Publications by authors named "Sidharth Mehan"

Introduction: Autism is a neurodevelopmental disorder associated with mitochondrial dysfunction, apoptosis, and neuroinflammation. These factors can lead to the overactivation of c-JNK and p38MAPK.

Methods: In rats, stereotactic intracerebroventricular (ICV) injection of propionic acid (PPA) results in autistic-like characteristics such as poor social interaction, repetitive behaviours, and restricted communication.

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Background: Multiple sclerosis (MS) is a persistent autoimmune condition characterized by inflammation and neurodegeneration. The current efficacy of treatments is limited, which has generated interest in developing neuroprotective strategies. Solid lipid nanoparticles (SLNs) and probiotics are potential drug delivery vehicles for targeting the CNS (Central nervous system), regulating immune responses, and supporting neuroprotection in neurological conditions.

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  • ALS is a progressive neurodegenerative disease affecting motor neurons, leading to severe motor dysfunction and respiratory failure, with varying global incidence primarily in individuals aged 45-80.
  • The disease is driven by genetic factors (like mutations in specific genes) and environmental influences, highlighting its complex pathogenesis involving protein misfolding, mitochondrial issues, oxidative stress, and neuroinflammation.
  • Current treatments focus on symptom management, with ongoing research into gene therapy and stem cell therapy, but effective solutions are still in early development, necessitating further exploration of ALS's genetics for targeted therapies.
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  • Autism is a complex condition with symptoms like repetitive behaviors and social communication difficulties, linked to genetic, environmental, and dietary factors, as well as neurobiological issues including mitochondrial dysfunction and neurotransmitter imbalances.
  • Propionic acid (PRPA), produced by gut bacteria, can worsen autism symptoms; however, Genistein (GNT), a natural compound, shows potential for improving these symptoms through its effects on cellular signaling pathways and mitochondrial function.
  • Research using a rat model of autism demonstrated that GNT significantly enhances motor and cognitive skills, reduces neuroinflammation and brain injuries, and normalizes key biological markers, indicating its promise as a treatment for autism.
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  • ALS is a serious neurodegenerative disease that weakens motor neurons, leading to muscle weakness and respiratory failure, influenced by factors like high glutamate levels and environmental toxins.
  • This study investigates the effectiveness of oleanolic acid (OLA) from olive trees in treating ALS, focusing on its ability to target specific harmful signaling pathways through various experimental methods on rats.
  • Results showed OLA significantly protects nerves, reduces inflammation, improves brain health, and enhances motor functions, especially when combined with another treatment, suggesting it could be a valuable addition to current ALS therapies pending further research.
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SIRT1 (Sirtuin 1) is a NAD+-dependent deacetylase that functions through nucleoplasmic transfer and is present in nearly all mammalian tissues. SIRT1 is believed to deacetylate its protein substrates, resulting in neuroprotective actions, including reduced oxidative stress and inflammation, increased autophagy, increased nerve growth factors, and preserved neuronal integrity in aging or neurological disease. Nrf2 is a transcription factor that regulates the genes responsible for oxidative stress response and substance detoxification.

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  • * Solanesol (SNL), a compound found in tobacco and various plants, may protect against nephrotoxicity induced by gentamicin, as shown in a study on Wistar albino rats.
  • * The study found that SNL treatment significantly reduced markers of kidney damage and inflammation, while restoring protective mechanisms in the kidneys, indicating its potential as a therapeutic option for drug-related kidney damage.
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Neuropathological diseases involve the death of neurons and the aggregation of proteins with altered properties in the brain. Proteins are used at the molecular level to categorize neurodegenerative disorders, emphasizing the importance of protein-processing mechanisms in their development. Natural herbal phytoconstituents, such as icariin, have addressed these neurological complications.

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Attempts to furnish antitumor structural templates that can prevent the occurrence of drug-induced hyperuricemia spurred us to generate xanthine oxidase inhibitor-based hydroxamic acids and anilides. Specifically, the design strategy involved the insertion of febuxostat (xanthine oxidase inhibitor) as a surface recognition part of the HDAC inhibitor pharmacophore model. Investigation outcomes revealed that hydroxamic acid 4 elicited remarkable antileukemic effects mediated via HDAC isoform inhibition.

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Magnesium (Mg) is a crucial mineral involved in numerous cellular processes critical for neuronal health and function. This review explores the multifaceted roles of Mg, from its biochemical interactions at the cellular level to its impact on cognitive health and behavioral regulation. Mg acts as a cofactor for over 300 enzymatic reactions, including those involved in ATP synthesis, nucleic acid stability, and neurotransmitter release.

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Obsessive-Compulsive Disorder (OCD), a prevalent neuropsychiatric condition, affects approximately 2%-3% of the global population. This paper provides an extensive overview of OCD, detailing its clinical manifestations, neurobiological underpinnings, and therapeutic approaches. It examines OCD's classification shift in the DSM-5, the role of the cortico-striatothalamo- cortical pathway in its development, and the various factors contributing to its etiology, such as genes, environmental factors, and genetic predispositions.

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Multiple sclerosis [MS] is a progressive autoimmune condition that primarily affects young people and is characterized by demyelination and neurodegeneration of the central nervous system [CNS]. This in-depth review explores the complex involvement of oligodendrocytes, the primary myelin- producing cells in the CNS, in the pathophysiology of MS. It discusses the biochemical processes and signalling pathways required for oligodendrocytes to function and remain alive, as well as how they might fail and cause demyelination to occur.

