Use of Multimodal Magnetic Resonance Imaging Techniques to Explore Cognitive Impairment in Leukoaraiosis

Yuan, Junliang; Feng, Li; Hu, Wenli; Zhang, Yumei

doi:10.12659/msm.912153

Cited by 11 publications

(7 citation statements)

References 43 publications

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“…LA is a common phenomenon in patients with ischemic stroke and has been characterized to be closely related to the increased risk of stroke and dementia. It is detected as a nonspecific image signal in cerebrovascular diseases and could be examined through MRI with high signals on the lateral ventricle or subcortical area (18,19). The pathogenesis of LA usually involves several factors, including advanced age, history of hypertension, smoking, and other characteristics, and these risk factors are also the main reason for severe symptoms and poor prognosis caused by stroke (20,21).…”

Section: ' Discussionmentioning

confidence: 99%

Claudin-1 and Claudin-3 as Molecular Regulators of Myelination in Leukoaraiosis Patients

Chen

Zhang

Mei

et al. 2021

Clinics

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Leukoaraiosis is described as white matter lesions that are associated with cognitive dysfunction, neurodegenerative disorders, etc. Myelin depletion is a salient pathological feature of, and the loss of oligodendrocytes is one of the most robust alterations evident in, white matter degeneration. Recent studies have revealed that claudin proteins are aberrantly expressed in leukoaraiosis and regulate oligodendrocyte activity. However, the roles of claudin-1 and claudin-3 in oligodendrocytes and leukoaraiosis are still not well-defined. METHODS: Quantitative polymerase chain reaction was used to measure the expression of claudin-1 (CLDN1), claudin-3 (CLDN3), and myelinogenesis-related genes such as myelin basic protein (MBP), proteolipid protein (PLP), oligodendrocyte transcription factor 2 (OLIG2), and SRY-box transcription factor 10 (SOX10) in leukoaraiosis patients (n=122) and healthy controls (n=122). The expression of claudin-1 and claudin-3 was either ectopically silenced or augmented in Oli-neu oligodendrocytes, and colony formation, apoptosis, and migration assays were performed. Finally, the expression of myelin proteins was evaluated by western blotting. RESULTS: Our results revealed that in addition to SOX10, the expression levels of claudin-1, claudin-3, and myelinogenesis-related proteins were prominently downregulated in leukoaraiosis patients, compared to those in healthy controls. Furthermore, the growth and migration of Oli-neu cells were downregulated upon silencing claudin-1 or claudin-3. However, the overexpression of claudin-1 or claudin-3 resulted in the reduction of the degree of apoptosis in Oli-neu cells. In addition, claudin-1 and claudin-3 promoted the expression of MBP, OLIG2, PLP, and SOX10 at the translational level. CONCLUSION: Our data has demonstrated that the abnormal expression of claudin-1 and claudin-3 regulates the pathological progression of leukoaraiosis by governing the viability and myelination of oligodendrocytes. These findings provide novel insights into the regulatory mechanisms underlying the roles of claudin-1 and claudin-3 in leukoaraiosis.

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Section: ' Discussionmentioning

confidence: 99%

Claudin-1 and Claudin-3 as Molecular Regulators of Myelination in Leukoaraiosis Patients

Chen

Zhang

Mei

et al. 2021

Clinics

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“…In contrast, a clearer correlation between imaging manifestations and neurological deficits can be observed on CT, as lesions found on CT reflect more severe neurodegenerative degeneration (Zagrajek and Pokryszko-Dragan, 2005). Gradient echo sequences (GRE) or more sensitive MRI magnetic susceptibility weighted imaging (SWI) can demonstrate the presence of cerebral microhemorrhages that cannot be distinguished from ischemic small vessel disease on CT and that are often characteristic of hypertensive small vessel disease and cerebral amyloid angiopathy (Yuan et al, 2018). LA can be divided into periventricular LA and deep/subcortical LA based on MRI features.…”

Section: Neuroimaging and Diagnosis Ct And Mrimentioning

confidence: 99%

Pathogenesis and research progress in leukoaraiosis

Sun

Lin

et al. 2022

Front. Hum. Neurosci.

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Leukoaraiosis is a common imaging marker of cerebral small vessel disease. In recent years, with the continuous advances in brain imaging technology, the detection rate of leukoaraiosis is higher and its clinical subtypes are gradually gaining attention. Although leukoaraiosis has long been considered an incidental finding with no therapeutic necessity, there is now growing evidence linking it to, among other things, cognitive impairment and a high risk of death after stroke. Due to different research methods, some of the findings are inconsistent and even contradictory. Therefore, a comprehensive and in-depth study of risk factors for leukoaraiosis is of great clinical significance. In this review, we summarize the literature on leukoaraiosis in recent years with the aim of elucidating the disease in terms of various aspects (including pathogenesis, imaging features, and clinical features, etc.).

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“…Similarly, a growing body of evidence also links cognition and mobility with white matter integrity detected by DTI [41,42,43]. These studies show that microstructural changes in normal-appearing white matter predict faster decline in psychomotor speed, executive functions, and working memory, regardless of WMH burden [24,44].…”

Section: White Matter Microstructure Vascular Risk Factors Cognimentioning

confidence: 99%

Brain White Matter: A Substrate for Resilience and a Substance for Subcortical Small Vessel Disease

Sorond

Gorelick

2019

Brain Sciences

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Age-related brain white matter disease is a form of small vessel disease (SVD) that may be associated with lacunar and other small subcortical infarcts, cerebral microbleeds, and perivascular spaces. This common form of cerebrovascular disease may manifest clinically as cognitive impairment of varying degrees and difficulty with mobility. Whereas some persons show cognitive decline and mobility failure when there are brain white matter hyperintensities (WMH) and acute stroke, others recover, and not everyone with brain white matter disease is disabled. Thus, repair or compensation of brain white matter may be possible, and furthermore, certain vascular risks, such as raised blood pressure, are targets for prevention of white matter disease or are administered to reduce the burden of such disease. Vascular risk modification may be useful, but alone may not be sufficient to prevent white matter disease progression. In this chapter, we specifically focus on WMH of vascular origin and explore white matter development, plasticity, and enduring processes of myelination across the health span in the context of experimental and human data, and compare and contrast resilient brain white matter propensity to a diseased white matter state. We conclude with thoughts on novel ways one might study white matter resilience, and predict future healthy cognitive and functional outcomes.

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Use of Multimodal Magnetic Resonance Imaging Techniques to Explore Cognitive Impairment in Leukoaraiosis

Cited by 11 publications

References 43 publications

Claudin-1 and Claudin-3 as Molecular Regulators of Myelination in Leukoaraiosis Patients

Claudin-1 and Claudin-3 as Molecular Regulators of Myelination in Leukoaraiosis Patients

Pathogenesis and research progress in leukoaraiosis

Brain White Matter: A Substrate for Resilience and a Substance for Subcortical Small Vessel Disease

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