White matter damage and glymphatic dysfunction in a model of vascular dementia in rats with no prior vascular pathologies

Venkat, Poornima; Chopp, Michael; Zacharek, Alex; Cui, Chengcheng; Zhang, Li; Li, Qingjiang; Lü, Mei; Zhang, Talan; Liu, Amy; Chen, Jieli

doi:10.1016/j.neurobiolaging.2016.11.002

Cited by 102 publications

(143 citation statements)

References 49 publications

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“…CAA and CADASIL) characterized by protein aggregation and deposition. Glymphatic function has been assessed in several highly relevant processes to SVD including aging(28) and diseases such as microinfarction (29, 30), stroke (31), Alzheimer’s disease (AD)(32), migraine(33), and diabetes(34). Extrapolating from the current literature, we will focus on the effects that altered PVS structure and function, arterial pulsatility, and clearance have on glymphatic function.…”

Section: Glymphatic Systemmentioning

confidence: 99%

“…General expression of AQP4 is increased within regions of diffuse reactive glial fibrillary acidic protein (GFAP)-positive gliosis. A vascular dementia (VaD) model characterized by diffuse multiple microinfarction (MMI) was achieved by intracarotid injection of cholesterol crystals (40–70μm) in two recent studies(29, 30). Both of these studies demonstrated severe glymphatic system impairment initially, with glymphatic influx returing to baseline by 14 days after the injury.…”

Section: Glymphatic Systemmentioning

confidence: 99%

“…Mislocalization of AQP4 at the astrocyte endfoot has also been confirmed in several mouse models of AD (32, 65, 66). To further extrapolate the role of perivascular AQP4 localization, a study using the same model of VaD as described above in rats, found that decreased perivascular AQP4 expression persisted up to 6 weeks after microinfarction(30). More importantly, perivascular AQP4 loss was positively correlated with cognitive impairment in three separate behavioral tasks (novel object recognition test, odor recognition, and Morris water maze)(30).…”

Section: Glymphatic Systemmentioning

confidence: 99%

“…To further extrapolate the role of perivascular AQP4 localization, a study using the same model of VaD as described above in rats, found that decreased perivascular AQP4 expression persisted up to 6 weeks after microinfarction(30). More importantly, perivascular AQP4 loss was positively correlated with cognitive impairment in three separate behavioral tasks (novel object recognition test, odor recognition, and Morris water maze)(30). Although an interesting relationship, the direct role that effective perivascular AQP4 polarization may play in cognitive function requires further exploration.…”

Section: Glymphatic Systemmentioning

confidence: 99%

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Perivascular spaces, glymphatic dysfunction, and small vessel disease

2017

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Cerebral small vessel diseases (SVD) range broadly in etiology but share a remarkably overlapping pathology. Features of SVD including enlarged perivascular spaces and formation of abluminal protein deposits cannot be completely explained by the putative pathophysiology. The recently discovered glymphatic system provides a new perspective to potentially address these gaps. This work provides a comprehensive review of the known factors that regulate glymphatic function and the disease mechanisms underlying glymphatic impairment emphasizing the role that aquaporin-4 (AQP4)-lined perivascular spaces, cerebrovascular pulsatility, and metabolite clearance play in normal CNS physiology. This review also discusses the implications that glymphatic impairment may have on SVD inception and progression with the aim of exploring novel therapeutic targets and highlighting the key questions that remain to be answered.

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Section: Glymphatic Systemmentioning

confidence: 99%

Section: Glymphatic Systemmentioning

confidence: 99%

Section: Glymphatic Systemmentioning

confidence: 99%

Section: Glymphatic Systemmentioning

confidence: 99%

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Perivascular spaces, glymphatic dysfunction, and small vessel disease

2017

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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%

Blood–Brain Barrier Disruption, Vascular Impairment, and Ischemia/Reperfusion Damage in Diabetic Stroke

Venkat

Chopp

Chen

2017

JAHA

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114

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Liver transplantation in rare late‐onset ornithine transcarbamylase deficiency with central nervous system injury: A case report and review of the literature

et al. 2022

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Background Ornithine transcarbamylase deficiency (OTCD) is a genetic metabolic disease. Its clinical manifestations are mainly central nervous system dysfunction caused by high blood ammonia. Late‐onset OTCD combined with central nervous system injury has a poor therapeutic response, which is one of the main factors affecting the prognosis and quality of life of patients. liver transplantation (LT) has gradually become a radical treatment for OTCD, which has achieved good results. However, there is no consensus on the timing of LT and problems of nervous system damage and repair. Methods We report the development of late‐onset OTCD with central nervous system injury in an 11‐year‐old child who received liver transplantation at our transplant center. His first symptoms were nonprojectile vomiting, followed by irritability and disturbance of consciousness, after which the disease progressed rapidly and finally resulted in a coma. After liver transplantation, the child's consciousness returned to normal, muscle strength of the limbs gradually recovered from grade 0 to grade 4, and muscle tone gradually recovered from grade 4 to grade 1, suggesting that the motor nerves had gradually recovered. However, the child is currently mentally retarded, and the language center has not yet fully recovered.At the same time, we made a literature review of OTCD. Conclusion For OTCD patients with central nervous system injury, liver transplantation can fundamentally solve the problem of ammonia metabolism in the liver and avoids further damage to the central nervous system caused by hyperammonemia. At the same time, children's nervous systems are in the developmental stage when neuroplasticity is greatest. If liver transplantation is performed as soon as possible, nerve repair is still possible.

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White matter damage and glymphatic dysfunction in a model of vascular dementia in rats with no prior vascular pathologies

Cited by 102 publications

References 49 publications

Perivascular spaces, glymphatic dysfunction, and small vessel disease

Perivascular spaces, glymphatic dysfunction, and small vessel disease

Blood–Brain Barrier Disruption, Vascular Impairment, and Ischemia/Reperfusion Damage in Diabetic Stroke

Liver transplantation in rare late‐onset ornithine transcarbamylase deficiency with central nervous system injury: A case report and review of the literature

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