ?

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