Neurovascular abnormalities in brain disorders: highlights with angiogenesis and magnetic resonance imaging studies

Chen, Chiao-Chi V.; Chen, Yu‐Chen; Hsiao, Han-Yun; Chang, Chen; Chern, Yijuang

doi:10.1186/1423-0127-20-47

Cited by 25 publications

(22 citation statements)

References 93 publications

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“…), contributing to the fine‐tuning of neurovascular coupling that critically impacts on the sustainability of function of neuronal networks (Chen et al . ; Kimbrough et al . ).…”

Section: The Adenosine Modulation System – Dynamics Of Its Extracellumentioning

confidence: 99%

How does adenosine control neuronal dysfunction and neurodegeneration?

Cunha

2016

Journal of Neurochemistry

368

385

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The adenosine modulation system mostly operates through inhibitory A 1 (A 1 R) and facilitatory A 2A receptors (A 2A R) in the brain. The activity-dependent release of adenosine acts as a brake of excitatory transmission through A 1 R, which are enriched in glutamatergic terminals. Adenosine sharpens salience of information encoding in neuronal circuits: highfrequency stimulation triggers ATP release in the 'activated' synapse, which is locally converted by ecto-nucleotidases into adenosine to selectively activate A 2A R; A 2A R switch off A 1 R and CB1 receptors, bolster glutamate release and NMDA receptors to assist increasing synaptic plasticity in the 'activated' synapse; the parallel engagement of the astrocytic syncytium releases adenosine further inhibiting neighboring synapses, thus sharpening the encoded plastic change. Brain insults trigger a large outflow of adenosine and ATP, as a danger signal. A 1 R are a hurdle for damage initiation, but they desensitize upon prolonged activation. However, if the insult is near-threshold and/or of short-duration, A 1 R trigger preconditioning, which may limit the spread of damage. Brain insults also up-regulate A 2A R, probably to bolster adaptive changes, but this heightens brain damage since A 2A R blockade affords neuroprotection in models of epilepsy, depression, Alzheimer's, or Parkinson's disease. This initially involves a control of synaptotoxicity by neuronal A 2A R, whereas astrocytic and microglia A 2A R might control the spread of damage. The A 2A R signaling mechanisms are largely unknown since A 2A R are pleiotropic, coupling to different G proteins and non-canonical pathways to control the viability of glutamatergic synapses, neuroinflammation, mitochondria function, and cytoskeleton dynamics. Thus, simultaneously bolstering A 1 R preconditioning and preventing excessive A 2A R function might afford maximal neuroprotection. Keywords: A 1 receptor, A 2A receptor, astrocyte, microglia, synaptic plasticity, synaptotoxicity. This article is part of a mini review series: "Synaptic Function and Dysfunction in Brain Diseases". Relevance of modulation systems to tune information flow in brain circuitsThe goal of understanding the flow of information in neuronal circuits has traditionally been centered in studying the key processes sustaining synaptic transmission and plasticity -i.e. the role of glutamate and glutamate receptors, as well as to a lesser extent the role of GABA and its receptors. If one considers an analogy to the experience of watching TV, this corresponds to studying how the ON/OFF button impacts all Received April 4, 2016; revised manuscript received May 23, 2016; accepted June 23, 2016. Address correspondence and reprint requests to R. A. Cunha, Center for Neurosciences and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal. E-mail: cunharod@gmail.com Abbreviations used: A 1 R, adenosine A 1 receptor; A 2A R, adenosine A 2A receptor; ADHD, attention deficit and hyperactivity disorder; BDNF, brain-derived neurotrophi...

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“…), contributing to the fine‐tuning of neurovascular coupling that critically impacts on the sustainability of function of neuronal networks (Chen et al . ; Kimbrough et al . ).…”

Section: The Adenosine Modulation System – Dynamics Of Its Extracellumentioning

confidence: 99%

How does adenosine control neuronal dysfunction and neurodegeneration?

Cunha

2016

Journal of Neurochemistry

368

385

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“…Vessel size index (VSI) and microvessel density (MVD) can be assessed with ssCE-MRI. These techniques have been the subject of several recent and thorough reviews (Ayata et al, 2004a, Chen et al, 2013). In addition, blood oxygenation level-dependent (BOLD) MRI and positron emission tomography (PET) are useful for the detection of increased oxygenated blood flow or metabolism as indirect evidence for angiogenesis (Marchal et al, 1993, Ding et al, 2008).…”

