Cognitive

Brain aging is associated mainly with a decline in cognitive function and is a major risk factor for various neurodegenerative disorders (NDDs). Major hallmarks of aging include oxidative stress, chronic neuroinflammation, mitochondrial dysfunction, and impaired proteostasis. Although caloric restriction (CR) has consistently demonstrated neuroprotective effects, its long-term effects in humans remain challenging. Consequently, CRMs such as metformin, spermidine, and curcumin have been widely us

Type 2 diabetes mellitus (T2DM) is a progressive metabolic disorder that often requires treatment intensification over time. In complex patients with multiple comorbidities and cognitive impairment, therapeutic decisions must balance glycemic control with safety and feasibility. We present a 59-year-old male with long-standing T2DM, marked body weight fluctuations, and emerging neurocognitive decline. Baseline glycated hemoglobin (HbA1c) was 9.4%, with progressive improvement to 7.1% under quadr

Alzheimer's disease (AD) and mild cognitive impairment (MCI) are major causes of cognitive decline. Antidiabetic medications such as metformin, pioglitazone, and GLP-1 receptor agonists have been proposed as potential neuroprotective therapies. We assessed whether these agents slow cognitive decline or disease progression in people with AD or MCI. PubMed, Embase, and Cochrane Central were searched for randomized controlled trials and observational studies of metformin, pioglitazone, or GLP-1 rec

Metformin is the first-line oral antihyperglycemic agent for type 2 diabetes mellitus (T2DM), with over 150 million individuals worldwide receiving treatment annually. Although synthesized in 1922, its clinical adoption began in the 1950s, and decades of widespread use have firmly established its efficacy in glycemic control and metabolic improvement. Nevertheless, growing evidence indicates that metformin exerts pleiotropic effects beyond glucose homeostasis-modulating neurocognitive function,

Diabetes is associated with a number of significant long-term effects. In this study we consider that purslane which possesses numerous of pharmacological properties, and metformin, an antidiabetic drug, may have a therapeutic effects on diabetes-induced memory impairments in rats. Forty male albino rats were randomly divided into five groups. Group I served as control group. The other four groups were first fed on HFD followed by a single interpretonial (i.p.) dose of STZ at a dose of (35) mg/k

Diabetes is significantly associated with cognitive impairment, particularly the risk of developing dementia. However, the impact of antidiabetic drugs on dementia risk remains unclear. This study aims to comprehensively evaluate the effects of different antidiabetic drugs on dementia risk using Bayesian network analysis. The study systematically searched databases including PubMed, Embase, and the Cochrane Library to identify relevant publications up to September 5, 2025. Eligible randomized co

Background Type 2 diabetes mellitus (T2DM) is associated with cognitive impairment, and metformin, the first-line pharmacotherapy, has been linked to vitamin B₁₂ deficiency with potential neurological consequences. Objective evidence linking early metformin-induced changes in vitamin B₁₂ levels to cognitive function remains limited, particularly in Indian populations. Objectives To evaluate changes in serum vitamin B₁₂ status and cognitive function, assessed using P300 event-related potentials (

Type 2 diabetes (T2D) is associated with cognitive impairment, with executive functions such as cognitive flexibility being particularly vulnerable. Growing evidence suggests that chronic inflammatory and metabolic stress contributes to diabetes -related brain dysfunction, yet behavioral assessment in animal models is often confounded by anxiety, altered motivation, and reduced response vigor. In this study, we used a translational touchscreen-based operant platform to distinguish associative le

This module synthesizes cognitive models, learning theory, and neurobiology to inform advanced CBT practice and research. It links dual‑process cognition, working memory, conditioning, and brain circuits (PFC, amygdala, hippocampus, neurotransmitters) to psychopathology and outlines integrated, evidence‑based interventions (psychotherapy + pharmacology).

This module integrates cognitive, behavioral, and neurobiological perspectives to explain psychopathology and guide evidence-based treatment, with emphasis on Cognitive Behavioral Therapy (CBT) as a core intervention. It reviews cognitive architecture (dual-process, working memory), learning principles, brain systems and neurotransmitters, stress biology, diagnostic frameworks, and combined pharmacological and psychotherapeutic approaches.