Article

Distinct MRI atrophy patterns in autopsy-proven Alzheimer's disease and frontotemporal lobar degeneration.

Memory and Aging Center, University of California, San Francisco, California 94143, USA.
American Journal of Alzheimer s Disease and Other Dementias (Impact Factor: 1.43). 01/2008; 22(6):474-88. DOI: 10.1177/1533317507308779
Source: PubMed

ABSTRACT To better define the anatomic distinctions between Alzheimer's disease (AD) and frontotemporal lobar degeneration (FTLD), we retrospectively applied voxel-based morphometry to the earliest magnetic resonance imaging scans of autopsy-proven AD (N = 11), FTLD (N = 18), and controls (N = 40). Compared with controls, AD patients showed gray matter reductions in posterior temporoparietal and occipital cortex; FTLD patients showed atrophy in medial prefrontal and medial temporal cortex, insula, hippocampus, and amygdala; and patients with both disorders showed atrophy in dorsolateral and orbital prefrontal cortex and lateral temporal cortex (P(FWE-corr) < .05). Compared with FTLD, AD patients had decreased gray matter in posterior parietal and occipital cortex, whereas FTLD patients had selective atrophy in anterior cingulate, frontal insula, subcallosal gyrus, and striatum (P < .001, uncorrected). These findings suggest that AD and FTLD are anatomically distinct, with degeneration of a posterior parietal network in AD and degeneration of a paralimbic fronto-insular-striatal network in FTLD.

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Available from: Stephen C Allison, May 20, 2014
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    • "the associated frontal circuit in comparison to other neurodegenerative conditions (Rabinovici et al., 2007). Grossman et al. (2010) examined the interpretation of positive and negative situations in individuals with bvFTD and found that these individuals were particularly impaired in interpreting negative consequences of a social situation (e.g., " rolling through a red light at 2 a.m. when there is a police car at the intersection , " p. 5). "
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    • "Aberrant projections from hippocampus and/or MTL could influence frontal cortex function prior to ADrelated anatomical changes. Pathology in mild AD is thought to be limited to the temporo-parietal junction (Rabinovici et al., 2007), which does not include the PEFs, so a lack of impairment in prosaccade generation is not surprising. It has been shown previously that volumetric changes in the SEF correlate with antisaccade latency, but that DLPFC and FEF volume were not correlated with antisaccade performance (Boxer et al., 2006), supporting the notion that functional changes probably precede anatomical changes in the frontal cortex of AD patients. "
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