Glocal University is a private and coeducational institution located in Saharanpur, Uttar Pradesh, India. It is situated in the foothills of Shivalik mountains. The university is a non-profit university established by the Uttar Pradesh Private Universities Act, 2011, (U.P. Act no. 2 of 2012) and is recognized by University Grant Commission. In keeping with its vision of Global canvass, local colours, the school's name is a portmanteau of "global" and "local". The university's 6 major schools offer more than 35 undergraduate, post-graduate, and professional courses.
Alzheimer's disease (AD) is the most common cause of dementia and cognitive impairment; yet, there is currently no treatment. A buildup of Aβ, tau protein phosphorylation, oxidative stress, and inflammation in AD is pathogenic. The accumulation of amyloid-beta (Aβ) peptides in these neurocognitive areas is a significant characteristic of the disease. Therefore, inhibiting Aβ peptide aggregation has been proposed as the critical therapeutic approach for AD treatment. Resveratrol has been demonstrated in multiple studies to have a neuroprotective, anti-inflammatory, and antioxidant characteristic and the ability to minimize Aβ peptides aggregation and toxicity in the hippocampus of Alzheimer's patients, stimulating neurogenesis and inhibiting hippocampal degeneration. Furthermore, resveratrol's antioxidant effect promotes neuronal development by activating the silent information regulator-1 (SIRT1), which can protect against the detrimental effects of oxidative stress. Resveratrol-induced SIRT1 activation is becoming more crucial in developing novel therapeutic options for AD and other diseases that have neurodegenerative characteristics. This review highlighted a better knowledge of resveratrol's mechanism of action and its promising therapeutic efficacy in treating AD. We also highlighted the therapeutic potential of resveratrol as an AD therapeutic agent, which is effective against neurodegenerative disorders.
Background: Alzheimer's disease (AD) is a prevalent neurodegenerative condition characterized by progressive cognitive decline and memory impairment resulting from the degeneration and death of brain neurons. Acetylcholinesterase (AChE) inhibitors are used in primary pharmacotherapy for numerous neurodegenerative conditions, providing their capacity to modulate acetylcholine levels crucial for cognitive function. Recently, quinazoline derivatives have emerged as a compelling model for neurodegenerative disease treatment, showcasing promising pharmacological features. Their unique structural features and pharmacokinetic profiles have sparked interest in their potential efficacy and safety across diverse neurodegenerative disorders. The exposure of quinazoline derivatives as a potential therapeutic way underscores the imperative for continued research exploration. Their multifaceted mechanisms of action and ability to target various pathways implicated in neurodegeneration offer exciting prospects for developing novel, effective, and well-tolerated treatments. Further investigations into their pharmacological activities and precise therapeutic roles are essential to advance our understanding of neurodegenerative disease pathophysiology and promote the development of modern therapeutic strategies to address this critical medical challenge. Methods: Quinazoline derivatives have gained eminent acetylcholinesterase (AChE) inhibitory activity. Their ability to effectively modulate AChE activity makes them promising candidates for treating neurological disorders, particularly Alzheimer's disease (AD). Their intricate molecular structures confer selectivity and affinity for AChE, offering potential for the development of novel therapeutic agents targeting cholinergic pathways. Hence, in this study, we designed, synthesized, and characterized a series of spiro[cycloalakane-1,2'-quinazoline derivatives (1-6) to assess their possible AChE inhibiting ability using docking into the active sites. Results: The AChE inhibitory potential of spiro[cycloalkane-1,2'-quinazoline derivatives (1-6) was explored via docking studies of the AChE active site. The findings revealed significant inhibitory activity and highlighted the promising nature of these derivatives. Conclusion: The synthesized spiro[cycloalkane-1,2'-quinazoline derivatives (1-6) exhibited their notable potential as AChE inhibitors. The observed significant inhibitory activity suggested that these derivatives warrant further exploration as candidates for developing therapeutic agents in AChE inhibitory pathways. This study emphasizes the relevance of quinazoline derivatives in searching for novel treatments for neurological disorders, particularly associated with cholinergic dysfunction, and they could be a useful alternative therapeutic agent.
