New Perspectives on Amyloid-β Dynamics After Acute Brain Injury

Magnoni, Sandra; Brody, David L.

doi:10.1001/archneurol.2010.214

Cited by 60 publications

(31 citation statements)

References 40 publications

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“…The accumulation of these factors is believed to be due to impaired axonal transport due to trauma, and it may lead to APP proteolysis and Aβ formation within the axonal membrane compartment [ 194 ]. Post-concussive Aβ plaque formation may help to explain the increased risk of Alzheimer disease after mild TBI through acceleration of the postulated amyloid cascade [ 195 ].…”

Section: Chronic Traumatic Encephalopathy and Late Risk Of Dementiamentioning

confidence: 99%

The Pathophysiology of Concussions in Youth

Shrey

Griesbach²,

Giza

2011

Physical Medicine and Rehabilitation Clinics of North America

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SYNOPSIS Mild traumatic brain injury, especially sport-related concussion, is particularly common among young persons. Consequences of transient pathophysiological dysfunction must be carefully considered in the context of a developing or immature brain, as must the potential for an accumulation of damage with repeated exposure over time. This review will summarize the underlying neurometabolic cascade of concussion with emphasis on the young brain in terms of acute pathophysiology, vulnerability, alterations in plasticity and activation, axonal injury, and cumulative risk from chronic, repetitive damage. The implications of these physiological changes will be discussed in the context of clinical care for the concussed youth, and areas for future investigation will be highlighted.

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Section: Chronic Traumatic Encephalopathy and Late Risk Of Dementiamentioning

confidence: 99%

The Pathophysiology of Concussions in Youth

Shrey

Griesbach²,

Giza

2011

Physical Medicine and Rehabilitation Clinics of North America

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“…One of the primary causes of CNS neuronal damage is trauma to the brain which can initiate chronic molecular events that may be important epigenetic factors that predispose an individual to neurodegenerative conditions such as Alzheimer's disease [39, 40], Parkinson's disease [41], and ALS [42, 43], at a later time in life [44–46]. Emerging evidence also suggests that mild traumatic brain injury (TBI), which consists of concussive and mild concussive trauma, such as those encountered during sporting activities, can provoke a distinctive neurodegenerative state known as chronic traumatic encephalopathy (CTE) [47–49].…”

Section: Neuronal Damage Arising From Traumamentioning

confidence: 99%

The Emerging Use ofIn VivoOptical Imaging in the Study of Neurodegenerative Diseases

Patterson

Booth

Saba

2014

BioMed Research International

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The detection and subsequent quantification of photons emitted from living tissues, using highly sensitive charged-couple device (CCD) cameras, have enabled investigators to noninvasively examine the intricate dynamics of molecular reactions in wide assortment of experimental animals under basal and pathophysiological conditions. Nevertheless, extrapolation of this in vivo optical imaging technology to the study of the mammalian brain and related neurodegenerative conditions is still in its infancy. In this review, we introduce the reader to the emerging use of in vivo optical imaging in the study of neurodegenerative diseases. We highlight the current instrumentation that is available and reporter molecules (fluorescent and bioluminescent) that are commonly used. Moreover, we examine how in vivo optical imaging using transgenic reporter mice has provided new insights into Alzheimer's disease, amyotrophic lateral sclerosis (ALS), Prion disease, and neuronal damage arising from excitotoxicity and inflammation. Furthermore, we also touch upon studies that have utilized these technologies for the development of therapeutic strategies for neurodegenerative conditions that afflict humans.

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“…In severe TBI, one study found decreased brain extracellular concentration of A β , a finding that may indicate TBI-induced suppression of neuronal activity [10]. In peripheral blood samples, only one study has linked A β to TBIs, with higher concentrations in the blood during the acute recovery period after severe TBIs and the highest concentrations correlating with mortality risk [11].…”

Section: Introductionmentioning

confidence: 99%

Active duty service members who sustain a traumatic brain injury have chronically elevated peripheral concentrations of Aβ40 and lower ratios of Aβ42/40

et al. 2016

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Primary objective: Excessive accumulation of amyloid beta (Aβ) and tau have been observed in older individuals with chronic neurological symptoms related to a traumatic brain injury (TBI), yet little is known about the possible role of Aβ in younger active duty service members following a TBI. The purpose of the study was to determine if Aβ 40 or 42 related to sustaining a TBI or to chronic neurological symptoms in a young cohort of military personnel. Research design: This was a cross-sectional study of active duty service members who reported sustaining a TBI and provided self-report of neurological and psychological symptoms and provided blood. Methods and procedures: An ultrasensitive single-molecule enzyme-linked immunosorbent assay was used to compare concentrations of Aβ in active duty service members with (TBI+; n = 53) and without (TBI–; n = 18) a history of TBI. Self-report and medical history were used to measure TBI occurrence and approximate the number of total TBIs and the severity of TBIs sustained during deployment. Main outcomes and results: This study reports that TBI is associated with higher concentrations of Aβ40 (F 1,68 = 6.948, p = 0.009) and a lower ratio of Aβ42/Aβ40 (F 1,62 = 5.671, p = 0.020). These differences remained significant after controlling for co-morbid symptoms of post-traumatic stress disorder and depression. Conclusions: These findings suggest that alterations in Aβ relate to TBIs and may contribute to chronic neurological symptoms.

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New Perspectives on Amyloid-β Dynamics After Acute Brain Injury

Cited by 60 publications

References 40 publications

The Pathophysiology of Concussions in Youth

The Pathophysiology of Concussions in Youth

The Emerging Use ofIn VivoOptical Imaging in the Study of Neurodegenerative Diseases

Active duty service members who sustain a traumatic brain injury have chronically elevated peripheral concentrations of Aβ40 and lower ratios of Aβ42/40

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