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IC–P–082: Atrophy in the parietotemporal regions increases the risk of developing Alzheimer's disease: A longitudinal MRI study
Author(s) -
Desikan Rahul S.,
Han Xiao,
Cabral Howard J.,
Fischl Bruce,
Blacker Deborah,
Guttmann Charles R.,
Albert Marilyn S.,
Killiany Ronald J.
Publication year - 2006
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2006.05.2287
Subject(s) - atrophy , medicine , neuropathology , neuroimaging , alzheimer's disease , temporal lobe , magnetic resonance imaging , pathology , brain size , disease , radiology , psychiatry , epilepsy
Background: Neuropathology and structural imaging studies have established the involvement of the medial temporal lobe in Alzheimer’s disease (AD). In contrast, the role of the posterior association areas is less well understood. Neuropathological analyses have described significant amyloid deposits in parietotemporal regions in the early stages of AD. Neuroimaging evidence from PET has, likewise, consistently shown abnormalities in the parietotemporal metabolism in AD. Structural abnormalities in this region have been difficult to quantify because identifying these cortices accurately on MRI has been methodologically challenging. Using procedures we recently developed (Fischl et al., 2004; Desikan et al, in press), we sought to determine whether progressive atrophy in the parietotemporal regions is evident on longitudinal MRI scans of subjects in the earliest stages of AD. Methods: 53 subjects (27 females) with SPGR scans at two time points (mean follow-up 2.74 years) were divided into two groups: subjects with normal cognition (CDR 0.0) at the time of both scans (n 23), and subjects with MCI (CDR 0.5) at the time of the first scan and had progressed to AD (CDR 1.0 AD) at the time of the follow-up scan (n 30). The scans were processed, subdividing the parietotemporal region into 17 anatomically defined ROIs per hemisphere. Logistic regression analyses, controlling for intracranial volume and time between scans, were used to assess the relationship between the longitudinal change in volume of each region and the likelihood of being in the control or MCI/AD group. Results: Odds ratios were generated to determine when increased rates of atrophy posed significant risk for being in the MCI/AD group. The hippocampus and supramarginal gyrus showed the most significant elevations of risk (p 0.03) followed by the precuneus, banks of the superior temporal gyrus, inferior parietal lobule, fusiform gyrus, parahippocampal gyrus, inferior temporal gyrus and the middle temporal gyrus. Conclusions: These findings suggest that progressive atrophy can be identified and followed longitudinally in both parietotemporal and medial temporal regions during the prodromal phase of AD. They are consistent with neuropathological findings and functional imaging data that describe abnormalities in parietotemporal regions early in the course of AD.