Dr.L.H.Hiranandani College of Pharmacy is a Pharmacy College in the Mumbai suburban and affiliation to the University of Mumbai.
Alzheimer’s disease (AD), the most common cause of dementia in the aging population, is marked by amyloid-beta (Aβ) plaques, tau tangles, and progressive neuronal degeneration, placing heavy clinical and socioeconomic burdens on healthcare worldwide. Aging remains the strongest risk factor, with chronic low-grade inflammation, oxidative stress, mitochondrial dysfunction, and impaired proteostasis creating a vulnerable brain environment that accelerates AD onset and progression. Recent evidence highlights the gut–glia–immune axis as a critical pathway linking age-related microbiome changes to glial dysfunction. Microbial metabolites, such as short-chain fatty acids and tryptophan derivatives, regulate microglial maturation, astrocytic activity, and neuroimmune signaling. However, age-associated dysbiosis disrupts glial homeostasis, amplifies neuroinflammation, and impairs amyloid clearance, thereby worsening neurodegeneration. Preclinical models including germ-free mice and fecal microbiota transplantation along with clinical studies of elderly AD patients, provide compelling evidence of microbiome-driven modulation of disease. From a therapeutic perspective, microbiome-targeted interventions including probiotics, prebiotics, synbiotics, and microbiota-directed small molecules offer promising strategies to restore glial balance, reduce inflammation, and protect cognitive function. This review highlights the therapeutic potential of probiotics, synbiotics, and fecal microbiota transplantation for mitigating neuroinflammation and cognitive decline in Alzheimer’s disease. However, given the multifactorial nature of neurodegenerative disorders, these strategies are unlikely to be universally effective and must be tailored to individual patient profiles.
Disorders related to the Central Nervous System (CNS) are the centre point of attraction these days due to their physical, mental, and genetic threat to human beings. The prevalence of diseases like multiple sclerosis, epilepsy, Parkinson's disease, Alzheimer’s, and stroke is rising, and it is responsible for serious financial, psychological, and physical challenges. Effective treatment and better patient outcomes depend on an accurate and timely diagnosis for CNS-related disorders. Biosensors, which combine biological elements with detectors, are valuable for diagnosing and treating central nervous system disorders. Biosensors, which provide sensitive, rapid, and efficient detection of disease-specific biomarkers, have become potent instruments in the diagnosis and treatment of CNS disorders. Biosensors successfully monitor disease progression, predict seizures, and track inflammatory markers. Therapeutically, they support personalized medicine by adjusting drug dosages in real time, aid in novel drug development, and facilitate brain-targeted drug delivery. Despite challenges like the brain's complex environment and the need for integration with existing technologies, the biosensors are promising tools for such cases. Future advancements, such as wearable biosensors, multiplexed detection, nanotechnology enhancements, and different tools for therapeutics or drug delivery systems, are paving the way for more effective and personalized CNS disorder management. Furthermore, the impact of nano-based materials in preparation and the requirement of biosensors in specific disorders to help in an early diagnosis and an effective approach towards treatments are highlighted.
Depression is a widespread neurological disorder, increasing the demand for safe, natural therapeutic alternatives. Since depression is a common neurological condition, there is a growing need for safe, all-natural treatment options. Mood regulation is significantly influenced by gamma-aminobutyric acid (GABA), and microbially synthesized GABA has created focus for potential psychobiotic uses. In this study, a probiotic strain that produces GABA was isolated from fermented buckwheat, and its functional and antidepressant potential was assessed both in vitro and in vivo. A strain of Cytobacillus oceanisediminis (G4) was found through screening, and GABA production was verified by TLC and quantified using HPLC. G4 isolate generated 152 µg/mL of GABA with a 4.61-minute retention period. Additionally, the strain showed significant anti-inflammatory properties and antioxidant activity. Foxtail millet was chosen as a fermentation substrate for in vivo testing because of its prebiotic significance. Fermented millet containing G4 decreased immobility (≈ 42
Abstract Background The current studies involve the development of a liquid chromatographic method that is highly effective (HPLC) for the Lumateperone Tosylate method that is simple, rapid, accurate, precise, and economical, all made possible by analytical quality by design (AQbD). The HPLC method’s experimental settings were multivariately optimised by using the design of experiments to determine critical method parameters, and the Ishikawa diagram was used for risk assessment. A two-factor, three-level design was used for the factor screening investigations. Mathematical models were created using two independent factors: the buffer’s pH and the composition of the mobile phase. The response surface methodology and the impacts of these independent aspects were thoroughly examined using central composite design, which allowed for the evaluation of the critical method attributes (CMAs). The parameters of method robustness include retention time, peak area, and symmetry factor. Utilising the desirability function, the optimisation of the CMAs took place at the same time. Results According to the contour diagram’s optimised data, 10 mM ammonium acetate buffer (pH = 3.2): acetonitrile (80:20 v/v) was selected as a mobile phase with a 1 mL/min flow rate. A Zorbax SB C18 250 × 4.6 mm, 5 μ chromatographic column with a UV detector at 230 nm was used and oven temperature was maintained at 25 °C. Lumateperone Tosylate showed linearity in the concentration range of 25–250 µg/mL (r2 = 0.9921). % RSD for interday and intraday precision was found to be 0.25–0.52 and 0.12–0.32, respectively. The % assay of drug content was found to be 100.01 ± 0.06, and accuracy was found to be 100.30–100.65%. In compliance with ICH recommendations, the optimised assay conditions were validated. Conclusion Therefore, it was clearly shown from the results that the AQbD methodology could be effectively used to optimise the HPLC method for Lumateperone Tosylate analysis. The technique was used to assess the Lumateperone Tosylate content in capsules as well.
Triple Negative Breast Cancer (TNBC) is a specific kind of breast cancer that is distinguished by the lack of expression of three specific receptors, namely human epidermal growth factor receptor 2 (HER2), estrogen receptor (ER), and progesterone receptor (PR) and are common in women under 40, especially among African American population or those with a BRCA1 genetic mutation. TNBC is characterized by its very aggressive behavior, elevated rates of recurrence, and restricted therapy alternatives in comparison to other subtypes of breast cancer. Chemotherapy is considered the most widely employed therapy against TNBC but experiences off-target toxicity due to its non-selectivity. Such a scenario led to the genetic profiling of the TNBC patients, which led to the identification of several targets and signaling pathways that can be considered as a therapeutic focus for the treatment of TNBC. In this review, we have compiled various therapeutic targets, including androgen receptor (AR) and PI3K/AKT/mTOR, Notch, Wnt/β-catenin, Hedgehog, and TGF-β signaling pathways, which are responsible for the progression of TNBC. In the current therapeutic landscape, the strategic targeting of key signaling pathways, coupled with the development of monoclonal antibody (mAb)-based immunotherapeutic interventions, has emerged as a promising and clinically relevant approach for the management of triple-negative breast cancer (TNBC). The mAbs reduce tumor development, modulate immune responses, and regulate the tumor microenvironment. This review summarizes their mechanisms, signaling pathway targets, clinical applications, and current therapeutic challenges.
