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The investigation of Alzheimer disease (AD) with neuroimaging has often focused on 2 different brain regions. Researchers using positron emission tomographic (PET) imaging of glucose metabolism with fludeoxyglucose F 18 described hypometabolism in the lateral temporoparietal cortex and especially the medial parietal cortex encompassing the precuneus and posterior cingulate.1 Investigations using magnetic resonance imaging showed that patients with AD had substantial atrophy in the medial temporal lobes (MTLs), specifically the hippocampus and entorhinal cortex. Considerable work has extended these findings to individuals who may be in early stages of AD as reflected by mild cognitive impairment. Although subsequently it has become clear that involvement of these anatomical areas is not modality specific (that is, medial temporal hypometabolism and medial parietal atrophy are both reported in AD), the pathological relationship of degeneration in these 2 brain regions has been difficult to understand.
Jagust W. Biomarkers and Brain Connectivity. JAMA Neurol. 2013;70(10):1233–1234. doi:10.1001/jamaneurol.2013.3743
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