Phytochemicals: Promising Alternatives for Metabolic Regulation in Neurodegenerative Diseases

Obesity has reached epidemic proportions globally and is increasingly recognized as a significant risk factor for cognitive decline and memory impairment. This comprehensive narrative review synthesizes current evidence on the molecular mechanisms underlying obesity-induced memory dysfunction, drawing upon insights from in vivo and in vitro models alongside human clinical and neuroimaging studies. We explore how chronic adiposity triggers a cascade of neuropathological events, beginning with peripheral metabolic dysregulation that propagates to the central nervous system. Key mechanisms include neuroinflammation mediated by pro-inflammatory cytokines and activated microglia, oxidative stress through reactive oxygen species generation, dysregulation of apoptosis pathways, suppression of neurotrophic factors (notably BDNF), neurotransmitter system imbalances, and central insulin resistance. Critically, obesity profoundly impairs hippocampal neurogenesis and synaptogenesis-processes fundamental to memory encoding and consolidation. These pathways exhibit extensive crosstalk, creating self-amplifying cycles that accelerate synaptic loss, neuronal dysfunction, and network disorganization. Emerging therapeutic strategies targeting these mechanisms, including GLP-1 receptor agonists, intranasal insulin, and anti-inflammatory agents, show promise in preclinical and early clinical studies. This review underscores the multifaceted nature of obesity-related cognitive decline and highlights the urgent need for mechanistic, longitudinal human studies to translate these findings into effective clinical interventions against the growing burden of obesity-associated neurodegeneration.

Molecular mechanisms underlying obesity-induced memory dysfunction: a comprehensive narrative review

Objectives In this study mice were fed a high-fat diet for 12 weeks to establish diet-induced obesity and syringic acid (SA) was assessed for anti-obese, neuroprotective, and neurogenesis.Method Animals were given HFD for 12 weeks to measure metabolic characteristics and then put through the Barns-maze and T-maze tests to measure memory. Additionally, the physiology of the blood–brain barrier, oxidative stress parameters, the expression of inflammatory genes, neurogenesis, and histopathology was evaluated in the brain.Result DIO raised body weight, BMI, and other metabolic parameters after 12 weeks of overfeeding. A reduced spontaneous alternation in behavior (working memory, reference memory, and total time to complete a task), decreased enzymatic and non-enzymatic antioxidants, oxidative biomarkers, increased neurogenesis, and impaired blood–brain barrier were all seen in DIO mice. SA (50 mg/kg) treatment of DIO mice (4 weeks after 8 weeks of HFD feeding) reduced diet-induced changes in lipid parameters associated with obesity, hepatological parameters, memory, blood–brain barrier, oxidative stress, neuroinflammation, and neurogenesis. SA also reduced the impact of malondialdehyde and enhanced the effects of antioxidants such as glutathione, superoxide dismutase (SOD), and total thiol (MDA). Syringic acid improved neurogenesis, cognition, and the blood–brain barrier while reducing neurodegeneration in the hippocampal area.Discussion According to the results of the study, syringic acid therapy prevented neurodegeneration, oxidative stress, DIO, and memory loss. Syringic acid administration may be a useful treatment for obesity, memory loss, and neurogenesis, but more research and clinical testing is needed. 

Impaired brain equanimity and neurogenesis in the diet-induced overweight mouse: a preventive role by syringic acid treatment

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Impaired brain equanimity and neurogenesis in the diet-induced overweight mouse: a preventive role by syringic acid treatment