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In 2020 the World Health Organization estimated that the number of people with dementia was 50 million in the world. Furthermore, it is expected about 10 million new cases every year. Alzheimer’s disease (AD) is the most common form of dementia, which represents more than 50% of the cases. Type 2 diabetes mellitus (T2DM) is a major risk factor for AD and dementia. Even in people without clinical dementia, diabetes is associated with decreased cognitive performance and with increased brain atrophy. If comparing general population and people with diabetes, patients with T2DM had a 73% higher risk of developing dementia and a 56% increased risk of developing AD. Typically, the first medication prescribed for T2DM is metformin and it has been associated with the reduction of cognitive decline and the risk of dementia in patients with T2DM when compared with diabetic patients without medication. A randomized, double-blinded, placebo-controlled study demonstrated that during metformin treatment there was an improvement of executive functioning, learning, memory, and attentional abilities. A possible explanations for the protective effect of metformin in patients with T2DM is that it prevents hyperinsulinemia and the formation of amyloid-β plaques in the brain and the onset of AD. Metformin does not only decrease the plasma glucose level in several mechanisms, but it also characterized to beneficially effect serum lipid profiles, reduce inflammatory cell adhesion to endothelium, and exert anti-inflammatory, anti-apoptotic and anti-oxidative properties. Method: A Clinical Scientific Research was made about correlation among dementia and metformin. Were searched and found in PubMed a total of 61 articles between 2015–2020, but only free access and those who correlated metformin and dementia were used. Results: Studies showed that T2DM patients taking metformin had decreased risk of developing dementia or AD if compared to others diabetic patients that were not taking metformin. However, it is being hard to test antidiabetic therapies in AD, because the mechanisms which tie T2DM to Alzheimer clinical syndrome are not totally known. Therefore, to be as effective as possible it is necessary to treat the patients before they develop extensive amyloid and tau tangle burden. Conclusion: Diabetic patients taking metformin have a protector factor to don’t develop dementia or AD, when compared to those who don’t take metformin since they started the treatment before accumulation of amyloid and tau protein in the brain.

Association Between Metformin and Prevention of Dementia in T2DM Adult Patients