scholarly journals Correlation of Brain Perfusion with White Matter Hyperintensity, Brain Atrophy, and Cognition in Patients with Posterior Cerebral Artery Stenosis and Subjective Cognitive Decline

2018 ◽  
Vol 24 ◽  
pp. 5729-5738
Author(s):  
Meng Liu ◽  
Zhi-Yu Nie ◽  
Ren-Ren Li ◽  
Wei Zhang ◽  
Hui Wang ◽  
...  
Keyword(s):  
White Matter ◽  
Cognitive Decline ◽  
Cerebral Artery ◽  
Brain Atrophy ◽  
Posterior Cerebral Artery ◽  
Brain Perfusion ◽  
Artery Stenosis ◽  
White Matter Hyperintensity ◽  
Subjective Cognitive Decline

scholarly journals White matter hyperintensities may be an early marker for age-related cognitive decline in the ADNI cohort

2021 ◽  
Author(s):  
Cassandra Morrison ◽  
Mahsa Dadar ◽  
Sylvia Villeneuve ◽  
D. Louis Collins
Keyword(s):  
White Matter ◽  
Cognitive Decline ◽  
White Matter Hyperintensities ◽  
White Matter Hyperintensity ◽  
Subjective Cognitive Decline ◽  
Age Related ◽  
Lower Baseline ◽  
Age Related Cognitive Decline ◽  
Linear Regressions

Background: Previous research suggests that white matter hyperintensities, amyloid, and tau contribute to age-related cognitive decline. It remains unknown as to how these factors relate to one another and how they jointly contribute to cognitive decline in normal aging. This project examines the association between these pathologies and their relationship to cognitive decline. Methods: Cognitively normal older adult data from the Alzheimers Disease Neuroimaging Initiative were examined. Participants were included if they had no subjective cognitive decline, had baseline white matter hyperintensity, CSF AB42/40, CSF pTau181, and cognitive scores. Of the 102 participants included, only 79 had follow-up cognitive scores. Linear regressions examined the influence of white matter hyperintensities, amyloid, and tau on baseline and follow-up cognitive scores. Linear regressions also examined the association of amyloid and tau on white matter hyperintensities and between tau and amyloid. Results: Increased white matter hyperintensity load was associated with lower baseline memory (B= -0.20, p =.046), follow-up executive functioning (B= -0.32, p<.001), and follow-up ADAS-13 (B=2.69, p<.001) scores. White matter hyperintensities were not related to pTau or AB42/40. Lower AB42/40 was associated with increased pTau (p=.025). pTau was not associated with decline in any cognitive score. Lower AB42/40 was associated with lower baseline (p=.015) but not follow-up executive function. Discussion: White matter hyperintensities may be one of the earliest pathologies observed in healthy older adults that contribute to cognitive decline. The inclusion of white matter hyperintensities as an additional marker for early cognitive decline may improve our current understanding of age-related changes.

scholarly journals Subjective Cognitive Decline Is Associated with Greater White Matter Hyperintensity Volume

2018 ◽  
Vol 66 (3) ◽  
pp. 1283-1294 ◽  
Author(s):  
Sanneke van Rooden ◽  
Annette A. van den Berg-Huysmans ◽  
Pauline H. Croll ◽  
Gerda Labadie ◽  
Jessica M. Hayes ◽  
...  
Keyword(s):  
White Matter ◽  
Cognitive Decline ◽  
White Matter Hyperintensity ◽  
Subjective Cognitive Decline

A-4 Amyloid Status Modifies the Association between Subjective Cognitive Decline and Brain MRI Metrics

2021 ◽  
Vol 36 (6) ◽  
pp. 1025-1025
Author(s):  
Marilyn J Steinbach ◽  
Omair A Khan ◽  
Dandan Liu ◽  
Camdyn Gilbert ◽  
Natalie Thwaites ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
White Matter ◽  
Cerebrovascular Disease ◽  
Cognitive Decline ◽  
Brain Mri ◽  
Ventricular Volume ◽  
White Matter Hyperintensity ◽  
Subjective Cognitive Decline ◽  
The Impact

