Contribution of White Matter Lesions to Gray Matter Atrophy in Multiple Sclerosis

Sepulcre, Jorge; Goñi, Joaquín; Masdeu, Joseph C.; Bejarano, Bartolomé; Mendizábal, Nieves Vélez de; Toledo, Jon B.; Villoslada, Pablo

doi:10.1001/archneurol.2008.562

Cited by 98 publications

(38 citation statements)

References 35 publications

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“…Our results demonstrate that GM atrophy occurred in the right supramarginal gyrus, right angular gyrus, right middle temporal gyrus, right anterior cingulum and left insula in OPVHs patients. These results are consistent with previous studies (Sepulcre et al, 2009; Raji et al, 2012). …”

Section: Discussionsupporting

confidence: 94%

Regional Gray Matter Atrophy Coexistent with Occipital Periventricular White Matter Hyper Intensities

Duan

Shen

et al. 2016

Front. Aging Neurosci.

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White matter hyperintensities (WMHs) and brain atrophy often coexist in the elderly. Additionally, WMH is often observed as occipital periventricular hyperintensities (OPVHs) with low-grade periventricular (PV) white matter (WM) lesions and is usually confined within an anatomical structure. However, the effects of OPVHs on gray matter (GM) atrophy remain largely unknown. In this study, we investigated GM atrophy in OPVHs patients and explored the relationship between such atrophy and clinical risk factors. T1-weighted and T2-weighted Magnetic resonance imaging (MRI) were acquired, and voxel-based morphometry (VBM) analysis was applied. The clinical (demographic and cardiovascular) risk factors of the OPVHs patients and healthy controls were then compared. Lastly, scatter plots and correlation analysis were applied to explore the relationship between the MRI results and clinical risk factors in the OPVHs patients. OPVHs patients had significantly reduced GM in the right supramarginal gyrus, right angular gyrus, right middle temporal gyrus, right anterior cingulum and left insula compared to healthy controls. Additionally, OPVHs patients had GM atrophy in the left precentral gyrus and left insula cortex, and such atrophy is associated with a reduction in low-density lipoprotein cholesterol (LDL-C) and apolipoprotein-B (Apo-B).

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Section: Discussionsupporting

confidence: 94%

Regional Gray Matter Atrophy Coexistent with Occipital Periventricular White Matter Hyper Intensities

Duan

Shen

et al. 2016

Front. Aging Neurosci.

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“…Work in Alzheimer disease patients has found cognitive reserve to attenuate the impact of pathology including β-amyloid (Roe et al, 2008), neuritic plaques, and diffuse plaques (Bennett et al, 2003) on cognitive function. Similar findings emerge in patients with multiple sclerosis, a disease known to predominately affect the white matter of the brain (Benedict et al, 2010; Sumowski, Chiaravalloti, & DeLuca, 2009; Sepulcre et al, 2009). Perhaps more directly related to the current sample, increased cognitive reserve mitigates the adverse effect of white matter hyperintensities on cognitive function in a sample of neurologically healthy older adults (Brickman et al, 2009).…”

Section: Discussionsupporting

confidence: 65%

Cognitive reserve moderates the association between heart failure and cognitive impairment

Alosco

Spitznagel

Raz

et al. 2012

Journal of Clinical and Experimental Neuropsychology

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Background Cognitive impairment in persons with heart failure is common. Theories of cognitive reserve suggest that premorbid factors, such as intellectual ability, may provide a buffer against cognitive impairment due to neuropathological insult. No study has examined the influence of cognitive reserve on cognitive functioning in older adults with heart failure. Aim This study examined whether cognitive reserve moderates the relationship between heart failure severity and cognitive function. Methods A total of 157 persons with heart failure (69.26 ± 9.26 years; 39% female) completed neuropsychological testing and a brief fitness assessment. Cognitive reserve was operationalized using estimated premorbid intellect on American National Adult Reading Test (AMNART). Results A moderation analysis was performed using a hierarchical regression models for each cognitive domain. An interaction term between the AMNART and 2-minute step test was created and entered into the final block of the model, with demographic, psychosocial, and heart failure severity entered in the previous blocks. The interaction term was significant for attention (t(155) = −2.54, p = .012), executive function (t(155) = −3.30, p = .001), and language (t(155) = −2.83, p = .005) domains. Conclusion The current findings suggest that cognitive reserve moderates the association between heart failure severity and cognitive function in multiple cognitive domains. Further work is needed to clarify the mechanisms by which cognitive reserve attenuates cognitive impairment in this population.

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“…Other observations that may support an association between WML and brain atrophy have come from studies in other neurological conditions, such as CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy), multiple sclerosis [84], amyotrophic lateral sclerosis [85], and HIV [86]. Of these conditions, CADASIL is of particular interest, because the WML in that condition are also presumed to be due to vascular disease [87].…”

Section: Discussionmentioning

confidence: 99%

White Matter Lesions and Brain Atrophy: More than Shared Risk Factors? A Systematic Review

Appelman¹,

et al. 2009

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Background: White matter lesions (WML) and brain atrophy are often found on MRI in the elderly. Shared vascular risk factors may be an explanation for their concomitance. However, disturbances of white matter integrity could also be involved in the pathogenesis of brain atrophy. Our objective was to systematically review studies that investigated the relation between WML and brain atrophy on MRI, and to investigate whether there is sufficient evidence to indicate that this relation is independent of shared risk factors. Methods: We searched PubMed for studies published in English between 1980 and October 2007, combining search terms for WML and brain atrophy. Articles that studied the relation between WML and brain atrophy were included if they met the following criteria: (1) original study, (2) MRI used for imaging, (3) assessment methods for WML and brain atrophy specified, and (4) a sample size of at least 20 participants. We recorded type and age of the study population, type and assessment of WML and brain atrophy, and variables for which adjustments were made in the analyses. Results: We identified 48 studies that met our inclusion criteria. A significant relation between WML and brain atrophy was found in 37 out of 48 studies. The source of the study population (e.g. clinic or population based) did not affect this relation. However, only 10 studies adjusted for shared risk factors, of which 9 found an association. Conclusions: The majority of studies found an association between WML and brain atrophy, but it is not yet clear if this association is independent of shared risk factors.

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Contribution of White Matter Lesions to Gray Matter Atrophy in Multiple Sclerosis

Cited by 98 publications

References 35 publications

Regional Gray Matter Atrophy Coexistent with Occipital Periventricular White Matter Hyper Intensities

Regional Gray Matter Atrophy Coexistent with Occipital Periventricular White Matter Hyper Intensities

Cognitive reserve moderates the association between heart failure and cognitive impairment

White Matter Lesions and Brain Atrophy: More than Shared Risk Factors? A Systematic Review

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