Neuroprotective role of Piceatannol in Chronic Unpredictable Stress induced memory dysfunction.

Background: Various studies have evidenced the neuroprotective role of SIRT1 activator. However, whether SIRT1 activator, Piceatannol pharmacological treatment is protective in chronic unpredictable stress induced memory dysfunction remains unknown. Therefore, this study design included testing the hypothesis that Piceatannol administered in chronic unpredictable stress induced memory dysfunction mice shows protective effects, explores & probes underlying the activation of SIRT1 pathway.

Gene Therapy: Towards a New Era of Medicine.

Over the past years, many significant advances have been made in the field of gene therapy and shown promising results in clinical trials conducted. Gene therapy aims at modifying or replacing a defective, inefficient, or nonfunctional gene with a healthy, functional gene by administration of genome material into the cell to cure genetic diseases. Various methods have been devised to do this by using several viral and non-viral vectors which are either administered by in vivo or ex vivo technique.

Emerging role of Nrf2 in Parkinson's disease therapy: a critical reassessment.

Parkinson's disease (PD) is the neurodegenerative disorder characterized by the progressive degeneration of nigrostriatal dopaminergic neurons, leading to the range of motor and non-motor symptoms. There is mounting evidence suggesting that oxidative stress, neuroinflammation and mitochondrial dysfunction play pivotal roles in the pathogenesis of PD. Current therapies only alleviate perturbed motor symptoms.

From Bench to Bedside: ROS-Responsive Nanocarriers in Cancer Therapy.

Reactive oxygen species (ROS) play a dual role in cancer, acting as both signaling molecules that promote tumour growth and as agents that can inhibit tumour progression through cytotoxic effects. In cancer therapy, ROS-responsive drug delivery systems take advantage of the elevated ROS levels found in tumors compared to healthy tissues. These systems are engineered to release drugs precisely in response to increased ROS levels in tumour cells, allowing targeted and controlled treatment, minimizing side effects, and enhancing therapeutic outcomes.

Exploring the Neuroprotective Effects of Rufinamide in a Streptozotocin-Induced Dementia Model.

Due to the complex pathophysiology of AD (Alzheimer's Disease), there are currently no effective clinical treatments available, except for acetylcholinesterase inhibitors. However, CREB (cyclic AMP-responsive element binding protein) has been identified as the critical factor for the transcription in memory formation. Understanding the effect of potential drugs on the CREB pathway could lead to the development of new therapeutic molecules.

Role of Flavonoids in Mitigating the Pathological Complexities and Treatment Hurdles in Alzheimer's Disease.

With the passage of time, people step toward old age and become more prone to several diseases associated with the age. One such is Alzheimer's disease (AD) which results into neuronal damage and dementia with the progression of age. The existing therapeutics has been hindered by various enkindles like less eminent between remote populations, affordability issues and toxicity profiles.

Mechanistic exploration of ubiquitination-mediated pathways in cerebral ischemic injury.

The ubiquitin-proteasome system (UPS) plays a pivotal role in regulating protein homeostasis and cellular processes, including protein degradation, trafficking, DNA repair, and cell signaling. During cerebral ischemia, ischemic conditions profoundly disrupt UPS activity, leading to proteasomal dysfunction and the accumulation of abnormal proteins. This imbalance contributes to neuronal injury and cell death observed in ischemic stroke.

Mechanistic insights and therapeutic potential of astilbin and apigenin in diabetic cardiomyopathy.

Diabetic cardiomyopathy (DCM) represents a critical complication of Diabetes mellitus (DM), characterized by structural and functional changes in the myocardium independent of coronary artery disease or hypertension. Emerging evidence highlights the significant roles of phytochemicals, particularly astilbin and apigenin, in modulating key molecular pathways implicated in DCM. This review synthesizes current mechanistic insights and therapeutic potential of these compounds, focusing on their interactions with AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptors (PPARs), O-linked N-acetylglucosamine (O-GlcNAc), sodium-glucose co-transporter 2 (SGLT2), protein kinase C (PKC), nuclear factor kappa B (NF-κB), mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK) pathways.

2,2'- Bipyridine Derivatives Exert Anticancer Effects by Inducing Apoptosis in Hepatocellular Carcinoma (HepG2) Cells.

Purpose: To elucidate the therapeutic potential of 2,2'-bipyridine derivatives [NPS (1-6)] on hepatocellular carcinoma HepG2 cells.

Methods: The effects on cell survival, colony formation, cellular and nuclear morphology, generation of reactive oxygen species (ROS), change in the integrity of mitochondrial membrane potential (MMP), and apoptosis were investigated. Additionally, docking studies were conducted to analyze and elucidate the interactions between the derivatives and AKT and BRAF proteins.

Diabetic Cardiomyopathy: An Update on Emerging Pathological Mechanisms.

Diabetic Cardiomyopathy (DCM) is a notable consequence of diabetes mellitus, distinguished by cardiac dysfunction that occurs separately from coronary artery disease or hypertension. A recent study has revealed an intricate interaction of pathogenic processes that contribute to DCM. Important aspects involve the dysregulation of glucose metabolism, resulting in heightened oxidative stress and impaired mitochondrial function.

A decade of pyridine-containing heterocycles in US FDA approved drugs: a medicinal chemistry-based analysis.

Heterocyclic scaffolds, particularly, pyridine-containing azaheterocycles, constitute a major part of the drugs approved in the past decade. In the present review, we explored the pyridine ring part of US FDA-approved small molecules (2014-2023). The analysis of the approved drugs bearing a pyridine ring revealed that a total of 54 drugs were approved.

