Microglia, as the immune guardians of the central nervous system (CNS), have the ability to maintain neural homeostasis, respond to environmental changes, and remodel the synaptic landscape. However, persistent microglial activation can lead to chronic neuroinflammation, which can alter neuronal signaling pathways, resulting in accelerated cognitive decline. Phosphoinositol 3-kinase (PI3K) has emerged as a critical driver, connecting inflammation to neurodegeneration, serving as the nexus of numerous intracellular processes that govern microglial activation. This review focuses on the relationship between PI3K signaling and microglial activation, which might lead to cognitive impairment, inflammation, or even neurodegeneration. The review delves into the components of the PI3K signaling cascade, isoforms, and receptors of PI3K, as well as the downstream effects of PI3K signaling, including its effectors such as protein kinase B (Akt) and mammalian target of rapamycin (mTOR) and the negative regulator phosphatase and tensin homolog (PTEN). Experiments have shown that the overproduction of certain cytokines, coupled with abnormal oxidative stress, is a consequence of poor PI3K regulation, resulting in excessive synapse pruning and, consequently, impacting learning and memory functions. The review also highlights the implications of autonomously activated microglia exhibiting M1/M2 polarization driven by PI3K on hippocampal, cortical, and subcortical circuits. Conclusions from behavioral studies, electrophysiology, and neuroimaging linking cognitive performance and PI3K activity were evaluated, along with new approaches to therapy using selective inhibitors or gene editing. The review concludes by highlighting important knowledge gaps, including the specific effects of different isoforms, the risks associated with long-term pathway modulation, and the limitations of translational potential, underscoring the crucial role of PI3K in mitigating cognitive impairment driven by neuroinflammation.

Metabolic syndrome (MetS) is a cluster of cardiometabolic abnormalities including central obesity, insulin resistance, dyslipidemia, and hypertension that markedly increases the risk of type 2 diabetes mellitus (T2DM) and cardiovascular disease. Lifestyle modification remains the cornerstone of management, but there is growing interest in adjunctive nutraceutical and phytopharmacological approaches capable of safely addressing multiple MetS components. Green tea, derived from the leaves of Camellia sinensis (family Theaceae), is one of the most widely consumed beverages worldwide and is rich in polyphenolic catechins, primarily (-)-epigallocatechin-3-gallate (EGCG), which have been extensively investigated for anti-obesity and metabolic benefits. This review provides a pharmacognostic and phytochemical perspective on C. sinensis as an anti-obesity agent in the context of MetS. Pharmacognostic sections summarize macroscopic and microscopic diagnostic features, physicochemical constants, and quality-control parameters for different tea types (green, white, oolong) based on recent standardization studies. Phytochemical sections describe major and minor constituents, with emphasis on catechins, caffeine, theaflavins, thearubigins, and other phenolics, and their quantitative variation by cultivar, processing, and extraction method. Mechanistic evidence from in vitro, animal, and human intervention studies is synthesized to delineate how tea polyphenols modulate body weight, adiposity, lipid and glucose metabolism, blood pressure, and inflammation. Proposed mechanisms include increased energy expenditure and fat oxidation via catechin-caffeine-induced sympathetic stimulation; inhibition of digestive enzymes and nutrient absorption; modulation of lipid metabolism and de novo lipogenesis; activation of AMP-activated protein kinase (AMPK); improvement of insulin signaling; regulation of adipokine secretion; and remodeling of gut microbiota composition and function. Pharmacokinetic, safety, and formulation aspects are discussed, alongside limitations and variability in clinical trial outcomes. The review concludes that standardized C. sinensis preparations, especially catechin-enriched green tea extracts, represent promising multi-target adjuncts for obesity and MetS management, while highlighting the need for rigorous pharmacognostic standardization, dose-response characterization, and biomarker-driven clinical trials.