Association of Cerebral Microbleeds with Cognitive Decline: A Longitudinal Study

Li, Lin; Wu, Danhong; Li, Hongqi; Tan, Lin; Xu, Wei; Dong, Qiang; Tan, Lan; Yu, Jin‐Tai; Initiative, Alzheimer’s Disease Neuroimaging

doi:10.3233/jad-191257

Cited by 24 publications

(16 citation statements)

References 31 publications

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“…The effect of cerebrovascular disease on cognition may be modulated by carriage of the APOE ε4 allele, which has far‐reaching effects via numerous Aβ‐dependent and independent pathways. Some studies reported APOE ε4‐independent associations between vascular disease and AD biomarkers 90,96 and/or cognitive decline 90,101 . However, in a study conducted in the Sunnybrook Dementia Cohort and replicated in ADNI, 102 greater WMH volume was associated with worse attention/executive functions and language in APOE ε4 carriers but not non‐carriers across the spectrum of AD and dementia with Lewy bodies.…”

Section: Beyond At(n): Other Influences On Disease Progressionmentioning

confidence: 99%

“…Some studies reported APOE ε 4-independent associations between vascular disease and AD biomarkers 90 , 96 and/or cognitive decline. 90 , 101 However, in a study conducted in the Sunnybrook Dementia Cohort and replicated in ADNI, 102 greater WMH volume was associated with worse attention/executive functions and language in APOE ε 4 carriers but not non-carriers across the spectrum of AD and dementia with Lewy bodies. Neuropathological assessment revealed that 100% of APOE ε 4 homozygotes but only 64% of heterozygotes had cerebral amyloid angiopathy, suggesting that accumulation of A β in the cerebral vasculature may be the etiology for WMH in APOE ε 4 carriers.…”

Section: Beyond At(n): Other Influences On Disease Progressionmentioning

confidence: 99%

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Using the Alzheimer's Disease Neuroimaging Initiative to improve early detection, diagnosis, and treatment of Alzheimer's disease

Veitch

Weiner

Aisen

et al. 2021

Alzheimer's & Dementia

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Introduction: The Alzheimer's Disease Neuroimaging Initiative (ADNI) has accumulated 15 years of clinical, neuroimaging, cognitive, biofluid biomarker and genetic data, and biofluid samples available to researchers, resulting in more than 3500 publications. This review covers studies from 2018 to 2020. Methods:We identified 1442 publications using ADNI data by conventional search methods and selected impactful studies for inclusion.Results: Disease progression studies supported pivotal roles for regional amyloid beta (Aβ) and tau deposition, and identified underlying genetic contributions to Alzheimer's disease (AD). Vascular disease, immune response, inflammation, resilience, and sex modulated disease course. Biologically coherent subgroups were identified at all clinical stages. Practical algorithms and methodological changes improved determination of Aβ status. Plasma Aβ, phosphorylated tau181, and neurofilament light were promising noninvasive biomarkers. Prognostic and diagnostic models were externally validated in ADNI but studies are limited by lack of ethnocultural cohort diversity.

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Section: Beyond At(n): Other Influences On Disease Progressionmentioning

confidence: 99%

Section: Beyond At(n): Other Influences On Disease Progressionmentioning

confidence: 99%

Using the Alzheimer's Disease Neuroimaging Initiative to improve early detection, diagnosis, and treatment of Alzheimer's disease

Veitch

Weiner

Aisen

et al. 2021

Alzheimer's & Dementia

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“…The prevalence of CMBs is significantly higher in the elderly population with multiple comorbidities and high-total cardiovascular risk, especially hypertension with subsequent hypertensive arteriopathy (13,14). Usually, CMBs are clinically silent in the terms of acute stroke care but might have a cumulative impact on patients in the following years, mainly because of the associations between the load of CMBs and cognitive impairment (15)(16)(17)(18)(19)(20).…”

Section: Introductionmentioning

confidence: 99%

New Remote Cerebral Microbleeds on T2*-Weighted Echo Planar MRI After Intravenous Thrombolysis for Acute Ischemic Stroke

