Drowning stars: reassessing the role of astrocytes in brain edema

Thrane, Alexander S.; Thrane, Vinita Rangroo

doi:10.1016/j.tins.2014.08.010

Cited by 187 publications

(172 citation statements)

References 110 publications

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“…Alternatively CAA may disrupt perivascular drainage via perturbations in normal arteriolar pulsation (Hawkes et al, 2014;Kress et al, 2014). It is also possible that the presence of hyper-phosphorylated tau has direct deleterious consequences for perivascular astrocytes, for example by directly disrupting their microtubular structure, or altering the expression or localisation of membrane channels (for example, aquaporin 4) that change normal interstitial fluid dynamics, with the eventual outcome of an enlarged perivascular space (Arima et al, 1998;Thrane et al, 2014;Iqbal et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

MRI-visible perivascular space location is associated with Alzheimer's disease independently of amyloid burden

Banerjee

Kim

Fox

et al. 2017

Brain

192

216

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MRI-visible perivascular spaces are a neuroimaging marker of cerebral small vessel disease.Their location may relate to the type of underlying small vessel pathology: those in the white matter centrum semi-ovale have been associated with cerebral amyloid angiopathy, whilst those in the basal ganglia have been associated with deep perforating artery arteriolosclerosis.Since cerebral amyloid angiopathy is an almost invariable pathological finding in Alzheimer's disease, we hypothesized that MRI-visible perivascular spaces in the centrum semi-ovale would be associated with a clinical diagnosis of Alzheimer's disease, whereas those in the basal ganglia would be associated with subcortical vascular cognitive impairment. We also hypothesised that MRI-visible perivascular spaces in the centrum semiovale would be associated with brain amyloid burden, as detected by amyloid-PET using subcortical vascular cognitive impairment n=116) with standardised MRI and PiB-PET imaging were included. MRI-visible perivascular spaces were rated using a validated 4-point visual rating scale, and then categorised by severity ("none/mild", "moderate" or "frequent/severe").

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Section: Discussionmentioning

confidence: 99%

MRI-visible perivascular space location is associated with Alzheimer's disease independently of amyloid burden

Banerjee

Kim

Fox

et al. 2017

Brain

192

216

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“…4 However, the cardiac pulsation provides no more than 15-25% of the propulsive energy and other pulsation mechanisms must contribute to the convective CSF fluid dynamics. 6 Early functional magnetic resonance imaging (fMRI) scans and other modalities have shown that there may be several sources of pulsations in the brain. [7][8][9][10][11] The spectrum of susceptibilityweighted blood oxygen level dependent (BOLD) signals shows a 1/f frequency profile with most pulsatile power in very low frequencies ( < 0.1 Hz) and distinct respiratory rate (0.2-0.3 Hz) and cardiac frequency (0.8-1.2 Hz) peaks.…”

Section: Introductionmentioning

confidence: 99%

Ultra-fast magnetic resonance encephalography of physiological brain activity – Glymphatic pulsation mechanisms?

Kiviniemi

Wang

Korhonen

et al. 2015

J Cereb Blood Flow Metab

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302

352

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The theory on the glymphatic convection mechanism of cerebrospinal fluid holds that cardiac pulsations in part pump cerebrospinal fluid from the peri-arterial spaces through the extracellular tissue into the peri-venous spaces facilitated by aquaporin water channels. Since cardiac pulses cannot be the sole mechanism of glymphatic propulsion, we searched for additional cerebrospinal fluid pulsations in the human brain with ultra-fast magnetic resonance encephalography. We detected three types of physiological mechanisms affecting cerebral cerebrospinal fluid pulsations: cardiac, respiratory, and very low frequency pulsations. The cardiac pulsations induce a negative magnetic resonance encephalography signal change in peri-arterial regions that extends centrifugally and covers the brain in &1 Hz cycles. The respiratory &0.3 Hz pulsations are centripetal periodical pulses that occur dominantly in peri-venous areas. The third type of pulsation was very low frequency (VLF 0.001-0.023 Hz) and low frequency (LF 0.023-0.73 Hz) waves that both propagate with unique spatiotemporal patterns. Our findings using critically sampled magnetic resonance encephalography open a new view into cerebral fluid dynamics. Since glymphatic system failure may precede protein accumulations in diseases such as Alzheimer's dementia, this methodological advance offers a novel approach to image brain fluid dynamics that potentially can enable early detection and intervention in neurodegenerative diseases.

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“…11,12) During TBI, cerebral ischemia, or hemorrhage, all of which cause BBB disruption, vasogenic edema is commonly observed and persists for several days after brain damage. 12,13) Severe damage to endothelial cells and a decrease of endothelial tight junction proteins results in BBB disruption leading to vasogenic edema. 11) In common with many types of brain damage, several physiological active substances including vascular endothelial growth factors (VEGFs) and matrix metalloproteinases (MMPs) are responsible for vasogenic edema formation through tight junction dysfunction.…”

Section: Brain Edemamentioning

confidence: 99%

“…3,13) Cerebral hemorrhage is a lethal condition, which results in sudden death, paralysis of the extremities, and cognitive dysfunctions. Hemorrhage results from a fracture of microvessels by cerebral contusions.…”

Section: Hemorrhagementioning

confidence: 99%

Protection of the Blood–Brain Barrier as a Therapeutic Strategy for Brain Damage

Michinaga

Kōyama

2017

Biological & Pharmaceutical Bulletin

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Severe brain damage by trauma, ischemia, and hemorrhage lead to fatal conditions including sudden death, subsequent complications of the extremities and cognitive dysfunctions. Despite the urgent need for treatments for these complications, currently available therapeutic drugs are limited. Blood-brain barrier (BBB) disruption is a common pathogenic feature in many types of brain damage. The characteristic pathophysiological conditions caused by BBB disruption are brain edema resulting from an excessive increase of brain water content, inflammatory damage caused by infiltrating immune cells, and hemorrhage caused by the breakdown of microvessel structures. Because these pathogenic features induced by BBB disruption cause fatal conditions, their improvement is a desirable strategy. Many studies using experimental animal models have focused on molecules involved in BBB disruption, including vascular endothelial growth factors (VEGFs), matrix metalloproteinases (MMPs) and endothelins (ETs). The inhibition of these factors in several experimental animals was protective against BBB disruption caused by several types of brain damage, and ameliorated brain edema, inflammatory damage, and hemorrhagic transformation. In patients with brain damage, the up-regulation of these factors was observed and was related to brain damage severity. Thus, BBB protection by targeting VEGFs, MMPs, and ETs might be a novel strategy for the treatment of brain damage.

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Drowning stars: reassessing the role of astrocytes in brain edema

Cited by 187 publications

References 110 publications

MRI-visible perivascular space location is associated with Alzheimer's disease independently of amyloid burden

MRI-visible perivascular space location is associated with Alzheimer's disease independently of amyloid burden

Ultra-fast magnetic resonance encephalography of physiological brain activity – Glymphatic pulsation mechanisms?

Protection of the Blood–Brain Barrier as a Therapeutic Strategy for Brain Damage

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