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P2‐371: Regional distribution of white matter hyperintensities in mild cognitive impairment
Author(s) -
Brickman Adam M.,
Muraskin Jordan,
Provenzano Frank A.,
Luchsinger Jose,
Manly Jennifer J.,
Apa Zoltan L.,
Yeung Lok-Kin,
Schupf Nicole,
Stern Yaakov,
Brown Truman R.,
Mayeux Richard
Publication year - 2010
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.2010.05.1423
Subject(s) - hyperintensity , cardiology , medicine , atrophy , hippocampus , leukoaraiosis , audiology , white matter , cognitive impairment , psychology , cognition , magnetic resonance imaging , fluid attenuated inversion recovery , neuroscience , disease , radiology
Background: Small vessel cerebrovascular disease, visualized as white matter hyperintensities (WMH) on MRI, has been linked to age-associated cognitive dysfunction, but whether it is related to Alzheimer’s disease (AD) is unclear. This study examined the regional distribution of WMH among older adults at high risk for developing AD drawn from a cohort of community-dwelling older adults. Because hippocampal atrophy, a putative marker for neurodegeneration, is typically increased among patients with AD, we also compared the ability of regional WMH volume with hippocampus volume to classify individuals as at-risk for AD (i.e., those with amnestic mild cognitive impairment) and as controls. Methods: Highresolution MRI was acquired in 717 non-demented, older (80.0+/5.5.8) and ethnically diverse adults from upper Manhattan. Participants were evaluated medically and neuropsychologically, and classified as normal controls (n 1⁄4 508); non-amnestic mild cognitive impairment (naMCI; n 1⁄4 74); and amnestic MCI (aMCI single/multiple domain; n 1⁄4 97), previously shown to be up to 4.3 times more likely to progress to AD than controls. Lobar (frontal, temporal, parietal, occipital) WMH volumes were quantified on T2-weighted FLAIR MRI scans. Hippocampal volumes were derived and normalized for head size, and presence/absence of infarct was recorded. Controlling for relevant demographic factors and infarct, we compared the regional distribution of WMH among the three groups with a mixed-design general linear model. We predicted group membership (aMCI vs. control) with regional WMH volume and hippocampus volume with logistic regression. Results: The aMCI group had significantly more overall WMH volume than controls. A Group by Region interaction revealed that both MCI groups had greater WMH volume in the frontal lobes than controls, but only the aMCI group had greater WMH in the parietal lobes. Parietal lobe WMH volume, but not hippocampus volume, reliably classified participants as aMCI or controls. Conclusions: While increased WMH volume in frontal lobes is related to cognitive dysfunction in aging, WMH volume in parietal lobes is elevated among those at greatest risk for developing AD specifically. Posterior WMH distribution reflects early vascular pathology that may precede neurodegeneration marked by hippocampal atrophy. Mechanistic links between small vessel cerebrovascular disease, particularly in posterior areas, and AD should continue to be evaluated.