et al. 2022

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BackgroundThe main and well-defined complication of intravenous administration of recombinant tissue plasminogen activator (tPA) in patients with acute ischemic stroke (AIS) is symptomatic intracranial hemorrhage (sICH). However, rtPA might also be connected with the formation of cerebral microbleeds (CMBs), located remotely from the ischemic lesions, that may remain clinically silent. This association might be important because the load of CMBs has been associated with cognitive impairment. We investigated whether administration of rtPA in AIS results in the appearance of new CMBs and if the initial load of CMBs is associated with hemorrhagic transformation.MethodsA total of fifty-nine consecutive patients with AIS treated with rtPA underwent MRI including T2*-weighted Echo Planar Imaging (T2*-EPI) shortly before and 7–9 days after rtPA administration. We calculated the load of new CMBs located outside the MR diffusion restriction area in the follow-up imaging and assessed hemorrhagic transformation with ECASS-II scoring.ResultsA total of forty-nine patients were included for the final analysis. On initial T2*-EPI-GRE, 37 baseline microbleeds (CMBs) were observed in 14 patients (28.6%). On follow-up T2*-EPI-GRE amount of CMBs increased to a total number of 103. New CMBs were found in 5 (14.3%) of 35 patients without and in 9 (64.3%) of 14 with any baseline CMBs. Multiple logistic regression analysis indicated that presence of baseline CMBs (risk ratio [RR] 5.95, 95% CI 2.69–13.20, p < 0.001) and lower platelets level (risk ratio [RR] 0.992, 95% CI 0.986–0.998, p = 0.007) were independently associated with new CMBs. The baseline load of CMBs was not associated with the risk of hemorrhagic transformation.ConclusionIn this study, new CMBs were found in nearly 30% of patients with AIS on the 7–9 days after rtPA treatment. Baseline CMBs correlated with a higher risk of new CMBs appearing after the rtPA treatment, independently of other factors. At the same time, in our sample, baseline CMBs did not correlate with an increased risk of hemorrhagic transformation. Since the associations between the CMBs load and cognitive impairment have already been proved, further studies are warranted to investigate possible associations between the thrombolytic treatment of patients with AIS, mainly those with baseline CMBs, and the risk of earlier cognitive decline.

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“…CC-BY 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. (which was not certified by peer review) 14), but associations between PVS and poorer cognitive ability, either cross-sectionally or longitudinally, are more variable (12). In recent years, several studies have quantified the 'total brain burden' of SVD using a simple 0-4 score, which allocates one point for the presence of each SVD marker (15)(16)(17)(18).…”

Section: Introductionmentioning

confidence: 99%

“…Similarly, the presence of lacunes and microbleeds have been associated with cognitive decline (12)(13)(14), but associations between PVS and poorer cognitive ability, either cross-sectionally or longitudinally, are more variable (12). In recent years, several studies have quantified the 'total brain burden' of SVD using a simple 0-4 score, which allocates one point for the presence of each SVD marker (15)(16)(17)(18).…”

Section: Introductionmentioning

confidence: 99%

Cerebral Small Vessel Disease Burden and Longitudinal Cognitive Decline from age 73 to 82: the Lothian Birth Cohort 1936

Hamilton

Cox

Okely

et al. 2021

Preprint

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Slowed processing speed is considered a hallmark feature of cognitive decline in cerebral small vessel disease (SVD), however, it is unclear whether SVDs association with slowed processing might be due to its association with overall declining general cognitive ability. We quantified the total MRI-visible SVD burden of 540 members of the Lothian Birth Cohort 1936 (age:72.6±0.7 years; 47% female). Using latent growth curve modelling, we tested associations between total SVD burden at mean age 73 and changes in general cognitive ability, processing speed, verbal memory, and visuospatial ability, measured at age 73, 76, 79 and 82. Covariates included age, sex, vascular risk, and childhood cognitive ability. In the fully-adjusted models, greater SVD burden was associated with greater declines in general cognitive ability (standardised β: -0.201; 95%CI: [-0.36, -0.04]; pFDR=0.022) and processing speed (-0.222; [-0.40, -0.04]; pFDR=0.022). SVD burden accounted for between 4 and 5% of variance in declines of general cognitive ability and processing speed. After accounting for the covariance between tests of processing speed and general cognitive ability, only SVDs association with greater decline in general cognitive ability remained significant, prior to FDR correction (-0.222; [-0.39, -0.06]; p=0.008; pFDR=0.085). Our findings do not support the notion that SVD has a specific association with declining processing speed, independent of decline in general cognitive ability (which captures the variance shared across domains of cognitive ability). The association between SVD burden and declining general cognitive ability supports the notion of SVD as a diffuse, whole-brain disease and suggests that trials monitoring SVD-related cognitive changes should consider domain-specific changes in the context of overall, general cognitive decline.

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Association of Cerebral Microbleeds with Cognitive Decline: A Longitudinal Study

Cited by 24 publications

References 31 publications

Using the Alzheimer's Disease Neuroimaging Initiative to improve early detection, diagnosis, and treatment of Alzheimer's disease

Using the Alzheimer's Disease Neuroimaging Initiative to improve early detection, diagnosis, and treatment of Alzheimer's disease

New Remote Cerebral Microbleeds on T2*-Weighted Echo Planar MRI After Intravenous Thrombolysis for Acute Ischemic Stroke

Cerebral Small Vessel Disease Burden and Longitudinal Cognitive Decline from age 73 to 82: the Lothian Birth Cohort 1936

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