Abstract Objective Subjective cognitive decline (SCD), a potential precursor to Alzheimer’s disease (ad), has been associated with increased neurodegeneration and cerebrovascular disease longitudinally. However, the impact of amyloid status, an early pathological marker of Alzheimer’s disease (ad) on these longitudinal associations is less clear. Here, we related baseline SCD to longitudinal biomarkers of brain health in the context of amyloid status. Method Participants included 139 non-demented older adults (72 ± 7 years) from the Vanderbilt Memory & Aging Project who completed a SCD questionnaire and fasting lumbar-puncture to quantify amyloid status (defined using published cutoffs of amyloid-beta42 levels) at baseline. 3 T brain-MRI to measure gray and white matter hyperintensity (WMH) volumes was collected at baseline, 18-months, 3-years, and 5-years. Linear mixed effects models assessed if baseline SCD X amyloid status was associated with longitudinal total and lobar grey and white matter volumes, covarying for baseline age, sex, race/ethnicity, education, diagnosis, mood, and apolipoprotein-Ee4 status. Models were also stratified by baseline amyloid status. Results Baseline SCD score and amyloid status interacted with total gray (p = 0.02) and WMH volume (p &lt; 0.05). In stratified models, higher total SCD predicted increased inferior lateral ventricular volume (p &lt; 0.001) among amyloid positive individuals. Conversely, in amyloid negative, greater baseline SCD was associated with increased WMH volumes globally (p = 0.03) and in the frontal and parietal lobes (p-values &lt;0.035). Conclusion In the presence of amyloid, the presence of SCD is predictive of neurodegeneration in ad-specific regions. Conversely, SCD without amyloidosis may reflect a cerebrovascular disease, indicated by WMHs. Results highlight how amyloid status may help delineate etiologies of SCD.

scholarly journals The Effects of Longitudinal White Matter Hyperintensity Change on Cognitive Decline and Cortical Thinning over Three Years

2020 ◽  
Vol 9 (8) ◽  
pp. 2663
Author(s):  
Seung Joo Kim ◽  
Dong Kyun Lee ◽  
Young Kyoung Jang ◽  
Hyemin Jang ◽  
Si Eun Kim ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
White Matter ◽  
Cognitive Decline ◽  
Dynamic Change ◽  
Surrogate Marker ◽  
Brain Magnetic Resonance Imaging ◽  
Longitudinal Change ◽  
White Matter Hyperintensity ◽  
Cortical Thinning ◽  
Automated Method

White matter hyperintensity (WMH) has been recognised as a surrogate marker of small vessel disease and is associated with cognitive impairment. We investigated the dynamic change in WMH in patients with severe WMH at baseline, and the effects of longitudinal change of WMH volume on cognitive decline and cortical thinning. Eighty-seven patients with subcortical vascular mild cognitive impairment were prospectively recruited from a single referral centre. All of the patients were followed up with annual neuropsychological tests and 3T brain magnetic resonance imaging. The WMH volume was quantified using an automated method and the cortical thickness was measured using surface-based methods. Participants were classified into WMH progression and WMH regression groups based on the delta WMH volume between the baseline and the last follow-up. To investigate the effects of longitudinal change in WMH volume on cognitive decline and cortical thinning, a linear mixed effects model was used. Seventy patients showed WMH progression and 17 showed WMH regression over a three-year period. The WMH progression group showed more rapid cortical thinning in widespread regions compared with the WMH regression group. However, the rate of cognitive decline in language, visuospatial function, memory and executive function, and general cognitive function was not different between the two groups. The results of this study indicated that WMH volume changes are dynamic and WMH progression is associated with more rapid cortical thinning.

Abstract TP181: Serum Eiocosapentaenoic Acids Is Protective Against White Matter Lesions

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Daiki Takano ◽  
Takashi Yamazaki ◽  
Tetsuya Maeda ◽  
Yuichi Satoh ◽  
Yasuko Ikeda ◽  
...  
Keyword(s):  
White Matter ◽  
Cognitive Decline ◽  
White Matter Hyperintensities ◽  
Small Vessel Disease ◽  
White Matter Lesions ◽  
White Matter Hyperintensity ◽  
Partial Regression Coefficient ◽  
The Relationship ◽  
Total Pufa ◽  
Periventricular Hyperintensity

