Serum biomarkers of spontaneous intracerebral hemorrhage induced secondary brain injury

Brunswick, Andrew; Hwang, Brian Y.; Appelboom, Geoffrey; Hwang, Richard Y.; Piazza, Matthew; Connolly, E. Sander

doi:10.1016/j.jns.2012.06.008

Cited by 57 publications

(41 citation statements)

References 119 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, early pathologies caused by transient opening of the BBB also influence secondary injury in the brain. 234 Therefore, BBB disruption may contribute to long-term transporter changes even after its resolution after TBI. CONCLUSION From the information presented in this review (summarized in Table 1), it is evident that Ab accumulation in the CNS can be both a cause and consequence of BBB dysfunction in AD.…”

Section: Alzheimer's Disease Risk Factors and The Blood-brain Barriermentioning

confidence: 99%

“…However, early pathologies caused by transient opening of the BBB also influence secondary injury in the brain. 234 Therefore, BBB disruption may contribute to long-term transporter changes even after its resolution after TBI. Cardiovascular Disease Cardiovascular disease is a risk factor for AD, and is associated with other AD risk factors such as diabetes and obesity.…”

Section: Alzheimer's Disease Risk Factors and The Blood-brain Barriermentioning

confidence: 99%

See 1 more Smart Citation

Blood–Brain Barrier Dysfunction as a Cause and Consequence of Alzheimer's Disease

Erickson

Banks

2013

J Cereb Blood Flow Metab

476

363

View full text Add to dashboard Cite

The blood-brain barrier (BBB) plays critical roles in the maintenance of central nervous system (CNS) homeostasis. Dysfunction of the BBB occurs in a number of CNS diseases, including Alzheimer's disease (AD). A prevailing hypothesis in the AD field is the amyloid cascade hypothesis that states that amyloid-b (Ab) deposition in the CNS initiates a cascade of molecular events that cause neurodegeneration, leading to AD onset and progression. In this review, the participation of the BBB in the amyloid cascade and in other mechanisms of AD neurodegeneration will be discussed. We will specifically focus on three aspects of BBB dysfunction: disruption, perturbation of transporters, and secretion of neurotoxic substances by the BBB. We will also discuss the interaction of the BBB with components of the neurovascular unit in relation to AD and the potential contribution of AD risk factors to aspects of BBB dysfunction. From the results discussed herein, we conclude that BBB dysfunction contributes to AD through a number of mechanisms that could be initiated in the presence or absence of Ab pathology. Keywords: Alzheimer's disease; blood-brain barrier; cerebrospinal fluid; diabetes; inflammation; neurovascular unit INTRODUCTION Alzheimer's disease (AD) is the most common type of dementia, and affects B36 million individuals worldwide (http://www.alz. co.uk/research/world-report). The majority of individuals afflicted with AD initially present with symptoms of memory loss and cognitive impairment late in life (Z65 years old). These symptoms increase in severity as AD progresses, often become so debilitating that institutionalization is necessary, and are eventually fatal. Therefore, AD is a disease with tremendous socioeconomic cost. Because of the growing aged population and lack of treatments that can prevent or slow disease progression, future AD prevalence is expected to increase to an extent that it may threaten the sustainability of healthcare systems worldwide. This necessitates a global effort to better understand AD, with the goal of developing treatments that can prevent or slow AD progression. Journal of Cerebral BloodMuch of the focus in AD research has been on amyloid-b peptide (Ab) and tau, which are the protein constituents of the hallmark senile plaques and neurofibrillary tangles that pathologically define AD. The amyloid cascade hypothesis, initially proposed by Hardy and Higgins in 1992, 1 updated by Hardy and Selkoe in 2002, 2 and still a prevalent focus of AD research today, states that deposition of Ab in the brain is the initiating event in AD. Although the hypothesis remains generally accepted, it is also increasingly evident that Ab plays a complex, multifaceted role in AD progression. In rare, familial forms of AD, mutations in the Ab precursor protein (APP) or in presenilin proteins, the enzymes that cleave Ab from APP, cause increased Ab deposition. In the remainder of AD cases, it is thought that Ab deposition results from deficient clearance. 2 Multiple routes of clearance have been elucidat...

show abstract

Section: Alzheimer's Disease Risk Factors and The Blood-brain Barriermentioning

confidence: 99%

“…However, early pathologies caused by transient opening of the BBB also influence secondary injury in the brain. 234 Therefore, BBB disruption may contribute to long-term transporter changes even after its resolution after TBI. Cardiovascular Disease Cardiovascular disease is a risk factor for AD, and is associated with other AD risk factors such as diabetes and obesity.…”

Section: Alzheimer's Disease Risk Factors and The Blood-brain Barriermentioning

confidence: 99%

Blood–Brain Barrier Dysfunction as a Cause and Consequence of Alzheimer's Disease

Erickson

Banks

2013

J Cereb Blood Flow Metab

476

363

View full text Add to dashboard Cite

show abstract

“…10 One mechanism underlying cytotoxic oedema is the perihaematomal accumulation of glutamate, which can lead to mitochondrial dysfunction and failure of cellular pumps. 16 Cytotoxic oedema does not directly cause tissue swelling, but creates a new transendothelial gradient of sodium that contributes to the osmotic force that drives ionic oedema. 10 The osmotic gradients created by clot retraction and cytotoxic oedema result in movement of water into the interstitial space.…”

Section: Pathophysiology Of Phomentioning

confidence: 99%

Targeting secondary injury in intracerebral haemorrhage—perihaematomal oedema

et al. 2015

View full text Add to dashboard Cite

Perihaematomal oedema (PHO) is an important pathophysiological marker of secondary injury in intracerebral haemorrhage (ICH). In this Review, we describe a novel method to conceptualize PHO formation within the framework of Starling's principle of movement of fluid across a capillary wall. We consider progression of PHO through three stages, characterized by ionic oedema (stage 1) and progressive vasogenic oedema (stages 2 and 3). In this context, possible modifiers of PHO volume and their value in identifying patients who would benefit from therapies that target secondary injury are discussed; the practicalities of using neuroimaging to measure PHO volume are also considered. We examine whether PHO can be used as a predictor of neurological outcome following ICH, and we provide an overview of emerging therapies. Our discussion emphasizes that PHO has clinical relevance both as a therapeutic target, owing to its augmentation of the mass effect of a haemorrhage, and as a surrogate marker for novel interventions that target secondary injury.

show abstract

“…Currently, clinical risk assessment tool such as National Institutes of Health Stroke Scale (NIHSS) score is the most commonly used method of risk stratification for ICH [7,17]. Nevertheless, some circulating biomarkers have shown some promise as prognostic predictors of ICH and also become the subject of research in recent years [2,12].…”

Section: Introductionmentioning

confidence: 99%

Neuropeptide proenkephalin A is associated with in-hospital mortality in patients with acute intracerebral hemorrhage

Yang¹,

An²,

Zhang

2014

Peptides

View full text Add to dashboard Cite

Serum biomarkers of spontaneous intracerebral hemorrhage induced secondary brain injury

Cited by 57 publications

References 119 publications

Blood–Brain Barrier Dysfunction as a Cause and Consequence of Alzheimer's Disease

Blood–Brain Barrier Dysfunction as a Cause and Consequence of Alzheimer's Disease

Targeting secondary injury in intracerebral haemorrhage—perihaematomal oedema

Neuropeptide proenkephalin A is associated with in-hospital mortality in patients with acute intracerebral hemorrhage

Contact Info

Product

Resources

About