1 billion in the USA, $124.6 billion in Italy, $30.5 billion in France, and $11.2 billion in England. The burden of this illness is such that investigators stress not only the importance of finding a cure, but also the necessity of intervening in the early stages of dementia to prolong functionality and extend the time before institutionalization.

These changing demographics will also impact the prevalence and incidence of MCI and AACD, since as many as 50% of individuals over age 65 currently fulfill the criteria for at least one of these conditions. Inhibitors,research,lifescience,medical Such impairments in cognition influence many day-to-day activities, from medication adherence to productivity in the workplace and at home.3 Additionally, extended selleck kinase inhibitor longevity rates and increasing numbers of older adults in our society suggest that older workers may be required to continue working to prevent financial overload on the retirement and pension systems. 4,5 The elimination of mandatory retirement for most occupations in the Inhibitors,research,lifescience,medical USA has made it possible for older adults to stay in the workplace. Maintaining memory and cognitive function is obviously important for older adults, who want

to – or are obliged to – continue working. The end result of these social changes is that older adults may not only want to live longer with better cognitive function, they may Inhibitors,research,lifescience,medical also need to. Additionally, preserving cognitive function helps maintain aspects of living, such as personal independence, that contribute to the good health and overall quality of life in older adults. In this article, we provide Inhibitors,research,lifescience,medical an overview of the current pharmacological and nonpharmacological approaches to the cognitive impairments associated with AD, MCI, and AACD, since these represent the most prevalent neurocognitive syndromes among older adults. Additionally, the neuropathological mechanisms hypothesized to underlie AD may also contribute to MCI and AACD. Indeed, many investigators suggest there is a spectrum of pathophysiological Inhibitors,research,lifescience,medical changes that accompany the

normal aging process, increase in severity to produce AACD and MCI, and, in their most severe form, result in dementia. most Such pathologies include neurotransmitter deficiencies (particularly cholinergic deficits), β-amyloid deposits, inflammation, neuroendocrine abnormalities, and immunological impairment. Additionally, the genetic and environmental risk factors for the development of dementia also appear to be associated with MCI and AACD.6,7 Thus, the therapeutic approaches developed to intervene with dementia have informed, and will continue to inform, similar approaches to MCI and AACD (Figure 1 and Figure 2).8 Figure 1. Potential physiological pathways to Alzheimer’s disease. APOE, apolipoprotein E; CSF, cerebrospinal fluid; PET, positron emission tomography; fMRI, functional magnetic resonance imaging. Reproduced from reference 8: Sunderland T. Alzheimer’s disease. … Figure 2. Typical clinical course: current and future therapeutic approaches.