[Introduction] White matter hyperintensities (WMH) are considered manifestation of arteriosclerotic small vessel disease and WMH burden increases risk of ischemic stroke and cognitive decline. There are only a few evidences concerning the relationship between polyunsaturated fatty acids (PUFA) and WMH. The present study was designed to elucidate the association between WMH and PUFA profile including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) and arachidonic acid (AA) in patients with Alzheimer’s disease (AD). [Methods] The present study was based on 119 patients who were diagnosed as having a probable AD according to the NINCDS-ADRDA criteria. Their mean age was 78.3 years old. All subjects underwent neuropsychological evaluation including mini mental state exam (MMSE) and 1.5-Tesla MRI. Fasting blood samples were also collected for the PUFA measurements. We measured the ratio of serum EPA, DHA and AA concentration to the total PUFA concentration. The WMH were evaluated on T2-weight images and classified into periventricular hyperintensity (PVH) and deep white matter hyperintensity (DWMH). The severity of WMH was graded 5 categories. We investigated the relationship between WMH and PUFA profiles. [Results] The EPA ratio correlated negatively with both PVH (rs=-0.2036, p=0.0264) and DWMH grade (rs=-0.3155, p=0.0005). It remained still significant after adjustment for age, sex, statins use, antithrombotics use, mean blood pressure and presence of hypertension (standardized partial regression coefficient(β)=-0.2516, p=0.0122 for PVH, β=-0.3598, p=0.0001 for DWMH). Neither DHA nor AA ratio correlated with DWMH or PVH grade. The EPA ratio but not DHA or AA ratio correlated positively with total MMSE score (rs=0.2310, p=0.0115). [Conclusions] Our data revealed that the serum EPA was protective against WMH as well as cognitive decline in AD patients. Pathophysiology underlying WMH is complex and the possible mechanisms involved in the pathogenesis of WMH encompass incomplete brain ischemia, increased permeability of blood-brain barrier, and inflammation responses. The relationship between serum EPA and WMH can be partly explained by those anti-ischemic and anti-arteriosclerotic effects of EPA.

Five-year follow-up of stenting for a symptomatic posterior cerebral artery stenosis

2011 ◽  
Vol 59 (3) ◽  
pp. 405
Author(s):  
Kangning Chen ◽  
Wei Chen ◽  
Jun Hu ◽  
Xiaofei Zhang ◽  
Shugui Shi
Keyword(s):  
Cerebral Artery ◽  
Posterior Cerebral Artery ◽  
Artery Stenosis

scholarly journals White matter hyperintensity increases are a feature of familial AD and are associated with increased brain atrophy

2020 ◽  
Vol 16 (S4) ◽  
Author(s):  
Phoebe Walsh ◽  
Carole H. Sudre ◽  
Emily N. Manning ◽  
Cassidy M. Fiford ◽  
Thomas Veale ◽  
...  
Keyword(s):  
White Matter ◽  
Brain Atrophy ◽  
White Matter Hyperintensity

scholarly journals White matter hyperintensities are common in midlife and already associated with cognitive decline

2019 ◽  
Vol 1 (1) ◽  
Author(s):  
Tracy d’Arbeloff ◽  
Maxwell L Elliott ◽  
Annchen R Knodt ◽  
Tracy R Melzer ◽  
Ross Keenan ◽  
...  
Keyword(s):  
White Matter ◽  
Cognitive Decline ◽  
White Matter Hyperintensities ◽  
Clinical Symptoms ◽  
White Matter Hyperintensity ◽  
Dementia Prevention ◽  
Increased Risk ◽  
Weighted Magnetic Resonance Imaging ◽  
Intervention Trials ◽  
The Brain

Abstract White matter hyperintensities proliferate as the brain ages and are associated with increased risk for cognitive decline as well as Alzheimer’s disease and related dementias. As such, white matter hyperintensities have been targeted as a surrogate biomarker in intervention trials with older adults. However, it is unclear at what stage of aging white matter hyperintensities begin to relate to cognition and if they may be a viable target for early prevention. In the Dunedin Study, a population-representative cohort followed since birth, we measured white matter hyperintensities in 843 45-year-old participants using T2-weighted magnetic resonance imaging and we assessed cognitive decline from childhood to midlife. We found that white matter hyperintensities were common at age 45 and that white matter hyperintensity volume was modestly associated with both lower childhood (ß = −0.08, P = 0.013) and adult IQ (ß=−0.15, P &lt; 0.001). Moreover, white matter hyperintensity volume was associated with greater cognitive decline from childhood to midlife (ß=−0.09, P &lt; 0.001). Our results demonstrate that a link between white matter hyperintensities and early signs of cognitive decline is detectable decades before clinical symptoms of dementia emerge. Thus, white matter hyperintensities may be a useful surrogate biomarker for identifying individuals in midlife at risk for future accelerated cognitive decline and selecting participants for dementia prevention trials.

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