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Structural MRI and functional imaging by SPECT as well as ^sup 18^F-FDG PET are widely used in the diagnosis of Alzheimer's disease (AD). Metabolic and perfusion reductions in the parietotemporal association cortex are recognized as a diagnostic pattern for AD. Outstanding progress in the diagnostic accuracy of these modalities has been achieved with statistical analysis on a voxel-by-voxel basis after anatomic standardization of individual scans to a standardized brain volume template instead of visual inspection or a volume-of-interest technique. In a very early stage of AD, this statistical approach revealed losses of gray matter in the entorhinal and hippocampal areas and hypometabolism or hypoperfusion in the posterior cingulate cortex and precuneus. This statistical approach also offers a prediction of the conversion from mild cognitive impairment (MCI) to AD. The presence of hypometabolism or hypoperfusion in parietal association areas and entorhinal atrophy at the MCI stage have been reported to predict a rapid conversion to AD. A recent advance in voxel-based statistical analysis has markedly enhanced the value of brain perfusion SPECT in diagnosing early AD at the stage of MCI.
Key Words: Alzheimer's disease; SPECT; PET; MRI; statistical image analysis
J Nucl Med 2007; 48:1289-1300
DOI: 10.2967/jnumed.106.037218
With increasing life expectancy in much of the world, the number of older people at risk of developing dementia is growing rapidly, and Alzheimer's disease (AD) remains the most common cause of dementia in all age groups. AD is a progressive neurodegenerative disorder associated with a disruption of neuronal function and a gradual deterioration in cognition, function, and behavior. AD is pathologically characterized by the presence of amyloid deposition and neurofibrillary tangles, together with the loss of cortical neurons and synapses (1). The most profound and earliest cognitive deficits seem to be impairment of episodic memory-the ability to recall events that are specific to a time and place. Medications such as Cholinesterase inhibitors are able to delay the progression of AD (2). Moreover, patients who have AD and in whom the start of Cholinesterase inhibitor therapy is delayed demonstrate fewer benefits than do patients starting therapy early in the course of AD (3). This fact has shifted the focus of present studies on AD toward earlier diagnosis and longitudinal investigations to assess the value of therapeutic interventions.