Topic: metformin

A lot of complications associated with type 2 diabetes mellitus (T2DM) are closely linked with the generation of reactive species or free radicals leading to oxidative/nitrosative stress. The aim of this study was to investigate the effect of combined administration of metformin with propionate on the degree of oxidative/nitrosative damage in the brain of rats with an experimental model of T2DM. Male Wistar rats were divided into control (healthy rats); rats with T2DM and no further therapy; rats with T2DM that received the following: metformin or propionate or propionate + metformin. Ventrome

Dementia is characterised by a profound decline in cognitive and behavioural functions, drastically affecting daily life and social interactions. There is a pressing need for novel therapeutic strategies, particularly if these can be repurposed from available medicine – recent research has suggested antidiabetic drugs may have neuroprotective properties, but validation requires translatable pre-clinical models paired with unbiased assessment. Rocky Mountain Laboratory (RML) scrapie is a well-characterised model that mimics many of the hallmarks of neurodegeneration seen in dementia but does no

Second generation antipsychotics (SGAs) are the first line treatment for psychosis and schizophrenia. SGAs are efficacious in reducing symptoms of these neuropsychiatric conditions; however, they are associated with metabolic side-effects that can be detrimental to a patient’s health and well-being. Patient’s taking SGAs have a three-fold increased risk of developing metabolic syndrome (MetS). MetS includes the development of type 2 diabetes, unprecedented weight gain, and dyslipidaemia. We hypothesised that SGAs disrupt mitochondrial function in the brain and periphery, and this may explain t

Aberrant insulin signalling was recently identified as a causative mechanism of Obsessive-Compulsive Disorder (OCD). Indeed, TALLYHO/JngJ mouse models of Type 2 diabetes are compulsive and anxious, with treatment with the Type 2 diabetes drug metformin generating partial rescue. Here, we aimed to establish the mechanisms behind this insulin-behavioural axis via proteomic analysis of brain and blood. Additionally, data from Genome-Wide Association studies (GWAS) of relevant disorders were compared using Ingenuity Pathway Analysis (IPA) (Qiagen). IPA analysis of proteomic results showed dysregul

Metabolic disorders like diabetes and obesity markedly elevate the risk of neurodegenerative diseases. While certain medications used to manage these conditions show neuroprotective potential, their exact mechanisms of action remain elusive. Here, we propose the utilization of brain histology in a mouse prion model as an effective approach for drug screening in dementia and for exploring the cellular mechanisms of neuroprotection offered by anti-diabetic drugs. Our primary objective was to establish the morphological criteria for brain pathology in prion-infected mice. To achieve this, C57BL/6

Alzheimer’s disease is the leading cause of dementia among aging population. Currently accepted treatments are focused on the symptoms while efforts are made to the develop therapies that target the major pathological hallmarks i.e., β-amyloid (Aβ) plaques and hyperphosphorylated Tau tangles. Evidence from epidemiology and neuroimaging studies suggest that Type 2 Diabetes (T2DM) and Alzheimer's disease (AD) have a shared pathogenesis. Moreover, insulin resistance has been shown to impact hyperphosphorylation and aggregation of Tau making this an important risk factor for the detection of early

Early Life Stress (ELS) can result in enduring health consequences, highlighting the need for exploring timely intervention approaches. Our study aims to investigate whether metformin, a long-recognized diabetes medication with neuroprotective and neurotrophic potential, can mitigate ELS-induced disruptions in hippocampal neurogenesis and dendritic growth. To test this hypothesis, both male and female neonatal Wistar rats were allocated into four distinct groups: control, metformin treatment, ELS model, and ELS model with metformin treatment (ELS+M). During the initial two weeks, ELS model was

We aimed to determine facial and hind paw allodynia in diabetic neuropathy model induced by streptozotocin (STZ) treatment and to determine the anti-allodynic effect of metformin treatment. STZ was intraperitoneally injected (150 mg/kg) to induce painful diabetic neuropathy, and 200 mg/kg of metformin was injected intraperitoneally on the 21st day. Both of the mechanical and cold sensitivity in facial and paw withdrawal region were quantified using von-Frey filaments and acetone solution, respectively. To test heat hyperalgesia, mice were placed into a plastic chamber with a glass floor and ra

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder marked by hyperglycemia, hyperinsulinemia, and altered insulin signaling. Current investigations propose that insulin not only participates in general metabolic processes but also exerts influence over brain functions. Also, altered insulin signaling is observed in conditions like Alzheimer's Disease and Obsessive-Compulsive Disorder. Despite evidence, current treatments targeting insulin signaling lack validation for mental disorders. Understanding insulin's role in concurrent mental and somatic disorders may reveal strategies fo