Commentary on “The Third Canadian Consensus Conference on the Diagnosis and Treatment of Dementia, 2006.”—An appraisal

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Since the second series of consensus documents from Canadian Alzheimer’s disease (AD) experts was published in 1999, the field has undergone major changes in the areas of genetics, risk and prevention, prodromal stages, diagnosis, and management. The methodology utilized by this Canadian group is well-constructed, and has yielded a new collection of papers that represents a major resource to students, general practitioners, specialists, and research scientists. It was a large effort, but the payoff is substantial. Most important, though, will be the efforts to assure optimal translation of the recommendations into clinical practice. I offer comments on a few specific areas within this very broad project. 1. There continue to be many areas of confusion surrounding the interpretation of observational studies of modifiable risk factors of dementia [1], such as blood pressure, cholesterol, smoking, and depression. This probably reflects the very difficult issue of bias in nonrandomized studies; it is a major problem with no ready solution. 2. With regard to the genetics of susceptibility to AD [2], the apolipoprotein E genotype is unquestionably important, but it remains uncertain whether any other genetic risk factor will have much impact. 3. The relationship between homocysteine, B vitamins, and cognitive impairment and dementia [3] is given a balanced review. Whereas homocysteine elevation is linked to both cerebrovascular disease and AD, there is insufficient evidence to justify testing for or treating homocysteine in the older population with or without cognitive dysfunction. We recently presented the results of a randomized, controlled trial of high-dose B vitamin supplementation in mild-to-moderate AD (conducted by the Alzheimer’s Disease Cooperative Study), with over