Mucosal Tolerization to E-Selectin Protects against Memory Dysfunction and White Matter Damage in a Vascular Cognitive Impairment Model

Wakita, Hideaki; Ruetzler, Christl; Illoh, Kachikwu; Chen, Yong; Takanohashi, Asako; Spatz, Maria; Hallenbeck, John M.

doi:10.1038/sj.jcbfm.9600528

Cited by 30 publications

(23 citation statements)

References 45 publications

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“…Such neurovascular dysfunction would aggravate the CBF reduction in critically perfused deep white matter regions and contribute to the white matter damage. Accordingly, scavenging of free radicals or approaches to suppress inflammation counteract white matter damage and behavioral deficits in rodent models of cerebral hypoperfusion (Dong et al, 2011; Kim et al, 2008a; Maki et al, 2011; Ueno et al, 2009; Wakita et al, 2008; Wang et al, 2010; Washida et al, 2010; Zhang et al, 2011). NADPH oxidase, a multiunit enzyme particularly enriched in cerebral blood vessels (Miller et al, 2005), has emerges as an important source in vascular oxidative stress in aging, hypertension, hyperlipidemia and diabetes (Faraci, 2011), and inhibition or genetic inactivation of this enzyme has been shown to ameliorate the vascular dysfunction (Drummond et al, 2011).…”

Section: Pathogenic Mechanisms Responsible For White Matter Injurymentioning

confidence: 99%

The Pathobiology of Vascular Dementia

Iadecola

2013

Neuron

1,464

1,399

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Vascular cognitive impairment defines alterations in cognition, ranging from subtle deficits to full-blown dementia, attributable to cerebrovascular causes. Often coexisting with Alzheimer’s disease, mixed vascular and neurodegenerative dementia has emerged as the leading cause of age-related cognitive impairment. Central to the disease mechanism is the crucial role that cerebral blood vessels play in brain health, not only for the delivery of oxygen and nutrients, but also for the trophic signaling that links inextricably the well being of neurons and glia to that of cerebrovascular cells. This review will examine how vascular damage disrupts these vital homeostatic interactions, focusing on the hemispheric white matter, a region at heightened risk for vascular damage, and on the interplay between vascular factors and Alzheimer’s disease. Finally, preventative and therapeutic prospects will be examined, highlighting the importance of midlife vascular risk factor control in the prevention of late-life dementia.

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Section: Pathogenic Mechanisms Responsible For White Matter Injurymentioning

confidence: 99%

The Pathobiology of Vascular Dementia

Iadecola

2013

Neuron

1,464

1,399

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“…In addition, activated microglia and astrocytes are present in WM lesions, which might exacerbate oxidative stress (Simpson et al, 2007). Therapeutic scavenging of ROS and anti-inflammatory approaches have been used to suppress inflammation and attenuate WM injuries in rodent models (Ma et al, 2015; Ueno et al, 2009; Wakita et al, 2008). …”

Section: Vascular Pathophysiology Underlying Vcid—how Does Vasculamentioning

confidence: 99%

The impact of cerebrovascular aging on vascular cognitive impairment and dementia

Yang

Sun

et al. 2017

Ageing Research Reviews

158

128

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As human life expectancy rises, the aged population will increase. Aging is accompanied by changes in tissue structure, often resulting in functional decline. For example, aging within blood vessels contributes to a decrease in blood flow to important organs, potentially leading to organ atrophy and loss of function. In the central nervous system, cerebral vascular aging can lead to loss of the integrity of the blood-brain barrier, eventually resulting in cognitive and sensorimotor decline. One of the major of types of cognitive dysfunction due to chronic cerebral hypoperfusion is vascular cognitive impairment and dementia (VCID). In spite of recent progress in clinical and experimental VCID research, our understanding of vascular contributions to the pathogenesis of VCID is still very limited. In this review, we summarize recent findings on VCID, with a focus on vascular age-related pathologies and their contribution to the development of this condition.

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“…151,152 A biologic product, E-selectin, has been shown to reduce inflammation after induction of nasal tolerance in the hypertensive rat. 153 Reliable end points will need to be established. For example, quantification of BBB permeability could show reduction in short-term studies of several months.…”

Section: Recommendations For Future Directionsmentioning

confidence: 99%

Consensus statement for diagnosis of subcortical small vessel disease

Rosenberg

Wallin

Wardlaw

et al. 2015

J Cereb Blood Flow Metab

186

132

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Vascular cognitive impairment (VCI) is the diagnostic term used to describe a heterogeneous group of sporadic and hereditary diseases of the large and small blood vessels. Subcortical small vessel disease (SVD) leads to lacunar infarcts and progressive damage to the white matter. Patients with progressive damage to the white matter, referred to as Binswanger's disease (BD), constitute a spectrum from pure vascular disease to a mixture with neurodegenerative changes. Binswanger's disease patients are a relatively homogeneous subgroup with hypoxic hypoperfusion, lacunar infarcts, and inflammation that act synergistically to disrupt the blood-brain barrier (BBB) and break down myelin. Identification of this subgroup can be facilitated by multimodal disease markers obtained from clinical, cerebrospinal fluid, neuropsychological, and imaging studies. This consensus statement identifies a potential set of biomarkers based on underlying pathologic changes that could facilitate diagnosis and aid patient selection for future collaborative treatment trials.

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Mucosal Tolerization to E-Selectin Protects against Memory Dysfunction and White Matter Damage in a Vascular Cognitive Impairment Model

Cited by 30 publications

References 45 publications

The Pathobiology of Vascular Dementia

The Pathobiology of Vascular Dementia

The impact of cerebrovascular aging on vascular cognitive impairment and dementia

Consensus statement for diagnosis of subcortical small vessel disease

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