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Pattern of regional white matter hyperintensity volume in mild cognitive impairment subtypes and associations with decline in daily functioning.

ABSTRACT: White matter hyperintensities (WMHs), a marker of small-vessel cerebrovascular disease, increase risk for mild cognitive impairment (MCI). Less is known about whether regional WMHs distinguish MCI subtypes and predict decline in everyday functioning. About 618 Alzheimer's Disease Neuroimaging Initiative participants (301 cognitively normal [CN]; 232 amnestic MCI [aMCI]; 85 nonamnestic MCI [naMCI]) underwent neuropsychological testing, MRI, and assessment of everyday functioning. aMCI participants showed greater temporal (p = 0.002) and occipital WMHs (p = 0.030) relative to CN whereas naMCI participants had greater frontal (p = 0.045), temporal (p = 0.003), parietal (p = 0.018), and occipital (p < 0.001) WMH compared with CN. Relative to those with aMCI, individuals with naMCI showed greater occipital WMH (p = 0.013). Greater WMH in temporal (p = 0.001) and occipital regions (p = 0.006) was associated with faster decline in everyday functioning across the sample. Temporal lobe WMHs were disproportionately associated with accelerated functional decline among naMCI (p = 0.045). Regional WMH volumes vary across cognitive groups and predict functional decline. Cerebrovascular markers may help identify individuals at risk for decline and distinguish subtypes of cognitive impairment.

SUBMITTER: Bangen KJ

PROVIDER: S-EPMC6995428 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature

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Subjective Cognitive Decline Is Associated with Greater White Matter Hyperintensity Volume.

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APOE ?2 is associated with white matter hyperintensity volume in CADASIL.

Project description:Apolipoprotein E (APOE) increases the risk for Alzheimer’s disease (?4 allele) and cerebral amyloid angiopathy (?2 and ?4), but its role in small vessel disease (SVD) is debated. Here we studied the effects of APOE on white matter hyperintensity volume (WMHV) in CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy), a nonamyloidogenic angiopathy and inherited early-onset form of pure SVD. Four hundred and eighty-eight subjects were recruited through a multicenter consortium. Compared with APOE ?3/?3, WMHV was increased in APOE ?2 (P?=?0.02) but not APOE ?4. The results remained significant when controlled for genome-wide genetic background variation. Our findings suggest a modifying influence of APOE ?2 on WMHV caused by pure SVD.

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