Increased Diameters of the Internal Cerebral Veins and the Basal Veins of Rosenthal Are Associated with White Matter Hyperintensity Volume

Houck, Alexander L.; Gutierrez, José; Gao, Fuqiang; Igwe, Kay C.; Colón, Juliet M.; Black, Sandra E.; Brickman, Adam M.

doi:10.3174/ajnr.a6213

Cited by 16 publications

(22 citation statements)

References 37 publications

(39 reference statements)

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“…Overall, significant collagenosis and stenosis of the venous system, in particular in the deep medullary veins, occurred in AD patients [47]. In combination with the results described by Moody and colleagues, these data indicate that venous collagenosis is enhanced by both age and AD-related pathology, such as white matter hyperintensities, and can impair cerebrovascular structure, cause venous insufficiency, increase fluid leakage/vasogenic edema, and occlude blood flow [30,46,47,52,54,55,[75][76][77].…”

Section: Venous Collagenosissupporting

confidence: 51%

Potential Role of Venular Amyloid in Alzheimer’s Disease Pathogenesis

Morrone

Bishay

McLaurin

2020

IJMS

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Insurmountable evidence has demonstrated a strong association between Alzheimer’s disease (AD) and cerebral amyloid angiopathy (CAA), along with various other cerebrovascular diseases. One form of CAA, which is the accumulation of amyloid-beta peptides (Aβ) along cerebral vessel walls, impairs perivascular drainage pathways and contributes to cerebrovascular dysfunction in AD. To date, CAA research has been primarily focused on arterial Aβ, while the accumulation of Aβ in veins and venules were to a lesser extent. In this review, we describe preclinical models and clinical studies supporting the presence of venular amyloid and potential downstream pathological mechanisms that affect the cerebrovasculature in AD. Venous collagenosis, impaired cerebrovascular pulsatility, and enlarged perivascular spaces are exacerbated by venular amyloid and increase Aβ deposition, potentially through impaired perivascular clearance. Gaining a comprehensive understanding of the mechanisms involved in venular Aβ deposition and associated pathologies will give insight to how CAA contributes to AD and its association with AD-related cerebrovascular disease. Lastly, we suggest that special consideration should be made to develop Aβ-targeted therapeutics that remove vascular amyloid and address cerebrovascular dysfunction in AD.

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Section: Venous Collagenosissupporting

confidence: 51%

Potential Role of Venular Amyloid in Alzheimer’s Disease Pathogenesis

Morrone

Bishay

McLaurin

2020

IJMS

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“…Recently, Houck et al. 28 discovered that increased diameters of the internal cerebral veins and the basal veins of Rosenthal were associated with WMH volume in elderly people, indicating the drainage relationship between cortical venous and white matter. However, due to lack of histologic evidence, the association between cortical venous disruption and white matter damage still needs further investigation.…”

Section: Discussionmentioning

confidence: 99%

Venous disruption affects white matter integrity through increased interstitial fluid in cerebral small vessel disease

Zhang

Huang

Jiaerken

et al. 2020

J Cereb Blood Flow Metab

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Deep medullary veins (DMVs) participate in the drainage of surrounding white matter. In cerebral small vessel disease (CSVD), disrupted DMVs were often observed together with damaged white matter, but the phenomenon lacked validation and explanation. We hypothesized that venous disruption might cause white matter damage through increased interstitial fluid resulting from hemodynamic alteration, and we designed a comprehensive multi-modality MRI study to testify our hypothesis. Susceptibility-weighted imaging was used to investigate the characteristics of DMVs and derive DMVs scores. Free water elimination diffusion tensor imaging model was used to analyze interstitial fluid fraction (fraction of free water, fFW) and white matter integrity (tissue fractional anisotropy, FAt). Totally, 104 CSVD patients were included. Total DMVs score was associated with FAt of DMVs drainage area. The effect of total DMVs score on FAt was mediated by fFW, after controlling for age, sex, hypertension, regional cerebral blood flow and lacune numbers. The relationships between DMVs score, fFW and FAt were also significant in most DMVs drainage subregions. Therefore, we discovered the DMVs disruption – increased interstitial fluid – white matter damage link in CSVD patients, which was independent of arterial perfusion variations.

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“…There is some evidence to suggest venous collagenosis may be associated with WMH [40,41]. The pathophysiology behind this finding is unknown, but one suggestion is that venous collagenosis is secondary to arterial disease [42]. Increased pulsatility could be a link between arterial and venous disease as kinetic energy may be transferred from arteries to veins by way of capillaries and/or CSF, and increased venous pulsatility has been tied to increasing WMH [16].…”

Section: Discussionmentioning

confidence: 99%

Cerebral arterial pulsatility is associated with features of small vessel disease in patients with acute stroke and TIA: a 4D flow MRI study

et al. 2019

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Cerebral small vessel disease (SVD) is a major cause of stroke and cognitive impairment. However, the underlying mechanisms behind SVD are still poorly understood. High cerebral arterial pulsatility has been suggested as a possible cause of SVD. In population studies, arterial pulsatility has been linked to white matter hyperintensities (WMH), cerebral atrophy, and cognitive impairment, all features of SVD. In stroke, pulsatility data are scarce and contradictory. The aim of this study was to investigate the relationship between arterial pulsatility and SVD in stroke patients. With a cross-sectional design, 89 patients with acute ischemic stroke or TIA were examined with MRI. A neuropsychological assessment was performed 1 year later. Using 4D flow MRI, pulsatile indices (PI) were calculated for the internal carotid artery (ICA) and middle cerebral artery (M1, M3). Flow volume pulsatility (FVP), a measure corresponding to the cyclic expansion of the arterial tree, was calculated for the same locations. These parameters were assessed for associations with WMH volume, brain volume and cognitive function. ICA-FVP was associated with WMH volume (β = 1.67, 95% CI: [0.1, 3.24], p = 0.037). M1-PI and M1-FVP were associated with decreasing cognitive function (β = − 4.4, 95% CI: [− 7.7, − 1.1], p = 0.009 and β = − 13.15, 95% CI: [− 24.26, − 2.04], p = 0.02 respectively). In summary, this supports an association between arterial pulsatility and SVD in stroke patients, and provides a potential target for further research and preventative treatment. FVP may become a useful biomarker for assessing pulsatile stress with PCMRI and 4D flow MRI.

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Increased Diameters of the Internal Cerebral Veins and the Basal Veins of Rosenthal Are Associated with White Matter Hyperintensity Volume

Cited by 16 publications

References 37 publications

Potential Role of Venular Amyloid in Alzheimer’s Disease Pathogenesis

Potential Role of Venular Amyloid in Alzheimer’s Disease Pathogenesis

Venous disruption affects white matter integrity through increased interstitial fluid in cerebral small vessel disease

Cerebral arterial pulsatility is associated with features of small vessel disease in patients with acute stroke and TIA: a 4D flow MRI study

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