Age at onset was estimated from the caregiver’s report of memory disturbances exceeding the episodic forgetfulness that might be regarded as usual for the patient or of other disturbances (language, praxis, orientation, visuospatial skills) that proved to be clearly related to the disease.
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To take into account the effect of Apo E polymorphism on brain morphology, the analysis was re-run including the presence of at least one ε4 allele as a nuisance covariate, but the results did not change appreciably.
We have shown that patients with early onset Alzheimer’s disease have greater temporoparietal atrophy and patients with late onset Alzheimer’s disease greater medial temporal atrophy than controls.
Both the patients and controls underwent high resolution sagittal T1-weighted volumetric MRI as previously described.) the main VBM steps: normalisation of the original MR images, segmentation of normalised images, cleaning of grey matter images, modulation of grey matter images, and smoothing of modulated images.
A “single subject: conditions and covariates” model was used.
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Figure 1A and table 1 show that patients with EOAD had greater atrophy than YC in the temporoparietal cortex.
The most significant voxel—that is, the voxel with the highest z score, was in the right temporoparietal junction, and the widest cluster was in the left parietal regions.
Intracranial volume and sex were included as nuisance covariates.
Regions specifically atrophic in EOAD and LOAD were detected by contrasting EOAD with YC and LOAD with OC, thresholding the resulting T maps at p 22.1 (4.1); p = 0.04), while the two groups were not significantly different on the verbal and non-verbal memory tasks as well as verbal fluency tasks.
Methods: We studied nine patients with early onset (age ⩽65 years), nine with late onset (age 65, n = 17) subjects.