Association of silent lacunar infarct with brain atrophy and cognitive impairment

Thong, Jamie Yu Jin; Hilal, Saima; Li, Han; Soon, Hock Wei; Dong, Yi; Collinson, Simon L.; Anh, Tuan Ta; Ikram, M. Kamran; Wong, Tien Yin; Venketasubramanian, Narayanaswamy; Chen, Christopher; Qiu, Anqi

doi:10.1136/jnnp-2013-305310

Cited by 54 publications

(46 citation statements)

References 43 publications

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“…Paths #1, #2 and #3 in Figure 2 were required to show significant associations. WMH and infarcts were associated with cognition, specifically PS/EF, as observed by others 7, 13, 36 . Second, for all 3 of our ROI’s, cortical volume was associated with cognition, which has also been frequently observed 37–42 .…”

Section: Discussionsupporting

confidence: 74%

Vascular Imaging Abnormalities and Cognition

Knopman

Griswold

Lirette

et al. 2015

Stroke

136

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Background and Purpose The relationships between cerebrovascular lesions visible on imaging and cognition are complex. We explored the possibility that cerebral cortical volume mediated the relationship. Methods 1906 non-demented participants (59% women; 25% African-American; mean age 76.6 years) in the Atherosclerosis Risk in Communities (ARIC) study underwent cognitive assessments, risk factor assessments, and quantitative MR imaging for white matter hyperintensities (WMH) and infarcts. The Freesurfer imaging analysis pipeline was used to determine regional cerebral volumes. We examined associations of cognitive domain outcomes with cerebral volumes (hippocampus, and separate groups of posterior and frontal cortical regions of interest (ROI)) and cerebrovascular imaging features (presence of large or small cortical/subcortical infarcts and WMH volume). We performed mediation pathway analyses to assess the hypothesis that hippocampal and cortical volumes mediated associations between cerebrovascular imaging features and cognition. Results In unmediated analyses, WMH and infarcts were both associated with worse psychomotor speed/executive function (PS/EF). In mediation analyses, WMH and infarcts associations on PS/EF were significantly attenuated, but not abolished, by the inclusion of the posterior cortical ROI volume in the models, and the infarcts on PS/EF association was attenuated, but not abolished, by inclusion of the frontal cortical ROI volume. Conclusions Both WMH and infarcts were associated with cortical volume, and both lesions were also associated with cognitive performance, implying shared pathophysiological mechanisms. Although cross-sectional, our findings suggest that WMH and infarcts could be proxies for clinically covert processes that directly damage cortical regions. Microinfarcts are one candidate for such a clinically covert process.

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Section: Discussionsupporting

confidence: 74%

Vascular Imaging Abnormalities and Cognition

Knopman

Griswold

Lirette

et al. 2015

Stroke

136

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“…“Silent” lacunar infarcts are frequently detected by MRI or CCT and are not accompanied by any overt clinical symptoms, but double the risk of subsequent stroke and dementia [133]. They have been shown to be associated with atrophy in multiple subcortical structures, ventricular enlargement, and widespread cortical thinning, supporting the assumption of a vascular contribution to neurodegeneration and cognitive impairment [134]. As opposed to large and lacunar infarcts, cortical microinfarcts (CMI) are usually not visible at gross neuropathological examination.…”

Section: Reviewmentioning

confidence: 99%

The overlap between vascular disease and Alzheimer’s disease - lessons from pathology

Attems

Jellinger

2014

BMC Med

582

420

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Recent epidemiological and clinico-pathological data indicate considerable overlap between cerebrovascular disease (CVD) and Alzheimer’s disease (AD) and suggest additive or synergistic effects of both pathologies on cognitive decline. The most frequent vascular pathologies in the aging brain and in AD are cerebral amyloid angiopathy and small vessel disease. Up to 84% of aged subjects show morphological substrates of CVD in addition to AD pathology. AD brains with minor CVD, similar to pure vascular dementia, show subcortical vascular lesions in about two-thirds, while in mixed type dementia (AD plus vascular dementia), multiple larger infarcts are more frequent. Small infarcts in patients with full-blown AD have no impact on cognitive decline but are overwhelmed by the severity of Alzheimer pathology, while in early stages of AD, cerebrovascular lesions may influence and promote cognitive impairment, lowering the threshold for clinically overt dementia. Further studies are warranted to elucidate the many hitherto unanswered questions regarding the overlap between CVD and AD as well as the impact of both CVD and AD pathologies on the development and progression of dementia.Electronic supplementary materialThe online version of this article (doi:10.1186/s12916-014-0206-2) contains supplementary material, which is available to authorized users.

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“…While extensive WMH can drive widespread cortical thinning and ventricular expansion 26–28 , regional WMH load may also be relevant. For example frontal WMH may have a greater impact on frontal lobe thinning 28–31 .…”

Section: Contribution Of Cerebrovascular Pathologies To Neurodegeneramentioning

confidence: 99%

The role of cerebrovascular disease when there is concomitant Alzheimer disease

Vemuri

Knopman

2016

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Cerebrovascular Pathologies (CVP) are the most common co-existent pathologies observed in conjunction with Alzheimer disease. CVP rarely exists in isolation in later life, and CVP most likely plays a supporting role, rather than a sole leading role, in the pathogenesis of dementia. Our goal is to illustrate CVP’s role using neuroimaging biomarkers. First, we discuss the frequency of CVP and present data from population-based Mayo Clinic Study of Aging. Here, we used a novel metric for identifying individuals with cerebrovascular imaging abnormalities (that we designate as “V+”) and present the frequency of V−/V+ in the context of absence and presence of β-amyloid elevation (designated A−/A+). Next, we discuss the contribution of CVP to neurodegeneration and use hippocampal volume loss over time in a subset of participants categorized as A−V−, A−V+, A+V−, A+V+. Lastly, we discuss the contribution of CVP to cognitive impairment and conclude with the considerations for design of future studies.

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Association of silent lacunar infarct with brain atrophy and cognitive impairment

Abstract: Our findings support a vascular contribution to neurodegeneration and cognitive impairment.

Cited by 54 publications

References 43 publications

Vascular Imaging Abnormalities and Cognition

Vascular Imaging Abnormalities and Cognition

The overlap between vascular disease and Alzheimer’s disease - lessons from pathology

The role of cerebrovascular disease when there is concomitant Alzheimer disease

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