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Twelve 3,5-disubstituted-thiazolidine-2,4-dione (TZD) hybrids were synthesized using solution phase chemistry. Continuing our previous work, nine -modified ethyl vanillin (8a-i) derivatives were synthesized and reacted with the TZD core Knoevenagel condensation under primary reaction conditions to obtain final derivatives 9a-i. Additionally, three isatin-TZD hybrids (11a-c) were synthesized.

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Alzheimer's disease (AD) poses a significant health challenge worldwide, affecting millions of individuals, and projected to increase further as the global population ages. Current pharmacological interventions primarily target acetylcholine deficiency and amyloid plaque formation, but offer limited efficacy and are often associated with adverse effects. Given the multifactorial nature of AD, there is a critical need for novel therapeutic approaches that simultaneously target multiple pathological pathways.

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Multiple sclerosis (MS), a prevalent neurological disorder, predominantly affects young adults and is characterized by chronic autoimmune activity. The study explores the immune system dysregulation in MS, highlighting the crucial roles of immune and non-neuronal cells in the disease's progression. This review examines the dual role of cytokines, with some like IL-6, TNF-α, and interferon-gamma (IFN-γ) promoting inflammation and CNS tissue injury, and others such as IL-4, IL-10, IL-37, and TGF-β fostering remyelination and protecting against MS.

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Dementia, an international health issue distinguished by the impairment of daily functioning due to cognitive decline, currently affects more than 55 million people worldwide, with the majority residing in low-income and middle-income countries. Globally, dementia entails significant economic burdens in 2019, amounting to a cost of 1.3 trillion US dollars.

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Over the last decade, nanoparticles have found great interest among scientists and researchers working in various fields within the realm of biomedicine including drug delivery, gene delivery, diagnostics, targeted therapy and biomarker mapping. While their physical and chemical properties are impressive, there is growing concern about the toxicological potential of nanoparticles and possible adverse health effects as enhanced exposure of biological systems to nanoparticles may result in toxic effects leading to serious contraindications. Toxicity associated with nanoparticles (nanotoxicity) may include the undesired response of several physiological mechanisms including the distressing of cells by external and internal interaction with nanoparticles.

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A series of new 2,5-disubstituted arylidene derivatives of thiazolidinedione () designed using molecular hybridization approach were synthesized, structurally characterized, and explored for their anti-obesity potential inhibition of Pancreatic Lipase (PL). Compound presented the most potent PL inhibitory activity with IC = 2.71 ± 0.

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Introduction: In the present study, solid lipid nanoparticles loaded with Rosiglitazone and probiotics were prepared solvent emulsification diffusion method which is patented. As a lipid and surfactant, Gleceryl monostearate and Pluronic -68 were used in the formulation process.

Methods: During characterization, it was determined that ingredient quantity variations significantly impacted Rosiglitazone loading capacity, particle size, polydispersity index, etc.

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Diabetes is one of the fastest-growing metabolic disorders, nearly doubling the number of patients each year. There are different treatment approaches available for the management of diabetes, which lacks due to their side effects. The inhibition of enzymes involved in the metabolism of complex polysaccharides to monosaccharides has proven beneficial in patients with type 2 diabetes mellitus.

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Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease that causes significant neurodegeneration. Methylmercury (MeHg+) is a neurotoxin that induces axonal neurodegeneration and motor nerve degeneration by destroying oligodendrocytes, degenerating white matter, inducing apoptosis, excitotoxicity, and reducing myelin basic protein (MBP). This study examines the inhibition of SIRT-1 (silence information regulator 1), Nrf-2 (nuclear factor E2-related factor 2), HO-1 (heme oxygenase 1), and TDP-43 (TAR-DNA-binding protein 43) accumulation in the context of ALS, as well as the modulation of these proteins by icariin (15 and 30 mg/kg, orally), a glycoside flavonoid with neuroprotective properties.

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Neurodegenerative and neuropsychiatric disorders are two broad categories of neurological disorders characterized by progressive impairments in movement and cognitive functions within the central and peripheral nervous systems, and have emerged as a significant cause of mortality. Oxidative stress, neuroinflammation, and neurotransmitter imbalances are recognized as prominent pathogenic factors contributing to cognitive deficits and neurobehavioral anomalies. Consequently, preventing neurodegenerative and neuropsychiatric diseases has surfaced as a pivotal challenge in contemporary public health.

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Amyotrophic lateral sclerosis (ALS) is a paralytic disease that damages the brain and spinal cord motor neurons. Several clinical and preclinical studies have found that methylmercury (MeHg) causes ALS. In ALS, MeHg-induced neurotoxicity manifests as oligodendrocyte destruction; myelin basic protein (MBP) deficiency leads to axonal death.

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Multiple sclerosis (MS) is a pathological condition characterized by the demyelination of nerve fibers, primarily attributed to the destruction of oligodendrocytes and subsequent motor neuron impairment. Ethidium bromide (EB) is a neurotoxic compound that induces neuronal degeneration, resulting in demyelination and symptoms resembling those observed in experimental animal models of multiple sclerosis (MS). The neurotoxic effects induced by EB in multiple sclerosis (MS) are distinguished by the death of oligodendrocytes, degradation of myelin basic protein (MBP), and deterioration of axons.

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