The present investigation determines the effects of rosiridin in cisplatin (CP)-induced renal toxicity in rats. The experimental animals were used and divided into four groups. Experimental rats were randomly divided into group-I normal control, group-II CP group (8 mg/kg i.p.), group-III CP + rosiridin (10 mg/kg, p.o.) and group-IV rosiridin (10 mg/kg p.o.). Various biochemical parameters, i.e., creatinine, urea, uric acid, cholesterol, blood urea nitrogen, antioxidant levels, inflammatory markers such as interleukins-1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α), nuclear factor kappa B (NF-κB), apoptosis markers including B cell lymphoma-2 (Bcl-2), caspase-3 and histopathological investigations were evaluated. Additionally, molecular docking and dynamics were performed to assess the interaction of rosiridin with target proteins. Rosiridin significantly minimized alteration in creatinine, urea, uric acid, cholesterol, blood urea nitrogen, antioxidant levels, and inflammatory, i.e., IL-1β, IL-6, TNF-α, NF-κB, Bcl-2, and caspase-3 which CP induced in rats. The interaction of rosiridin showed a favorable docking energy. The MD simulation results showed the higher stability of the complex generated from rosiridin. The current study exhibited rosiridin having a protective effect on CP-induced renal toxicity.
The ability of neurons to communicate via synapses is called synaptic transmission, and it is an essential process of brain functioning and plasticity. Its interference has been discovered as a common molecular trait in a broad range of neurological and psychiatric ailments. Nevertheless, in spite of increasing evidence within the disease context, the existing knowledge is still rather disunified, and the molecular processes are poorly incorporated into coherent, cross-disorder models. This narrative review addresses this gap by concisely synthesising recent advances in molecular genetics, synaptic proteomics, neuroimaging, and systems neuroscience to provide an integrated overview of synaptic dysfunction across neurological and psychiatric disorders. It reviews the role of the changes in vesicle trafficking, calcium dynamics, neurotransmitter receptor signalling, brain-derived neurotrophic factor (BDNF) action, and glia-mediated synaptic plasticity in the pathophysiology of conditions like schizophrenia, autism spectrum disorder (ASD), Alzheimer's disease (AD), epilepsy, major depressive disorder (MDD), and Parkinson's disease (PD). The emerging tools that have translational relevance, as pointed out by the review, include single-cell RNA sequencing, spatial proteomics, and synaptic positron emission tomography (PET) imaging, with the capabilities of providing disease-specific and patient-level insights into the pathology of synapses. This review establishes the convergence of the dysfunction, as well as therapeutic potential, through the presentation of a systems-level, cross-diagnostic framework at the level of the synapse. It ends with a prospective report of where precision medicine, development of new biomarkers, and lifespan research efforts are required to incorporate synaptic biology in translational neuroscience.
This study explores the factors influencing green entrepreneurial intentions (GEI) among higher education students and their significance in cultivating sustainable competencies within an emerging economy. The research utilises Partial Least Squares Structural Equation Modelling (PLS-SEM) to examine how perceived educational support, environmental awareness, self-efficacy, and attitudes influence students’ inclination toward green entrepreneurship. Empirical data were collected from 399 university students enrolled at three universities in northern India.The results indicate that environmental understanding, perceived educational support, and self-efficacy significantly influence green entrepreneurial intention. Furthermore, attitude plays a significant role in shaping GEI and functions as an important mediating mechanism between environmental understanding and green entrepreneurial intention. However, the moderating role of attitude between perceived educational support and GEI was not statistically significant. These findings highlight the importance of strengthening sustainability-oriented entrepreneurship education to develop favourable attitudes and entrepreneurial confidence among students. The study offers implications for policymakers, educators, and institutions seeking to foster sustainable entrepreneurial competencies among young people in emerging economies.
