Interaction between hypertension and cerebral hypoperfusion in the development of cognitive dysfunction and white matter pathology in rats

Choi, Jun Young; Cui, Yunkang; Kim, Byung Gon

doi:10.1016/j.neuroscience.2015.06.056

Cited by 33 publications

(26 citation statements)

References 41 publications

(43 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies have confirmed that hypertension plays a role in the loss of BBB integrity (Choi et al, 2015) and is a strong predictor of WMI. Adequate control of hypertension might alleviate the progression of WMI.…”

Section: Management and Treatmentmentioning

confidence: 98%

White matter injury in ischemic stroke

Wang

Liu

Hong

et al. 2016

Progress in Neurobiology

220

206

View full text Add to dashboard Cite

Stroke is one of the major causes of disability and mortality worldwide. It is well known that ischemic stroke can cause gray matter injury. However, stroke also elicits profound white matter injury, a risk factor for higher stroke incidence and poor neurological outcomes. The majority of damage caused by stroke is located in subcortical regions and, remarkably, white matter occupies nearly half of the average infarct volume. Indeed, white matter is exquisitely vulnerable to ischemia and is often injured more severely than gray matter. Clinical symptoms related to white matter injury include cognitive dysfunction, emotional disorders, sensorimotor impairments, as well as urinary incontinence and pain, all of which are closely associated with destruction and remodeling of white matter connectivity. White matter injury can be noninvasively detected by MRI, which provides a three-dimensional assessment of its morphology, metabolism, and function. There is an urgent need for novel white matter therapies, as currently available strategies are limited to preclinical animal studies. Optimal protection against ischemic stroke will need to encompass the fortification of both gray and white matter. In this review, we discuss white matter injury after ischemic stroke, focusing on clinical features and tools, such as imaging, manifestation, and potential treatments. We also briefly discuss the pathophysiology of WMI and future research directions.

show abstract

Section: Management and Treatmentmentioning

confidence: 98%

White matter injury in ischemic stroke

Wang

Liu

Hong

et al. 2016

Progress in Neurobiology

220

206

View full text Add to dashboard Cite

show abstract

“…Starting from these evidences, it is intriguing to speculate that in the presence of hyperuricemia, the diffusion of UA through blood-brain barrier could increase the concentrations of UA in CSF to levels that might exert detrimental effects on cells biology by promoting the onset and/or progression of neuronal damage. An alteration of integrity of blood-brain barrier, which can occur in patients with AD (Bowman et al, 2010) as well as in the presence of cerebrovascular disease (Kalaria et al, 2016) or high blood pressure levels (Choi et al, 2015;Fan et al, 2015;Borghi and Desideri, 2016) could further contribute to achieve potentially "toxic" levels of UA in CSF. Indeed, the alteration of blood-brain barrier integrity is associated with a further increase of UA levels in CSF (Bowman et al, 2010).…”

Section: Journal Of Cellular Physiologymentioning

confidence: 99%

Uric Acid Amplifies Aβ Amyloid Effects Involved in the Cognitive Dysfunction/Dementia: Evidences From an Experimental Model In Vitro

Desideri

Gentile

Antonosante

et al. 2016

Journal Cellular Physiology

View full text Add to dashboard Cite

There is still a considerable debate concerning whether uric acid is neuroprotective or neurotoxic agent. To clarify this topic, we tested the effects of uric acid on neuronal cells biology by using differentiated SHSY5Y neuroblastoma cells incubated with amyloid β to reproduce an in vitro model of Alzheimer's disease. The incubation of cells with uric acid at the dose of 40 µM or higher significantly reduced cell viability and potentiated the proapoptotic effect of amyloid β. Finally, uric acid enhanced the generation of 4-hydroxynonenal and the expression of PPARβ/δ promoted by amyloid β, indicating a prooxidant effects. In conclusion, uric acid could exert a detrimental influence on neuronal biology being this influence further potentiated by the concomitant exposure to neurotoxic stimuli. This effect is evident for uric acid concentrations close to those achievable in cerebrospinal fluid in presence of mild hyperuricemia thus suggesting a potential role of uric acid in pathophysiology of cognitive dysfunction. These effects are influenced by the concentrations of uric acid and by the presence of favoring conditions that commonly occur in neurodegenerative disorders and well as in the aging brain, including increased oxidative stress and exposure to amyloid β. J. Cell. Physiol. 232: 1069-1078, 2017. © 2016 Wiley Periodicals, Inc.

