In addition to the association between overweight/obesity and cardiovascular disorders, with the presence of a vascular burden as a cofactor, recent studies have particularly focused on the association between indicators of adiposity and dementia. Particularly, renewed predictive value has been addressed to body mass index (BMI). A high BMI can increase the risk for dementia when measured before clinical dementia onset. Although the use of BMI in population-based and clinical studies is feasible, this is an index of weight excess and shows limits in its ability to distinguish between fat and fat-free mass or between deep (visceral) abdominal fat and subcutaneous abdominal fat. In this scenario, we suggest that visceral adipose tissue (VAT) rather than BMI should be considered as a concurrent factor in the development of dementia. Several physiopathologic theories (neurochemical, hormonal, atherosclerotic and inflammatory) have been proposed to explain the decline of cognitive functions. Along with this, well known cardiovascular risk factors (dyslipidaemia, insulin resistance, blood pressure, adipocytokine/chemokines, atherosclerosis) contributing to the development of cognitive decline seem more strongly related to body fat distribution, particularly visceral adipose tissue (VAT), rather than to BMI. With this regard, VAT may be reasonably considered to play a predominant role.
