Correction: Tian et al. The Underlying Role of the Glymphatic System and Meningeal Lymphatic Vessels in Cerebral Small Vessel Disease. Biomolecules 2022, 12, 748

Tian, Yu; Zhao, Mingxia; Chen, Yiyi; Yang, Mo; Wang, Yilong

doi:10.3390/biom13040705

Cited by 5 publications

(2 citation statements)

References 1 publication

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“…Such impairment impedes the clearance of neurotoxic substances. 31 Subsequently, neuroinflammation, myelin damage, and neurodegeneration occur, leading to clinical symptoms. The evolution of these pathological processes may go through a decade-long subclinical phase before clinical symptoms arise.…”

Section: Vascular Etiologies and Pathophysiology Of Vci Ischemic And ...mentioning

confidence: 99%

“…Compromised neurovascular units, BBB integrity, and glymphatic system are causative in triggering amyloid/tau accumulation (eg, increased production and reduced clearance of amyloid) and the subsequent pathological cascades of AD. 31,[35][36][37] This causative role of cSVD is not only evident in the early development of late-onset AD but also in familial young onset autosomal dominant AD and in APOE ε4 carriers. 38,39 Clinical observational study using amyloid PET imaging showed that the number of midlife vascular risk factors (eg, hypertension, diabetes, hypercholesterolemia, obesity, smoking) was associated with increased amyloid deposition.…”

Section: Vascular Etiologies and Pathophysiology Of Vci Ischemic And ...mentioning

confidence: 99%

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Current and Future Treatments of Vascular Cognitive Impairment

Ip,

Ko,

Lam

et al. 2024

Stroke

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Nonamyloid sporadic cSVD is considered the most prevalent cause or pathological substrate of VCI. 20,21 It refers to diseased microscopic perforating cerebral arterioles, capillaries, and venules giving rise to abnormalities in the cerebral white and deep gray matter. 5 Driven by arteriosclerosis and fibrinoid necrosis, the arteriolar wall can be stenosed, occluded, dilated, or ruptured, which may result in lacunar infarcts or deep microparenchymal/macroparenchymal hemorrhages. 22 In addition, recent studies suggested that cSVD is a dynamic process that affects the whole brain, beginning at the cellular level that involves the components of neurovascular units, including endothelial cells, pericytes, vascular smooth muscle cells, glia, neurons, immune cells, and extracellular matrix. 23,24 These units regulate cerebral blood flow, endothelial function, BBB integrity, and neuroinflammation. 5,23,25 Endothelial dysfunction, astrocytopathy, and BBB leakage may occur when components of neurovascular units are diseased or damaged due to aging, vascular risk factors (eg, hypertension, hyperlipidemia, hyperhomocysteinemia, diabetes, smoking), 26,27 increase in pulsatile flow being transmitted to the cerebral small vessels secondary to aortic stiffness, 28 and genetic factors. 5,24,29,30 These pathological changes may lead to compromised cerebral

show abstract

Section: Vascular Etiologies and Pathophysiology Of Vci Ischemic And ...mentioning

confidence: 99%

Section: Vascular Etiologies and Pathophysiology Of Vci Ischemic And ...mentioning

confidence: 99%

Current and Future Treatments of Vascular Cognitive Impairment

Ip,

Ko,

Lam

et al. 2024

Stroke

View full text Add to dashboard Cite

show abstract

Spinal Lymphatic Dysfunction Aggravates the Recovery Process After Spinal Cord Injury

Zhang,

Zheng,

Zhang

et al. 2024

Neuroscience

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Vascular cognitive impairment and dementia: Mechanisms, treatment, and future directions

Mok,

Cai,

Markus

2024

International Journal of Stroke

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Worldwide, around 50 million people live with dementia, and this number is projected to triple by 2050. It has been estimated that 20% of all dementia cases have a predominant cerebrovascular pathology, while perhaps another 20% of vascular diseases contribute to a mixed dementia picture. Therefore, the vascular contribution to dementia affects 20 million people currently and will increase markedly in the next few decades, particularly in lower- and middle-income countries. In this review, we discuss the mechanisms of vascular cognitive impairment (VCI) and review management. VCI refers to the spectrum of cerebrovascular pathologies that contribute to any degree of cognitive impairment, ranging from subjective cognitive decline, to mild cognitive impairment, to dementia. While acute cognitive decline occurring soon after a stroke is the most recognized form of VCI, chronic cerebrovascular disease, in particular cerebral small-vessel disease, can cause insidious cognitive decline in the absence of stroke. Moreover, cerebrovascular disease not only commonly co-occurs with Alzheimer’s disease (AD) and increases the probability that AD pathology will result in clinical dementia, but may also contribute etiologically to the development of AD pathologies. Despite its enormous health and economic impact, VCI has been a neglected research area, with few adequately powered trials of therapies, resulting in few proven treatments. Current management of VCI emphasizes prevention and treatment of stroke and vascular risk factors, with most evidence for intensive hypertension control. Reperfusion therapies in acute stroke may attenuate the risk of VCI. Associated behavioral symptoms such as apathy and poststroke emotionalism are common. We also highlight novel treatment strategies that will hopefully lead to new disease course-modifying therapies. Finally, we highlight the importance of including cognitive endpoints in large cardiovascular prevention trials and the need for an increased research focus and funding for this important area.

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Correction: Tian et al. The Underlying Role of the Glymphatic System and Meningeal Lymphatic Vessels in Cerebral Small Vessel Disease. Biomolecules 2022, 12, 748

Abstract: In the published publication [...]

Cited by 5 publications

References 1 publication

Current and Future Treatments of Vascular Cognitive Impairment

Current and Future Treatments of Vascular Cognitive Impairment

Spinal Lymphatic Dysfunction Aggravates the Recovery Process After Spinal Cord Injury

Vascular cognitive impairment and dementia: Mechanisms, treatment, and future directions

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