Predictors of Alzheimers disease

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27 subjects with MCI for 24 months and 26% developed AD (Jelic and Nordberg, 2000). All these MCI patients underwent PET studies of brain glucose metabolism before the longitudinal study started. Impairments in cerebral glucose metabolism were already present at the beginning of the follow-up period in the group of MCI patients who progressed to AD, with a 93% predictive power of converting to AD (Jelic and Nordberg, 2000; Nordberg et al., 2001). Similarly, in a group of 20 MCI patients followed for 36 months, 9 patients converted to AD while 11 patients remained clinically stable (and were classified as stable MCI). Neuropsychological assessments, such as Block Design, gave a correct classification of 65% while the combined measure of Block Design and cerebral glucose metabolism gave a correct classification of 90% (Arnaiz et al., 2001). It is apparent that early functional metabolic changes can be observed in subjects with MCI and that the degree of functional disturbances in glucose metabolism as measured by PET can be used as a predictive marker for conversion from MCI to AD, especially when combined with neuropsychological testing. CSF markers will probably also represent another valuable complement in a near future (Knopman et al., 2001).

Mild cognitive impairment

How important is an early detection of MCI patients? How important is it to initiate drug treatment in MCI patients before they may convert to AD? Is there any possibility of predicting which MCI patients are likely to convert to AD? MCI is considered as an intermediate in the continuum from normalcy to dementia (Almkvist et al., 1998). The most commonly used criteria for MCI include memory complaints and memory impairment, but normal general cognitive function and daily living (Petersen et al., 1999). In a four year follow-up of 76 subjects selected for MCI, the annual conversion rate to AD was 12% compared to 1% in normal subjects (Petersen et al., 1999), whereas in a two year follow-up study, it was estimated to be 25% (Flicker et al., 1991). It has recently been estimated that, among subjects with MCI, the rate of progression to dementia or AD is 6-c25% per year (Petersen et al., 2001). We followed

Apolipoprotein E e4 carriers

Two independent studies have reported that the APOE s4 allele is not associated with specific alterations in glucose metabolism in patients with AD (Corder et al., 1997; Hirono et al., 1998). There is evidence that the presence of the "4 allele could cause preclinical deficits similar to what can be observed in manifest disease (Small et al., 1996; Reiman et al., 1996). Small et al. (2000) also showed recently that, in nondemented APOE "4 carriers followed longitudinally for two year, the memory performance scores did not decline significantly, while there was a significant decline in cortical metabolic ratio. Similar findings were also reported by Reiman et al. (2001), who found a significant decline in cerebral glucose metabolism in the temporal cortex, posterior cingulate cortex, prefrontal cortex, basal forebrain, parahippocampal gyri and thalamus of "4

heterozygotes, in the absence of cognitive alterations during two years. Reiman et al. (2001) estimated that 50-150 cognitively normal s4 heterozygotes would probably be a sufficient number of subjects for testing the outcome of a preventive AD therapy. Cerebral metabolic rates and genetic factors may provide a means for preclinical AD detection and importantly assist in the evaluation of the efficiency of preventive drug treatments in the future.

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