Reduced subventricular zone proliferation and white matter damage in juvenile ferrets with kaolin-induced hydrocephalus

Curzio, Domenico L. Di; Buist, Richard; Bigio, Marc R. Del

doi:10.1016/j.expneurol.2013.06.004

Cited by 49 publications

(62 citation statements)

References 75 publications

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“…[22][23][24][25]27,57,79,80,136 Metabolic disturbances contribute to reversible dysfunction, but the clinical syndrome of hydrocephalic brain dysfunction may be due predominantly to a subcortical disconnection syndrome. Possible causes of ventricular dilation include obstructed CSF flow with associated increased CSF pulsatility.…”

Section: Pathophysiological Modificationsmentioning

confidence: 99%

An update on research priorities in hydrocephalus: overview of the third National Institutes of Health-sponsored symposium “Opportunities for Hydrocephalus Research: Pathways to Better Outcomes”

McAllister

Williams

Walker

et al. 2015

JNS

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abbreviatioNs CPC = choroid plexus cauterization; DTI = diffusion tensor imaging; ETV = endoscopic third ventriculostomy; HCRN = Hydrocephalus Clinical Research Network; ICP = intracranial pressure; iNPH = idiopathic NPH; LPA = lysophosphatidic acid; NIH = National Institutes of Health; NPC = neural precursor cell; NPH = normal pressure hydrocephalus; NSC = neural stem cell; PreOL = precursor oligodendroglia; RCT = randomized controlled trial; SVZ = subventricular zone; TNF = tumor necrosis factor; VP = ventriculoperitoneal; VZ = ventricular zone. . International experts gave plenary talks, and extensive group discussions were held for each of the major themes.The conference emphasized patient-centered care and translational research, with the main objective to arrive at a consensus on priorities in hydrocephalus that have the potential to impact patient care in the next 5 years. The current state of hydrocephalus research and treatment was presented, and the following priorities for research were recommended for each theme. 1) Causes of Hydrocephalus-CSF absorption, production, and related drug therapies; pathogenesis of human hydrocephalus; improved animal and in vitro models of hydrocephalus; developmental and macromolecular transport mechanisms; biomechanical changes in hydrocephalus; and age-dependent mechanisms in the development of hydrocephalus. 2) Diagnosis of Hydrocephalus-implementation of a standardized set of protocols and a shared repository of technical information; prospective studies of multimodal techniques including MRI and CSF biomarkers to test potential pharmacological treatments; and quantitative and cost-effective CSF assessment techniques. 3) Treatment of Hydrocephalus-improved bioengineering efforts to reduce proximal catheter and overall shunt failure; external or implantable diagnostics and support for the biological infrastructure research that informs these efforts; and evidencebased surgical standardization with longitudinal metrics to validate or refute implemented practices, procedures, or tests. 4) Outcome in Hydrocephalus-development of specific, reliable batteries with metrics focused on the hydrocephalic 1427

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Section: Pathophysiological Modificationsmentioning

confidence: 99%

An update on research priorities in hydrocephalus: overview of the third National Institutes of Health-sponsored symposium “Opportunities for Hydrocephalus Research: Pathways to Better Outcomes”

McAllister

Williams

Walker

et al. 2015

JNS

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“…Hence, oligodendrocyte function is not restricted to myelination, but includes a possible supportive role in the survival and development of cortical axon. In another study, depletion of the glial precursor cells was noted in a 14-day-old model of kaolin-induced hydrocephalus [13] . Also the optic nerve of a rat model of 21-day kaolin-induced hydrocephalus revealed a reduction in the density of oligodendrocytes [14] .…”

mentioning

confidence: 99%

Cortical Oligodendrocytes in Kaolin-Induced Hydrocephalus in Wistar Rat: Impact of Degree and Duration of Ventriculomegaly

