Aging, the Metabolic Syndrome, and Ischemic Stroke

Lucke‐Wold, Brandon; Logsdon, Aric F.; Turner, Ryan C.; Rosen, Charles L.; Huber, Jason D.

doi:10.1016/bs.apha.2014.07.001

Cited by 34 publications

(16 citation statements)

References 195 publications

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“…These include aging, hypertension, hyperlipidemia and hyperglycemia and they are known to enhance BBB dysfunction after stroke [81]. The effects of such co-morbidities on CP injury after ischemic stroke are unknown.…”

Section: Choroid Plexus As a Site Of Injurymentioning

confidence: 99%

The choroid plexus as a site of damage in hemorrhagic and ischemic stroke and its role in responding to injury

Xiang

Routhe

Wilkinson

et al. 2017

Fluids Barriers CNS

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While the impact of hemorrhagic and ischemic strokes on the blood–brain barrier has been extensively studied, the impact of these types of stroke on the choroid plexus, site of the blood-CSF barrier, has received much less attention. The purpose of this review is to examine evidence of choroid plexus injury in clinical and preclinical studies of intraventricular hemorrhage, subarachnoid hemorrhage, intracerebral hemorrhage and ischemic stroke. It then discusses evidence that the choroid plexuses are important in the response to brain injury, with potential roles in limiting damage. The overall aim of the review is to highlight deficiencies in our knowledge on the impact of hemorrhagic and ischemic strokes on the choroid plexus, particularly with reference to intraventricular hemorrhage, and to suggest that a greater understanding of the response of the choroid plexus to stroke may open new avenues for brain protection.

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Section: Choroid Plexus As a Site Of Injurymentioning

confidence: 99%

The choroid plexus as a site of damage in hemorrhagic and ischemic stroke and its role in responding to injury

Xiang

Routhe

Wilkinson

et al. 2017

Fluids Barriers CNS

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“…MetS is a complex clustering of metabolic disorders with a combination of components, such as abdominal fat, high blood pressure, elevated triglyceride level, low high-density lipoprotein (HDL) cholesterol levels, and glucose intolerance [2]. Each MetS component is a known risk factor for increased blood vessel occlusion, incidence and mortality of cardiovascular disease, type 2 diabetes mellitus, and stroke [3–7]. …”

Section: Introductionmentioning

confidence: 99%

Association Between Alcohol Consumption and Metabolic Syndrome in a Community-Based Cohort of Korean Adults

et al. 2017

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BackgroundThe relationship between alcohol consumption and metabolic syndrome (MetS) remains controversial. This study investigated the relationship between alcohol consumption and MetS components and prevalence.Material/MethodsWe analyzed 10 037 subjects (3076 MetS and 6961 non-MetS) in a community-based cohort.MetS was defined according to the ATP III Guidelines. Subjects were divided according to amount of alcohol consumption; non-drinker, very light (0.1–5.0 g/day), light (5.1–15.0 g/day), moderate (15.1–30.0 g/day), and heavy drinker (>30 g/day). Multiple logistic regression models were performed to estimate odds ratios (ORs) and confidence intervals (CIs). The analyses were performed in men and women separately. SPSS statistical software was used for analyses.ResultsThe prevalence of MetS in both males and females was associated with alcohol drinking status (p<0.0001). Amount of alcohol consumption (0.1–5.0 g/day) was significantly associated with lower prevalence of MetS in both genders compared to non-drinkers. Amount of alcohol consumption (>30.0 g/day) did not show a significant association with prevalence of MetS. However, alcohol consumption (>30.0 g/day) showed an association with glucose and HDL cholesterol among the components of MetS.ConclusionsOur results indicate that alcohol drinking (0.1–5.0 g/day) contributed to decrease prevalence of MetS and components, including triglyceride and HDL cholesterol.

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“…Aging is associated with numerous neurobiological alterations over time, including elevations in hypothalamic-pituitary-adrenal (HPA) axis activity, oxidative radicals, microglia activation and blood-brain barrier (BBB) permeability, coupled with decreases in brain-derived neurotrophic factor (BDNF; Pan, 2011; Jurgens and Johnson, 2012; Derecki et al, 2014; Lucke-Wold et al, 2014). It is well known that these changes can interact to promote “wear and tear” on the individual and modulate susceptibility to environmental insults (Blau et al, 2012; Chapman et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Age and Chronicity of Administration Dramatically Influenced the Impact of Low Dose Paraquat Exposure on Behavior and Hypothalamic-Pituitary-Adrenal Activity

Rudyk

McNeill

Prowse

et al. 2017

Front. Aging Neurosci.

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Little is known of the age-dependent and long-term consequences of low exposure levels of the herbicide and dopaminergic toxicant, paraquat. Thus, we assessed the dose-dependent effects of paraquat using a typical short-term (3 week) exposure procedure, followed by an assessment of the effects of chronic (16 weeks) exposure to a very low dose (1/10th of what previously induced dopaminergic neuronal damage). Short term paraquat treatment dose-dependently induced deficits in locomotion, sucrose preference and Y-maze performance. Chronic low dose paraquat treatment had a very different pattern of effects that were also dependent upon the age of the animal: in direct contrast to the short-term effects, chronic low dose paraquat increased sucrose consumption and reduced forced swim test (FST) immobility. Yet these effects were age-dependent, only emerging in mice older than 13 months. Likewise, Y-maze spontaneous alternations and home cage activity were dramatically altered as a function of age and paraquat chronicity. In both the short and long-term exposure studies, increased corticosterone and altered hippocampal glucocorticoid receptor (GR) levels were induced by paraquat, but surprisingly these effects were blunted in the older mice. Thus, paraquat clearly acts as a systemic stressor in terms of corticoid signaling and behavioral outcomes, but that paradoxical effects may occur with: (a) repeated exposure at; (b) very low doses; and (c) older age. Collectively, these data raise the possibility that repeated “hits” with low doses of paraquat in combination with aging processes might have promoted compensatory outcomes.

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Aging, the Metabolic Syndrome, and Ischemic Stroke

Cited by 34 publications

References 195 publications

The choroid plexus as a site of damage in hemorrhagic and ischemic stroke and its role in responding to injury

The choroid plexus as a site of damage in hemorrhagic and ischemic stroke and its role in responding to injury

Association Between Alcohol Consumption and Metabolic Syndrome in a Community-Based Cohort of Korean Adults

Age and Chronicity of Administration Dramatically Influenced the Impact of Low Dose Paraquat Exposure on Behavior and Hypothalamic-Pituitary-Adrenal Activity

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