Demyelinating processes in aging and stroke in the central nervous system and the prospect of treatment strategy

Chen, Di; Huang, Yichen; Shi, Ziyu; Li, Jiaying; Zhang, Yue; Wang, Ke; Smith, Amanda D.; Gong, Yi; Gao, Yanqin

doi:10.1111/cns.13497

Cited by 41 publications

(29 citation statements)

References 99 publications

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“…However, none of the patients was known to suffer from a demyelinating disease. Furthermore, although advanced age is related to white matter demyelination [86,87], age was not associated with tissue elasticity in the sample of the present work. These results agree with observations on mammalian brain tissue, where white matter elasticity did not differ between young and old subjects, with the exception of striatal white matter [85].…”

Section: Discussioncontrasting

confidence: 59%

Atomic Force Microscope Nanoindentation Analysis of Diffuse Astrocytic Tumor Elasticity: Relation with Tumor Histopathology

Tsitlakidis

Tsingotjidou

Κritis

et al. 2021

Cancers

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This study aims to investigate the influence of isocitrate dehydrogenase gene family (IDH) mutations, World Health Organization (WHO) grade, and mechanical preconditioning on glioma and adjacent brain elasticity through standard monotonic and repetitive atomic force microscope (AFM) nanoindentation. The elastic modulus was measured ex vivo on fresh tissue specimens acquired during craniotomy from the tumor and the peritumoral white matter of 16 diffuse glioma patients. Linear mixed-effects models examined the impact of tumor traits and preconditioning on tissue elasticity. Tissues from IDH-mutant cases were stiffer than those from IDH-wildtype ones among anaplastic astrocytoma patients (p = 0.0496) but of similar elasticity to IDH-wildtype cases for diffuse astrocytoma patients (p = 0.480). The tumor was found to be non-significantly softer than white matter in anaplastic astrocytomas (p = 0.070), but of similar elasticity to adjacent brain in diffuse astrocytomas (p = 0.492) and glioblastomas (p = 0.593). During repetitive indentation, both tumor (p = 0.002) and white matter (p = 0.003) showed initial stiffening followed by softening. Stiffening was fully reversed in white matter (p = 0.942) and partially reversed in tumor (p = 0.015). Tissue elasticity comprises a phenotypic characteristic closely related to glioma histopathology. Heterogeneity between patients should be further explored.

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Section: Discussioncontrasting

confidence: 59%

Atomic Force Microscope Nanoindentation Analysis of Diffuse Astrocytic Tumor Elasticity: Relation with Tumor Histopathology

Tsitlakidis

Tsingotjidou

Κritis

et al. 2021

Cancers

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“…These cells are responsible for the long process of intracortical myelination and increase the local cholesterol and iron levels in the process causing increased toxicity to the intracortical environment ( Bartzokis, 2004 ). The loss of myelin in aging WM may be caused by immune-mediated, metabolic, ischaemic, and excitotoxic pathways ( Chen et al, 2020b ). Immune-mediated myelin injury is mostly driven by activated microglial cells or macrophages which are thus activated, release toxins, and ultimately cause myelin sheath and oligodendrocyte degeneration.…”

Section: White Matter Aging Mechanismsmentioning

confidence: 99%

“…Moreover, oligodendrocytes and glial cells are particularly sensitive to ischemia-induced apoptosis ( Lassmann, 2001 ). Hypertensive vascular alterations may gradually obstruct blood flow to WM regions and cause chronic ischemia which leads to progressive loss of myelin and oligodendrocytes ( Chen et al, 2020b ).…”

Section: White Matter Aging Mechanismsmentioning

confidence: 99%

Brain aging mechanisms with mechanical manifestations

Blinkouskaya

Caçoilo

Gollamudi

et al. 2021

Mechanisms of Ageing and Development

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Brain aging is a complex process that affects everything from the subcellular to the organ level, begins early in life, and accelerates with age. Morphologically, brain aging is primarily characterized by brain volume loss, cortical thinning, white matter degradation, loss of gyrification, and ventricular enlargement. Pathophysiologically, brain aging is associated with neuron cell shrinking, dendritic degeneration, demyelination, small vessel disease, metabolic slowing, microglial activation, and the formation of white matter lesions. In recent years, the mechanics community has demonstrated increasing interest in modeling the brain’s (bio)mechanical behavior and uses constitutive modeling to predict shape changes of anatomically accurate finite element brain models in health and disease. Here, we pursue two objectives. First, we review existing imaging-based data on white and gray matter atrophy rates and organ-level aging patterns. This data is required to calibrate and validate constitutive brain models. Second, we review the most critical cell- and tissue-level aging mechanisms that drive white and gray matter changes. We focuse on aging mechanisms that ultimately manifest as organ-level shape changes based on the idea that the integration of imaging and mechanical modeling may help identify the tipping point when normal aging ends and pathological neurodegeneration begins.

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“…Secondly, oligodendrocytes are extremely sensitive to ischemia and can rapidly undergo apoptosis in the setting of chronic CBF reduction 78 . And finally, other glial cells also participate in exacerbating oligodendrocyte injury and demyelination through releasing TIMP‐3, TNF‐α, and MMP‐3, etc 79 . Notably, reduced myelin component production may occur independent of oligodendrocyte death 79 …”

Section: Introductionmentioning

confidence: 99%

“…And finally, other glial cells also participate in exacerbating oligodendrocyte injury and demyelination through releasing TIMP‐3, TNF‐α, and MMP‐3, etc 79 . Notably, reduced myelin component production may occur independent of oligodendrocyte death 79 …”

Section: Introductionmentioning

confidence: 99%

Pathological changes in neurovascular units: Lessons from cases of vascular dementia

Wang

Yan

et al. 2021

CNS Neurosci Ther

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Vascular dementia (VD) is the second leading cause of dementia after Alzheimer's disease (AD). The decrease of cerebral blood flow (CBF) to different degrees is one of the main causes of VD. Neurovascular unit (NVU) is a vessel‐centered concept, emphasizing all the cellular components play an integrated role in maintaining the normal physiological functions of the brain. More and more evidence shows that reduced CBF causes a series of changes in NVU, such as impaired neuronal function, abnormal activation of glial cells, and changes in vascular permeability, all of which collectively play a role in the pathogenesis of VD. In this paper, we review NVU changes as CBF decreases, focusing on each cellular component of NVU. We also highlight remote ischemic preconditioning as a promising approach for VD prevention and treatment from the NVU perspective of view.

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Demyelinating processes in aging and stroke in the central nervous system and the prospect of treatment strategy

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 41 publications

References 99 publications

Atomic Force Microscope Nanoindentation Analysis of Diffuse Astrocytic Tumor Elasticity: Relation with Tumor Histopathology

Atomic Force Microscope Nanoindentation Analysis of Diffuse Astrocytic Tumor Elasticity: Relation with Tumor Histopathology

Brain aging mechanisms with mechanical manifestations

Pathological changes in neurovascular units: Lessons from cases of vascular dementia

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