Physical exercise advantages have been manifested in several neurodegenerative and/or neuropsychiatric disorders implying that these, largely non-invasive, non-pharmacologic interventions, ought to be examined closely in the Alzheimer's disease (AD) and other dementias context. Thus, according to the tenets of an increasingly broad consensus, preventative and interventional agents for AD and dementia conditions should include physical activity, proper and appropriate lifestyle ingredients, cognitive-affective and intellectual stimulation and the management of conditions such as hypertension, diabetes and obesity.Keywords: AD; Cardiovascular disorders; Exercise; Cognition; Biomarkers; Prevention; Intervention
EditorialThe economic, logistic and caregiver burdens of worldwide Alzheimer's disease (AD), and in dementia of other causes also, is fasting approaching epic and insurmountable proportions, and among individuals motivation to improve 'brain health' through new information and/or their own efforts is markedly limited [1]. Healthy nutritional habits, including drinking plenty of water and maintaining hydration, are fundamental components for sustaining life, health and wellbeing with dietary patterns and lifestyles involved intimately in delaying the progression of the ageing process and reducing the risk of AD. Nutritional factors and physical exercise benefits have been manifested in other neurodegenerative disorders [2], implying that these, largely non-invasive interventions, ought to be examined closely in the AD context. In a large meta-analysis of putative protective factors for the disorder [3], grade I evidence for four medical treatments (oestrogen, statin, antihypertensive medications and nonsteroidal anti-inflammatory drugs therapy) and four dietary interventions (folate, vitamin E/C and coffee) was obtained. Epidemiological, biomarker, metabolic, neurocognitive and neuroimaging studies have furnished markedly copious evidence indicating the presence of indolent prodromal AD neuropathology long in advance of symptomatic onset with mechanistic links existing possibly between epigenomic status, DNA damage, and chronically unhealthy/dysfunctional body systems in the expression of disorder. For example, Hishikawa et al. [4] showed that greater cognitive and affective decline occurred in patients presenting AD with metabolic syndrome than those patients, with marked insulin resistance and vascular endothelial dysfunction observed in the former together with pathological brain white matter alterations. Dietary supplements aimed at reducing pro-inflammatory cytokine availability may also retard AD progression under conditions of exacerbated immunosenescence. The consensus seems to warrant individual-based combinations of early, multi-component nutritional approaches (a Mediterranean-style diet, multivitamins and key combinatorial supplements, etc), together with particular lifestyle modifications, such as social activities merged with intellectual and physical exercise. Assessment-based, tailored...