Ayannuga

Naicker

2017

Ann Neurosci

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Background: Oligodendrocytes are critical to the function of the brain. They generate the myelin sheath which ensures saltatory conduction, which is a more energy saving and efficient means of axonal impulse transmission. Ventriculomegaly results in neuronal degeneration and astrogliosis. Purpose: The effect of the degree of ventriculomegaly on oligodendrocyte in kaolin-induced hydrocephalus and the timeline have not been extensively documented, hence this study. Methods: A total of 81 rats that were 3 weeks old were divided into 4 groups each consisting of control and experimental subgroups. Kaolin suspension was intracisternally injected to induce hydrocephalus and the animal sacrificed post-induction at 1, 2, 3, and 4 weeks. Two 1-mm-thick coronal slices at optic chiasma level were fixed in 10% buffered formal-saline and Karnovsky's fixative for light and transmission electron microscopy (TEM), respectively. The former slices were processed and stained with hematoxylin and eosin for glial density, cortical thickness, and oligodendrocyte evaluations. Subcortical white matter region of the latter were processed by conventional techniques for TEM. Results: Compared with their corresponding control rats, thickness of the dorsolateral cortex was significantly reduced across the 2-4 week post-induction (WPI), glial density was significantly increased in the mild and moderate ventriculomegaly subgroups 1 WPI but only in mild ventriculomegaly subset 2 WPI. In the 4 WPI group, there was significant increase in glial density across the 3 ventriculomegaly subsets. Early hydropic changes of oligodendrocytes were noted in the inner pyramidal layer mostly in the 4 WPI experimental rats. Dilation of the endoplasmic reticulum precedes that of mitochondria, while mitochondrial crista disruption was noted in the 3 and 4 WPI rats. The nuclear membrane of the oligodendrocytes was progressively deformed from the 2nd to 4th WPI. Conclusion: This study reported degenerative changes of oligodendrocytes and its organelles in kaolin-induced hydrocephalus. Degeneration was worse with duration and in the deep cortical layers.

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“…Activation of astrocytes, which play a critical role in synapse formation, control of neurotransmission, and regulation of cerebral blood flow, accompanies most central nervous system pathologies and has been associated with injury repair (Pekny et al, 2014). Up-regulation of the astrocytic intermediate filament protein glial fibrillary acidic protein (GFAP) is a hallmark of astrocytic activation (Pekny et al, 2014) and has been reported in models of hydrocephalus (Catalao et al, 2014; Di Curzio et al, 2013; Olopade et al, 2012; Xu et al, 2012a; Xu et al, 2012b). Analysis of GFAP shows only a low level of staining in WT mice (Fig.…”

Section: Resultsmentioning

confidence: 99%

Strain-dependent brain defects in mouse models of primary ciliary dyskinesia with mutations in Pcdp1 and Spef2

2014

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Hydrocephalus is caused by the accumulation of cerebrospinal fluid in the cerebral ventricular system which results in an enlargement of the cranium due to increased intraventricular pressure. The increase in pressure within the brain typically results in sloughing of ciliated ependymal cells, loss of cortical grey matter, and increased gliosis. Congenital hydrocephalus is associated with several syndromes including primary ciliary dyskinesia (PCD), a rare, genetically heterogeneous, pediatric syndrome that results from defects in motile cilia and flagella. We have examined the morphological and physiological defects in the brains of two mouse models of PCD, nm1054 and bgh, which have mutations in Pcdp1 (also known as Cfap221) and Spef2, respectively. Histopathological and immunohistochemical analyses of mice with these mutations on the C57BL/6J and 129S6/SvEvTac genetic backgrounds demonstrate strain-dependent morphological brain damage. Alterations in astrocytosis, microglial activation, myelination, and the neuronal population were identified and are generally more severe on the C57BL/6J background. Analysis of ependymal ciliary clearance ex vivo and cerebrospinal fluid flow in vivo demonstrate a physiological defect in nm1054 and bgh mice on both genetic backgrounds, indicating that abnormal cilia-driven flow is not the sole determinant of the severity of hydrocephalus in these models. These results suggest that genetic modifiers play an important role in susceptibility to severe PCD-associated hydrocephalus.

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Reduced subventricular zone proliferation and white matter damage in juvenile ferrets with kaolin-induced hydrocephalus

Cited by 49 publications

References 75 publications

An update on research priorities in hydrocephalus: overview of the third National Institutes of Health-sponsored symposium “Opportunities for Hydrocephalus Research: Pathways to Better Outcomes”

An update on research priorities in hydrocephalus: overview of the third National Institutes of Health-sponsored symposium “Opportunities for Hydrocephalus Research: Pathways to Better Outcomes”

Cortical Oligodendrocytes in Kaolin-Induced Hydrocephalus in Wistar Rat: Impact of Degree and Duration of Ventriculomegaly

Strain-dependent brain defects in mouse models of primary ciliary dyskinesia with mutations in Pcdp1 and Spef2

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