Section: The Role Of Angiogenesis In Cerebrovascular Diseases and mentioning

confidence: 99%

Vascular remodeling after ischemic stroke: Mechanisms and therapeutic potentials

Liu

Wang

Akamatsu

et al. 2014

Progress in Neurobiology

274

224

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The brain vasculature has been increasingly recognized as a key player that directs brain development, regulates homeostasis, and contributes to pathological processes. Following ischemic stroke, the reduction of blood flow elicits a cascade of changes and leads to vascular remodeling. However, the temporal profile of vascular changes after stroke is not well understood. Growing evidence suggests that the early phase of cerebral blood volume (CBV) increase is likely due to the improvement in collateral flow, also known as arteriogenesis, whereas the late phase of CBV increase is attributed to the surge of angiogenesis. Arteriogenesis is triggered by shear fluid stress followed by activation of endothelium and inflammatory processes, while angiogenesis induces a number of pro-angiogenic factors and circulating endothelial progenitor cells (EPCs). The status of collaterals in acute stroke has been shown to have several prognostic implications, while the causal relationship between angiogenesis and improved functional recovery has yet to be established in patients. A number of interventions aimed at enhancing cerebral blood flow including increasing collateral recruitment are under clinical investigation. Transplantation of EPCs to improve angiogenesis is also underway. Knowledge in the underlying physiological mechanisms for improved arteriogenesis and angiogenesis shall lead to more effective therapies for ischemic stroke.

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“…Transverse relaxation-based ΔR 2 and ΔR 2 * micro-MR angiography (MRA) is being investigated for the imaging of the cerebral vasculature in rodent brains in vivo, in conjunction with exogenous blood pool contrast agents, such as superparamagnetic iron oxide nanoparticles (SPION) (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11). Compared with conventional T 1 contrast MRA with a gadolinium-based contrast agent, ΔR 2 and ΔR 2 * MRAs exhibit higher sensitivity as a result of the increased intravascular transverse relaxivity/residence and the extravascular signal decay from diffusing spins in the presence of susceptibility-induced magnetic field gradients with intravascular SPION (especially at higher field strengths, >7 T).…”

Section: Introductionmentioning

confidence: 99%

UTE-ΔR₂-ΔR₂* combined MR whole-brain angiogram using dual-contrast superparamagnetic iron oxide nanoparticles

et al. 2016

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The ability to visualize whole-brain vasculature is important for quantitative in vivo investigation of vascular malfunctions in cerebral small vessel diseases, including cancer, stroke and neurodegeneration. Transverse relaxation-based ΔR2 and ΔR2 * MR angiography (MRA) provides improved vessel-tissue contrast in animal deep brain with the aid of intravascular contrast agents; however, it is susceptible to orientation dependence, air-tissue interface artifacts and vessel size overestimation. Dual-mode MRA acquisition with superparamagnetic iron oxide nanoparticles (SPION) provides a unique opportunity to systematically compare and synergistically combine both longitudinal (R1 ) and transverse (ΔR2 and ΔR2 *) relaxation-based MRA. Through Monte Carlo (MC) simulation and MRA experiments in normal and tumor-bearing animals with intravascular SPION, we show that ultrashort TE (UTE) MRA acquires well-defined vascularization on the brain surface, minimizing air-tissue artifacts, and combined ΔR2 and ΔR2 * MRA simultaneously improves the sensitivity to intracortical penetrating vessels and reduces vessel size overestimation. Consequently, UTE-ΔR2 -ΔR2 * combined MRA complements the shortcomings of individual angiograms and provides a strategy to synergistically merge longitudinal and transverse relaxation effects to generate more robust in vivo whole-brain micro-MRA. Copyright © 2016 John Wiley & Sons, Ltd.

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Neurovascular abnormalities in brain disorders: highlights with angiogenesis and magnetic resonance imaging studies

Cited by 25 publications

References 93 publications

How does adenosine control neuronal dysfunction and neurodegeneration?

How does adenosine control neuronal dysfunction and neurodegeneration?

Vascular remodeling after ischemic stroke: Mechanisms and therapeutic potentials

UTE-ΔR₂-ΔR₂* combined MR whole-brain angiogram using dual-contrast superparamagnetic iron oxide nanoparticles

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Neurovascular abnormalities in brain disorders: highlights with angiogenesis and magnetic resonance imaging studies

Cited by 25 publications

References 93 publications

How does adenosine control neuronal dysfunction and neurodegeneration?

How does adenosine control neuronal dysfunction and neurodegeneration?

Vascular remodeling after ischemic stroke: Mechanisms and therapeutic potentials

UTE-ΔR2-ΔR2* combined MR whole-brain angiogram using dual-contrast superparamagnetic iron oxide nanoparticles

Contact Info

Product

Resources

About

UTE-ΔR₂-ΔR₂* combined MR whole-brain angiogram using dual-contrast superparamagnetic iron oxide nanoparticles