Thus, every risk factor discussed above could contribute to a different phase of plaque formation or consolidation. Although this theory provides an opportunity for an integrative conceptualization regarding the role of the various risk factors involved in the AD pathway, we are aware of the fact that it is still speculative in nature and demands further evidence.

Because some of the cardiovascular risk factors are modifiable, Inhibitors,research,lifescience,medical investigating the mechanisms by which they contribute to AD pathology and the manifestation of dementia has implications in prevention. This is particularly interesting, since in other multifactorial diseases, such as stroke, coronary heart, disease,123 and colon cancer,124 modifiable environmental factors such as diet, physical activity, and smoking may account for over half of the variability leading to the disease. Not surprising Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical therefore are studies demonstrating that physical and total activity in midlife,125-127 diet,40 and mild-to-moderate alcohol consumption128 are protective

against AD. However, these data should be seen with caution since there are not enough prospective studies Inhibitors,research,lifescience,medical to set clear guidelines regarding the medical and

nonmedical strategies for dementia prevention or delay. Selected abbreviations and acronyms AD Alzheimer’s disease AGE advanced glycation end-product ApoE Apolipoprotein E APP amyloid precursor protein HDL high-density lipoprotein IDE insulin-degrading enzyme MCI mild cognitive impairment MID multi-infarct dementia VD vascular dementia
Alzheimer’s disease Inhibitors,research,lifescience,medical (AD) is one of the most, devastating and costly disorders affecting the aging population. This disease has an estimated prevalence of up to 40% in Ergoloid those over age 80.1 Its financial cost to society has been estimated at between $70 and $100 billion annually.2 Currently approved therapies, arguably modest in effect, focus on symptomatic treatment.3-5 Preventive ATM Kinase Inhibitor strategics, on the other hand, remain elusive. Better understanding of this disorder, as well as the development, of both preventive and improved symptomatic treatments, has been limited by difficulties encountered in clinical diagnosis and the lack of adequate quantitative biomarkers for the disease. Clinical diagnosis depends on the definition of cognitive deficits and the separation of normal age-related decline from pathological deterioration.