Neuroinflammation in intracerebral haemorrhage: immunotherapies with potential for translation

Xue, Mengzhou; Yong, V. Wee

doi:10.1016/s1474-4422(20)30364-1

Cited by 165 publications

(137 citation statements)

References 77 publications

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“… 9 , 29 However, to improve outcomes for most patients with ICH, our findings suggest that future research efforts should be aimed at treatment of IVH and PHE. 6 , 30 , 31 …”

Section: Discussionmentioning

confidence: 99%

Disability-Adjusted Life-Years Associated With Intracerebral Hemorrhage and Secondary Injury

et al. 2021

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“… 9 , 29 However, to improve outcomes for most patients with ICH, our findings suggest that future research efforts should be aimed at treatment of IVH and PHE. 6 , 30 , 31 …”

Section: Discussionmentioning

confidence: 99%

Disability-Adjusted Life-Years Associated With Intracerebral Hemorrhage and Secondary Injury

et al. 2021

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“…Iron overload can cause neurotoxicity (Hua et al, 2007 ), and injection of deferoxamine can reduce hydrocephalus caused by red blood cell lysate (Gao et al, 2014 ). When the BBB is severely damaged or opens in the early stage of hemorrhagic stroke, the immune cells in the blood vessels, such as T cells (Kunis et al, 2013 ) and neutrophils (Wang et al, 2016 ), may also enter the perivascular space of the brain parenchyma, and can be induced by antigen-presenting cells, such as activated microglia and astrocytes (Xue and Yong, 2020 ), to proliferate, differentiate, and release proinflammatory cytokines, which will exacerbate the destruction of the BBB and the formation of vasogenic edema.…”

Section: The Molecular Mechanisms Of Brain Edema Formation After Strokementioning

confidence: 99%

Glymphatic System in the Central Nervous System, a Novel Therapeutic Direction Against Brain Edema After Stroke

Zhou

Lenahan³

et al. 2021

Front. Aging Neurosci.

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Stroke is the destruction of brain function and structure, and is caused by either cerebrovascular obstruction or rupture. It is a disease associated with high mortality and disability worldwide. Brain edema after stroke is an important factor affecting neurologic function recovery. The glymphatic system is a recently discovered cerebrospinal fluid (CSF) transport system. Through the perivascular space and aquaporin 4 (AQP4) on astrocytes, it promotes the exchange of CSF and interstitial fluid (ISF), clears brain metabolic waste, and maintains the stability of the internal environment within the brain. Excessive accumulation of fluid in the brain tissue causes cerebral edema, but the glymphatic system plays an important role in the process of both intake and removal of fluid within the brain. The changes in the glymphatic system after stroke may be an important contributor to brain edema. Understanding and targeting the molecular mechanisms and the role of the glymphatic system in the formation and regression of brain edema after stroke could promote the exclusion of fluids in the brain tissue and promote the recovery of neurological function in stroke patients. In this review, we will discuss the physiology of the glymphatic system, as well as the related mechanisms and therapeutic targets involved in the formation of brain edema after stroke, which could provide a new direction for research against brain edema after stroke.

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“…In previous studies of the nervous system development and function in health and human pathologies, the following models have been used: animal models in vivo [ 1 , 2 , 3 , 4 , 5 ]; intravital sections of the brain ex vivo [ 6 , 7 , 8 ]; primary neuronal culture of cells or brain tissue in vitro [ 9 , 10 , 11 , 12 , 13 ], and, to a lesser extent, post-mortem material [ 14 , 15 , 16 , 17 , 18 ]. All these experimental methodological approaches have their limitations.…”

Section: Introductionmentioning

confidence: 99%

Cerebral Organoids—Challenges to Establish a Brain Prototype

Eremeev

Lebedeva

Bogomiakova

et al. 2021

Cells

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The new cellular models based on neural cells differentiated from induced pluripotent stem cells have greatly enhanced our understanding of human nervous system development. Highly efficient protocols for the differentiation of iPSCs into different types of neural cells have allowed the creation of 2D models of many neurodegenerative diseases and nervous system development. However, the 2D culture of neurons is an imperfect model of the 3D brain tissue architecture represented by many functionally active cell types. The development of protocols for the differentiation of iPSCs into 3D cerebral organoids made it possible to establish a cellular model closest to native human brain tissue. Cerebral organoids are equally suitable for modeling various CNS pathologies, testing pharmacologically active substances, and utilization in regenerative medicine. Meanwhile, this technology is still at the initial stage of development.

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Neuroinflammation in intracerebral haemorrhage: immunotherapies with potential for translation

Cited by 165 publications

References 77 publications

Disability-Adjusted Life-Years Associated With Intracerebral Hemorrhage and Secondary Injury

Disability-Adjusted Life-Years Associated With Intracerebral Hemorrhage and Secondary Injury

Glymphatic System in the Central Nervous System, a Novel Therapeutic Direction Against Brain Edema After Stroke

Cerebral Organoids—Challenges to Establish a Brain Prototype

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