It was rational to apply these techniques

to mild cognitive deficit, in order to characterize these states and identify predictors of progression to AD. Neuropathological studies have shown the hippocampus to be one of the earliest, affected structures in AD,71 and so it is a region of choice for neuroimaging studies. Although hippocampal atrophy, as measured by volumetric Inhibitors,research,lifescience,medical techniques is not entirely specific, it is now considered to be a hallmark of AD,72 and its absence in addition to minor or unilateral atrophy is believed to be strong evidence against the diagnosis. In mild cognitive deficit, several studies have shown lesser73-76 or similar77 hippocampal Inhibitors,research,lifescience,medical atrophy to that found in AD. Age transformation of combined hippocampal and amygdala volume increases the accuracy of classifying AD, MCI, and normal elderly subjects.78 MCI subjects

had hippocampal volume correlated with cognitive and performance measures79 and those who declined over time had also a greater annualized rate of hippocampal atrophy than nondeclincrs, close to that of AD patients.80 Atrophy of various regions at baseline, Inhibitors,research,lifescience,medical including hippocampus79, 81, 82 ERC,83-84 fusiform gyrus,85 caudal cingulate cortex,83 and medial temporal lobe,76 was found predictive of progression to AD. White matter lesions have been found to be associated with subjective cognitive decline,86 lowered attention and speed of mental processing,87 and progression to dementia.88 There Inhibitors,research,lifescience,medical is an agreement on the fact that established AD is characterized by altered cerebral blood flow (CBF) and metabolism in posterior parietal and temporal lobes as well as by, according to stage and neuropsychological Inhibitors,research,lifescience,medical profile, frontal cortex deficits, and hemispheric asymmetry.89 That functional imaging is able to detect selleckchem preclinical AD is suggested by positron emission tomography (PET) studies, which found regional cerebral glucose metabolism (rCMRGlu) alterations in nondemented subjects at risk of AD (ie, those carrying the apolipoprotein E type 4 allele [ ApoE ε4] and with familial

Cilengitide history of AD)90, 9190-91; those in the inferior parietal and posterior cingulate cortices correlated with later memory decline.92 Studies comparing CBF and rCMRGlu in normal and mildly impaired subjects found deficits in the latter, in various regions including bilateral parietal cortex,56 hippocampus,77 and posterior cingulate gyrus.93-95 Prediction of outcome was found for defects in parietal or temporoparietal cortex,56, 96 posterior cingulate gyrus,94, 95 and for temporoparietal asymmetry97 and lowered postcroanterior ratio89; others were predictive when combined with performance on specific cognitive tasks98, 99 and/or demographic selleck chem characteristics.99 Progress in functional imaging can come from activation studies.