Exploring Therapeutic Strategies: The Relationship between Metabolic Disorders and FOXO Signalling in Alzheimer's Disease.

Alzheimer's disease is an ailment that is linked with the degeneration of the brain cells, and this illness is the main cause of dementia. Metabolic stress affects the activity of the brain in AD via FOXO signaling. The occurrence of AD will significantly surge as the world's population ages, along with lifestyle changes perceived in current decades, indicating a main contributor to such augmented prevalence.

Proposed Hypothesis of TWEAK/Fn14 Receptor Modulation in Autism Spectrum Disorder.

Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder with a complex, multiple etiology that is marked by impaired social interaction, communication, and repetitive behaviour. There is presently no pharmaceutical treatment for the core symptoms of ASD, even though the prevalence of ASD is increasing worldwide. Treatment of autism spectrum disorder involves the interaction of numerous signalling pathways, such as the Wnt/beta-catenin pathway, probiotics and kynurenine pathway, PPAR pathway, PI3K-AKT-mTOR pathway, Hedgehog signaling pathway, etc.

Hypoxia-inducible Factor-1α Pathway in Cerebral Ischemia: From Molecular Mechanisms to Therapeutic Targets.

Introduction: Ischemic injury to the brain can result in a variety of life-threatening conditions, mortality, or varying degrees of disability. Hypoxia-inducible factor 1α (HIF 1α), an oxygen- sensitive transcription factor that controls the adaptive metabolic response to hypoxia, is a critical constituent of cerebral ischemia. It participates in numerous processes, such as metabolism, proliferation, and angiogenesis, and plays a major role in cerebral ischemia.

Therapeutic approaches targeting aging and cellular senescence in Huntington's disease.

Huntington's disease (HD) is a devastating neurodegenerative disease that is manifested by a gradual loss of physical, cognitive, and mental abilities. As the disease advances, age has a major impact on the pathogenic signature of mutant huntingtin (mHTT) protein aggregation. This review aims to explore the intricate relationship between aging, mHTT toxicity, and cellular senescence in HD.

The role of sirtuin 1 in ageing and neurodegenerative disease: A molecular perspective.

Sirtuin 1 (SIRT1), an NAD+-dependent deacetylase, has emerged as a key regulator of cellular processes linked to ageing and neurodegeneration. SIRT1 modulates various signalling pathways, including those involved in autophagy, oxidative stress, and mitochondrial function, which are critical in the pathogenesis of neurodegenerative diseases. This review explores the therapeutic potential of SIRT1 in several neurodegenerative disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and Amyotrophic Lateral Sclerosis (ALS).

Aquaporin proteins: A promising frontier for therapeutic intervention in cerebral ischemic injury.

Cerebral ischemic injury is characterized by reduced blood flow to the brain, remains a significant cause of morbidity and mortality worldwide. Despite improvements in therapeutic approaches, there is an urgent need to identify new targets to lessen the effects of ischemic stroke. Aquaporins, a family of water channel proteins, have recently come to light as promising candidates for therapeutic intervention in cerebral ischemic injury.

Nrf2 and Ferroptosis: Exploring Translational Avenues for Therapeutic Approaches to Neurological Diseases.

Nrf2, a crucial protein involved in defense mechanisms, particularly oxidative stress, plays a significant role in neurological diseases (NDs) by reducing oxidative stress and inflammation. NDs, including Alzheimer's, Parkinson's, Huntington's, amyotrophic lateral sclerosis, stroke, epilepsy, schizophrenia, depression, and autism, exhibit ferroptosis, iron-dependent regulated cell death resulting from lipid and iron-dependent reactive oxygen species (ROS) accumulation. Nrf2 has been shown to play a critical role in regulating ferroptosis in NDs.

Exploring the nexus of cGAS STING pathway in neurodegenerative terrain: A therapeutic odyssey.

By detecting and responding to cytosolic DNA, the cGAS STING pathway regulates the innate immune responses bymediatinginflammatory reactions and antiviral defense. Thederegulation and modification of this system have been linked to variousneurodegenerative diseases like AD, PD and ALS. Accumulation of tau protein and Aβ aggregates to activate the pathway and releases neuroinflammatory cytokines which accelerates neuronal dysfunction and cognitive impairment as the symptom of AD.

Vincristine in Cancer Therapy: Mechanisms, Efficacy, and Future Perspectives.

Cancer remains one of the predominant causes of mortality globally, accounting for over 10 million deaths each year. Despite advancements in medical treatments, the challenge of resistance and treatment failure persists, necessitating innovative approaches. Traditional cancer treatments include surgery, chemotherapy, radiation therapy, and pharmaceutical therapy.

Exploring therapeutic potential: Targeting TRPM7 in neurodegenerative diseases.

The ions Ca and Mg, which are both present in the body, have been demonstrated to be crucial in the control of a variety of neuronal processes. Transient melastatin-7 (TRPM7) channel plays an important role in controlling Ca and Mg homeostasis, which is crucial for biological processes. The review will also examine how changes in TRPM7 function or expression can lead to neurodegeneration.

Exploring the potential of an and honey extract loaded bi-layered nanofibrous scaffold of PCL-Col and PCL-SBMA mimicking the skin architecture for the treatment of diabetic wounds.

Diabetic wounds are often chronic in nature, and issues like elevated blood sugar, bacterial infections, oxidative stress and persistent inflammation impede the healing process. To ensure the appropriate healing of wounds, scaffolds should promote complete tissue regeneration in wounds, both functionally and structurally. However, the available scaffolds lack the explicit architecture and functionality that could match those of native skin, thus failing to carry out the scar-free skin regeneration in diabetic wounds.