Citations 273

O3‐01‐02: Treatment with 17β‐estradiol in postmenopausal women is associated with lower PiB‐PET retention

Alzheimer's & Dementia | December 15, 2015 | Volume: 11 | Issue: 7S_Part_5 | Pages: No page available

10.1016/j.jalz.2015.07.237

P4‐245: Predicting survival in dementia with lewy bodies: The importance of hippocampal volume

Alzheimer's & Dementia | December 15, 2015 | Volume: 11 | Issue: 7S_Part_19 | Pages: No page available

10.1016/j.jalz.2015.08.074

O5‐06‐04: Systems fail before molecules spread: A cascading failure model of Alzheimer's disease

Alzheimer's & Dementia | December 15, 2015 | Volume: 11 | Issue: 7S_Part_7 | Pages: No page available

10.1016/j.jalz.2015.07.478

P2‐163: Arterial stiffness and white matter hyperintensity load in normotensive postmenopausal women

Alzheimer's & Dementia | December 15, 2015 | Volume: 11 | Issue: 7S_Part_12 | Pages: No page available

10.1016/j.jalz.2015.06.702

F3‐02‐01: The relationship of primary age‐related tauopathy (PART) to snap: Controversy or parallel?

Alzheimer's & Dementia | December 15, 2015 | Volume: 11 | Issue: 7S_Part_4 | Pages: No page available

10.1016/j.jalz.2015.07.226

IC‐04‐04: Optimizing PiB‐PET change‐over‐time measurement by analysis of longitudinal reliability, plausibility, and separability

Alzheimer's & Dementia | December 15, 2015 | Volume: 11 | Issue: 7S_Part_1 | Pages: No page available

10.1016/j.jalz.2015.06.018

Characterizing White Matter Tract Degeneration in Syndromic Variants of Alzheimer’s Disease: A Diffusion Tensor Imaging Study

Journal of Alzheimer's Disease | December 14, 2015 | Volume: 49 | Issue: 3 | Pages: 633-643

10.3233/jad-150502 | PMID 26484918

Background: Different clinical syndromes can arise from Alzheimer’s disease (AD) neuropathology, including dementia of the Alzheimer’s type (DAT), logopenic primary progressive aphasia (lvPPA), and posterior cortical atrophy (PCA). Objective: To assess similarities and differences in patterns of white matter tract degeneration across these syndromic variants of AD. Methods: Sixty-four subjects (22 DAT, 24 lvPPA, and 18 PCA) that had diffusion tensor imaging and showed amyloid-β deposition on PET were assessed in this case-control study. A whole-brain voxel-based analysis was performed to assess differences in fractional anisotropy, mean diffusivity, axial diffusivity, and radial diffusivity across groups. Results: All three groups showed overlapping diffusion abnormalities in a network of tracts, including fornix, corpus callosum, posterior thalamic radiations, superior longitudinal fasciculus, inferior longitudinal fasciculus, inferior fronto-occipital fasciculus, and uncinate fasciculus. Subtle regional differences were also observed across groups, with DAT particularly associated with degeneration of fornix and cingulum, lvPPA with left inferior fronto-occipital fasciculus and uncinate fasciculus, and PCA with posterior thalamic radiations, superior longitudinal fasciculus, posterior cingulate, and splenium of the corpus callosum. Conclusion: These findings show that while each AD phenotype is associated with degeneration of a specific structural network of white matter tracts, striking spatial overlap exists among the three network patterns that may be related to AD pathology.
Atrial fibrillation, cognitive impairment, and neuroimaging

Alzheimer's & Dementia | October 25, 2015 | Volume: 12 | Issue: 4 | Pages: 391-398

10.1016/j.jalz.2015.08.164 | PMID 26607820

AbstractIntroductionThe objective of our study was to investigate cross‐sectional associations of atrial fibrillation with neuroimaging measures of cerebrovascular disease and Alzheimer's disease and their interactions with mild cognitive impairment (MCI).MethodsMagnetic resonance imaging scans of individuals from a population‐based study were analyzed for infarctions, total gray matter, and hippocampal and white matter hyperintensity volumes. A subsample underwent positron emission tomography imaging.ResultsAtrial fibrillation was associated with infarctions and lower total gray matter volume. Compared with subjects with no atrial fibrillation and no infarction, the odds ratio (95% confidence intervals) for MCI was 2.99 (1.57–5.70; P = .001) among participants with atrial fibrillation and infarction, 0.90 (0.45–1.80; P = .77) for atrial fibrillation and no infarction, and 1.50 (0.96–2.34; P = .08) for no atrial fibrillation and any infarction.DiscussionParticipants with both atrial fibrillation and infarction are more likely to have MCI than participants with either infarction or atrial fibrillation alone.
Role of β-Amyloidosis and Neurodegeneration in Subsequent Imaging Changes in Mild Cognitive Impairment

JAMA Neurology | October 5, 2015 | Volume: 72 | Issue: 12 | Pages: 1475

10.1001/jamaneurol.2015.2323 | PMID 26437123

Age, Sex, andAPOEε4 Effects on Memory, Brain Structure, and β-Amyloid Across the Adult Life Span

JAMA Neurology | March 16, 2015 | Volume: 72 | Issue: 5 | Pages: 511

10.1001/jamaneurol.2014.4821 | PMID 25775353