show abstract

“…It has been reported that many diseases such as heart disease (de la Torre, 2012), hypertension (Farkas et al, 2002; Choi et al, 2015), diabetes (Kwon et al, 2015) and atherosclerosis (McColl et al, 2009) contribute to vascular constriction and cause CCH.…”

Section: Introductionmentioning

confidence: 99%

“…The mechanisms underlying dementia caused by CCH involve neuronal loss (Pappas et al, 1996; Bang et al, 2013), white matter lesion (Tomimoto et al, 2003; Chida et al, 2011), glial activation (Simpson et al, 2007), synaptic dysfunction (Simpson et al, 2007), oxidative stress (Ritchie et al, 2004; Kašparová et al, 2005), accumulation of Aβ (Li et al, 2009b; Okamoto et al, 2012) and aggravation of progressive cognitive deficits (de la Torre, 2012; Choi et al, 2015). …”

Section: Introductionmentioning

confidence: 99%

Dl-3-n-Butylphthalide Treatment Enhances Hemodynamics and Ameliorates Memory Deficits in Rats with Chronic Cerebral Hypoperfusion

Xiong

Zhu

et al. 2017

Front. Aging Neurosci.

View full text Add to dashboard Cite

Our previous study has revealed that chronic cerebral hypoperfusion (CCH) activates a compensatory vascular mechanism attempting to maintain an optimal cerebral blood flow (CBF). However, this compensation fails to prevent neuronal death and cognitive impairment because neurons die prior to the restoration of normal CBF. Therefore, pharmacological invention may be critical to enhance the CBF for reducing neurodegeneration and memory deficit. Dl-3-n-butylphthalide (NBP) is a compound isolated from the seeds of Chinese celery and has been proven to be able to prevent neuronal loss, reduce inflammation and ameliorate memory deficits in acute ischemic animal models and stroke patients. In the present study, we used magnetic resonance imaging (MRI) techniques, immunohistochemistry and Morris water maze (MWM) to investigate whether NBP can accelerate CBF recovery, reduce neuronal death and improve cognitive deficits in CCH rats after permanent bilateral common carotid artery occlusion (BCCAO). Rats were intravenously injected with NBP (5 mg/kg) daily for 14 days beginning the first day after BCCAO. The results showed that NBP shortened recovery time of CBF to pre-occlusion levels at 2 weeks following BCCAO, compared to 4 weeks in the vehicle group, and enhanced hemodynamic compensation through dilation of the vertebral arteries (VAs) and increase in angiogenesis. NBP treatment also markedly reduced reactive astrogliosis and cell apoptosis and protected hippocampal neurons against ischemic injury. The escape latency of CCH rats in the MWM was also reduced in response to NBP treatment. These findings demonstrate that NBP can accelerate the recovery of CBF and improve cognitive function in a rat model of CCH, suggesting that NBP is a promising therapy for CCH patients or vascular dementia.

show abstract

Interaction between hypertension and cerebral hypoperfusion in the development of cognitive dysfunction and white matter pathology in rats

Cited by 33 publications

References 41 publications

White matter injury in ischemic stroke

White matter injury in ischemic stroke

Uric Acid Amplifies Aβ Amyloid Effects Involved in the Cognitive Dysfunction/Dementia: Evidences From an Experimental Model In Vitro

Dl-3-n-Butylphthalide Treatment Enhances Hemodynamics and Ameliorates Memory Deficits in Rats with Chronic Cerebral Hypoperfusion

Contact Info

Product

Resources

About