Dataset Information

Reduced coupling between the global blood-oxygen-level-dependent signal and cerebrospinal fluid inflow is associated with the severity of small vessel disease.

ABSTRACT:

Background

Small vessel disease (SVD) is highly prevalent in the elderly and associated with an increased risk of dementia and stroke. SVD may have disturbed cerebrospinal fluid (CSF) flow, which can compromise waste clearance and accelerate disease progression.

Methods

We retrospectively included 146 SVD patients from a prospectively collected dataset, with one- or two-year follow-up data in 61 patients. The coupling strength between the global blood-oxygen-level-dependent (gBOLD) signal and CSF inflow was used to reflect CSF dynamics. We performed regression analyses to investigate the association between the gBOLD-CSF coupling index and the severity of SVD and vascular risk factors. Longitudinal analysis was carried out to investigate causal relationships.

Results

Patients with severe SVD had significantly decreased gBOLD-CSF coupling (β = -0.180, p = 0.032). Dilation of perivascular spaces in the basal ganglia area (β = -0.172, p = 0.033) and diabetes (β = -0.204, p = 0.014) were associated with reduced gBOLD-CSF coupling. In longitudinal analyses, diabetes was associated with faster decline in gBOLD-CSF coupling (β = 0.20, p = 0.039), while perivascular space (PVS) dilation in the centrum semiovale showed a opposite relationship (β = -0.20, p = 0.041). The gBOLD-CSF coupling could not predict SVD progression.

Conclusion

Altered CSF flow is associated with the severity of SVD.

SUBMITTER: Zhang Y

PROVIDER: S-EPMC9668594 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature

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Publications

Reduced coupling between the global blood-oxygen-level-dependent signal and cerebrospinal fluid inflow is associated with the severity of small vessel disease.

Zhang Yao Y Zhang Ruiting R Wang Shuyue S Hong Hui H Jiaerken Yeerfan Y Li Kaicheng K Zeng Qingze Q Luo Xiao X Yu Xinfeng X Zhang Minming M Huang Peiyu P

NeuroImage. Clinical 20221012

<h4>Background</h4>Small vessel disease (SVD) is highly prevalent in the elderly and associated with an increased risk of dementia and stroke. SVD may have disturbed cerebrospinal fluid (CSF) flow, which can compromise waste clearance and accelerate disease progression.<h4>Methods</h4>We retrospectively included 146 SVD patients from a prospectively collected dataset, with one- or two-year follow-up data in 61 patients. The coupling strength between the global blood-oxygen-level-dependent (gBOLD ...[more]

PMID: 36252555

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Project description:The identification of molecular biomarkers in CSF from individuals affected by Huntington disease may help improve predictions of disease onset, better define disease progression and could facilitate the evaluation of potential therapies. The primary objective of our study was to investigate novel CSF protein candidates and replicate previously reported protein biomarker changes in CSF from Huntington disease mutation carriers and healthy controls. Our secondary objective was to compare the discriminatory potential of individual protein analytes and combinations of CSF protein markers for stratifying individuals based on the severity of Huntington disease. We conducted a hypothesis-driven analysis of 26 pre-specified protein analytes in CSF from 16 manifest Huntington disease subjects, eight premanifest Huntington disease mutation carriers and eight healthy control individuals using parallel-reaction monitoring mass spectrometry. In addition to reproducing reported changes in previously investigated CSF biomarkers (NEFL, PDYN, and PENK), we also identified novel exploratory CSF proteins (C1QB, CNR1, GNAL, IDO1, IGF2, and PPP1R1B) whose levels were altered in Huntington disease mutation carriers and/or across stages of disease. Moreover, we report strong associations of select CSF proteins with clinical measures of disease severity in manifest Huntington disease subjects (C1QB, CNR1, NEFL, PDYN, PPP1R1B, and TTR) and with years to predicted disease onset in premanifest Huntington disease mutation carriers (ALB, C4B, CTSD, IGHG1, and TTR). Using receiver operating characteristic curve analysis, we identified PENK as being the most discriminant CSF protein for stratifying Huntington disease mutation carriers from controls. We also identified exploratory multi-marker CSF protein panels that improved discrimination of premanifest Huntington disease mutation carriers from controls (PENK, ALB and NEFL), early/mid-stage Huntington disease from premanifest mutation carriers (PPP1R1B, TTR, CHI3L1, and CTSD), and late-stage from early/mid-stage Huntington disease (CNR1, PPP1R1B, BDNF, APOE, and IGHG1) compared with individual CSF proteins. In this study, we demonstrate that combinations of CSF proteins can outperform individual markers for stratifying individuals based on Huntington disease mutation status and disease severity. Moreover, we define exploratory multi-marker CSF protein panels that, if validated, may be used to improve the accuracy of disease-onset predictions, complement existing clinical and imaging biomarkers for monitoring the severity of Huntington disease, and potentially for assessing therapeutic response in clinical trials. Additional studies with CSF collected from larger cohorts of Huntington disease mutation carriers are needed to replicate these exploratory findings.

Dataset Information

Reduced coupling between the global blood-oxygen-level-dependent signal and cerebrospinal fluid inflow is associated with the severity of small vessel disease.

Background

Methods

Results

Conclusion

Publications

Reduced coupling between the global blood-oxygen-level-dependent signal and cerebrospinal fluid inflow is associated with the severity of small vessel disease.

Similar Datasets

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