It is commonly understood that. different levels of cognitive functioning are expected from a 90 year old than a 60 year old, or a university graduate versus an illiterate person. Instead, the clinical diagnosis of dementia usually relies on the characterization of intraindividual decline from premorbid level of functioning. Typically, however, firm quantitative data about premorbid status are lacking, and the diagnostic process relies instead on interviews at the time of Inhibitors,research,lifescience,medical symptomatic onset, that. attempt to characterize premorbid performance

levels. This approach is 3MA limited in its accuracy, and suffers from possible sources of diagnostic bias. Inhibitors,research,lifescience,medical In addition to these

problems of isolating mild, initial AD from normal aging, the clinical diagnosis is sometimes ambiguous due to overlap of symptoms between AD and other dementing illnesses. To address these issues and improve diagnostic accuracy, we need to support, the clinical diagnosis by laboratory Inhibitors,research,lifescience,medical markers. Many have been sought, 6-8 this article addresses one of the most promising and best documented, based on imaging of cerebral structure and function. Several modalities as well as strategies (eg, quantitative versus qualitative) have been evaluated for their role in the imaging diagnosis of AD. Computed tomography (CT) and magnetic resonance imaging (MRI) have focused primarily on the structural changes observed in specific brain Inhibitors,research,lifescience,medical areas during the course of the disease. Studies evaluating the diagnosis of AD using these techniques

are based on impressionistic (or interpretive) measures (eg, qualitative determination of atrophy) or more rigorous quantitative measures where linear or volumetric parameters are obtained from the imaging Inhibitors,research,lifescience,medical data. The mesial temporal lobe (MTL), especially the hippocampus, has emerged as the most Pifithrin-�� cost sensitive area to examine for AD-relatcd atrophy. Functional neuroimaging, such as single photon emission computed tomography (SPECT) or positron emission tomography (PET), typically measures cerebral perfusion or metabolism, reflecting alteration in cerebral function. These studies are also based on either qualitative impression or objective measured parameters. The area most, sensitive to such functional deficits in AD is the inferior parietal cortex. There is a large body of evidence regarding the validity of both measures (hippocampal atrophy and parietal metabolic deficit.) as markers of AD. The relationship between the two is obscure, and despite their promise, imaging findings lack compelling evidence for their diagnostic value.