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Commentary on “A roadmap for the prevention of dementia II: Leon Thal Symposium 2008.” Comments from abroad
Author(s) -
Korczyn Amos D.
Publication year - 2009
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2009.01.009
Subject(s) - tel aviv , library science , citation , medicine , psychology , computer science
It is imperative to change public and governmental views of the expanding dementia epidemic by stressing the urgency of action, but at the same time by also providing a strategy to show that the prospects are good to find a solution, provided the right path is followed. We have to demonstrate that the developments so far are not trivial, and that a lot has been achieved. The fight against cancer is a valuable example, where the gains have been used to convince authorities that the prospects for even greater achievements are within reach. In a similar vein, we can and should demonstrate the great advances during the last 20 years in the understanding of the mechanisms leading to brain failure on the molecular, cellular, and system levels, as well as the therapeutic achievements. On that background, there is an obvious need for a concerted action in several fronts. One target is the importance of early intervention. To do so, we must eliminate the nonuseful definition of Alzheimer’s disease (AD) and of dementia in general, a definition that we have created. We know all too well that biologic changes precede full-blown dementia by several years or decades, and we must emphasize that these provide us with a window of opportunity for successful early intervention. In this context, the present requirements for a person to be severely affected before the diagnosis of dementia can be made (on the basis of clinical dementia rating or Diagnostic and Statistical Manual [of Mental Disorders], Fourth Edition criteria) are outdated. As we all know, there is no biologic demarcation separating dementia from milder form of cognitive impairment. Objective biologic markers of disease will be very helpful in this regard. Evidence of minor functional decline, if accompanied by the existence of a biologic marker (such as impaired cerebral metabolism evidenced by positron emission tomography, hippocampal atrophy, or amyloid deposi-