Type 2 diabetes reduces the proliferation and survival of oligodendrocyte progenitor cells in ishchemic white matter lesions

Yatomi, Yutaka; Tanaka, Ryota; Shimada, Yoshiaki; Yamashiro, Kazuo; Liu, M; Mitome-Mishima, Yumiko; Miyamoto, Nobukazu; Ueno, Yoshio; Urabe, Takao

doi:10.1016/j.neuroscience.2014.12.054

Cited by 32 publications

(33 citation statements)

References 34 publications

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“…Consistent with these findings, Chen et al found that hyperglycemia aggravates WMI in the ischemic area and worsens functional prognosis in diabetic mice (Chen et al, 2011). The underlying mechanism may be that hyperglycemia inhibits the proliferation and survival of OPCs by promoting oxidative stress and stimulating MMP-9 activity (Yatomi et al, 2015). …”

Section: Management and Treatmentmentioning

confidence: 99%

White matter injury in ischemic stroke

Wang

Liu

Hong

et al. 2016

Progress in Neurobiology

227

206

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Stroke is one of the major causes of disability and mortality worldwide. It is well known that ischemic stroke can cause gray matter injury. However, stroke also elicits profound white matter injury, a risk factor for higher stroke incidence and poor neurological outcomes. The majority of damage caused by stroke is located in subcortical regions and, remarkably, white matter occupies nearly half of the average infarct volume. Indeed, white matter is exquisitely vulnerable to ischemia and is often injured more severely than gray matter. Clinical symptoms related to white matter injury include cognitive dysfunction, emotional disorders, sensorimotor impairments, as well as urinary incontinence and pain, all of which are closely associated with destruction and remodeling of white matter connectivity. White matter injury can be noninvasively detected by MRI, which provides a three-dimensional assessment of its morphology, metabolism, and function. There is an urgent need for novel white matter therapies, as currently available strategies are limited to preclinical animal studies. Optimal protection against ischemic stroke will need to encompass the fortification of both gray and white matter. In this review, we discuss white matter injury after ischemic stroke, focusing on clinical features and tools, such as imaging, manifestation, and potential treatments. We also briefly discuss the pathophysiology of WMI and future research directions.

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Section: Management and Treatmentmentioning

confidence: 99%

White matter injury in ischemic stroke

Wang

Liu

Hong

et al. 2016

Progress in Neurobiology

227

206

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“…Nevertheless, the detailed mechanisms are not entirely clear. A plethora of remarkable pathological changes have been identified during the CCCI process, such as cerebral cortex atrophy, neuronal degeneration, WMLs, and glial cell proliferation . The evidence of oxidative stress, apoptosis, enhanced expression of inflammatory factors, and increased Aβ deposition in the brain tissue is also invariably observed .…”

Section: Experimental Researchmentioning

confidence: 99%

Advances in chronic cerebral circulation insufficiency

Zhou

et al. 2017

CNS Neurosci Ther

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Chronic cerebral circulation insufficiency (CCCI) may not be an independent disease; rather, it is a pervasive state of long-term cerebral blood flow insufficiency caused by a variety of etiologies, and considered to be associated with either occurrence or recurrence of ischemic stroke, vascular cognitive impairment, and development of vascular dementia, resulting in disability and mortality worldwide. This review summarizes the features and recent progress of CCCI, mainly focusing on epidemiology, experimental research, pathophysiology, etiology, clinical manifestations, imaging presentation, diagnosis, and potential therapeutic regimens. Some research directions are briefly discussed as well.

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“…DM decreases neuronal dendrite outgrowth and neuronal cell survival and increases cell death of myelin‐producing oligodendrocytes 9. In the diabetic brain, ischemia induces significant white matter rarefaction, decreases axon and myelin density, and decreases the proliferation and survival of oligodendrocytes progenitor cells, and delays remyelination 53, 79, 80, 81. Loss of myelin and axon density hinders the conduction of nerve signals and interneuronal communications affecting sensorimotor functions 76.…”

Section: White Matter Damage In Diabetic Strokementioning

confidence: 99%