Detection of brain amyloid β deposition in patients with neuropsychological impairment after traumatic brain injury: PET evaluation using Pittsburgh Compound-B

Kawai, Nobuyuki; Kawanishi, Masahiko; Kudomi, Nobuyuki; Maeda, Yukito; Yamamoto, Yuka; Nishiyama, Yoshihiro; Tamiya, Takashi

doi:10.3109/02699052.2013.794963

Cited by 50 publications

(46 citation statements)

References 25 publications

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“…[55][56][57][58][59] Alpha-synuclein is significantly increased in TBI patient cerebrospinal fluid. 60 Deposition of aberrant proteins is seen in TBI animal models and patients.…”

Section: Fig 2 Electron Micrographs Of Neocortical Neurons After Trmentioning

confidence: 99%

“…60 Deposition of aberrant proteins is seen in TBI animal models and patients. 55,57 CMA is a major cellular system for removal of a-synuclein, Tau, huntingtin, ubiquitin carboxyl-terminal esterase L1, calcineurin 1, and the cytoplasmic tail of amyloid precursor protein. 58,61 Many of these neurodegenerative disease-related proteins can act as CMA inhibitors and thus compromise CMA.…”

Section: Fig 2 Electron Micrographs Of Neocortical Neurons After Trmentioning

confidence: 99%

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Chaperone-Mediated Autophagy after Traumatic Brain Injury

Park

Liu

Luo

et al. 2015

Journal of Neurotrauma

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Chaperone-mediated autophagy (CMA) and the ubiquitin-proteasomal system (UPS) are two major protein degradation systems responsible for maintaining cellular homeostasis, but how these two systems are regulated after traumatic brain injury (TBI) remains unknown. TBI produces primary mechanical damage that must be repaired to maintain neuronal homeostasis. The level of lysosomal-associated membrane protein type 2A (LAMP2A) is the hallmark of CMA activity. The level of polyubiquitinated proteins (ubi-proteins) reflects UPS activity. This study utilized a moderate fluid percussion injury model in rats to investigate the changes in CMA and the UPS after TBI. Induction of CMA was manifested by significant upregulation of LAMP2A and secondary lysosomes during the periods of 1-15 days of recovery after TBI. In comparison, the levels of ubiproteins were increased only moderately after TBI. The increases in the levels of LAMP2A and 70 kDa heat-shock protein for CMA after TBI were seen mainly in the secondary lysosome-containing fractions. Confocal and electron microscopy further showed that increased LAMP2A or lysosomes were found mainly in neurons and proliferated microglia. Because CMA and the UPS are two major routes for elimination of different types of cellular aberrant proteins, the consecutive activation of these two pathways may serve as a protective mechanism for maintaining cellular homeostasis after TBI.

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“…[55][56][57][58][59] Alpha-synuclein is significantly increased in TBI patient cerebrospinal fluid. 60 Deposition of aberrant proteins is seen in TBI animal models and patients.…”

Section: Fig 2 Electron Micrographs Of Neocortical Neurons After Trmentioning

confidence: 99%

Section: Fig 2 Electron Micrographs Of Neocortical Neurons After Trmentioning

confidence: 99%

Chaperone-Mediated Autophagy after Traumatic Brain Injury

Park

Liu

Luo

et al. 2015

Journal of Neurotrauma

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“…235 Another study reported [ 11 C] PiB binding in three of 12 patients with neuropsychological impairment studied 5 to 129 months after injury. 236 Further studies will be required to determine the prevalence and time sequence of b-amyloid deposition in TBI, and its relation to degree of initial injury and subsequent impairment.…”

Section: Chronic Tbimentioning

confidence: 99%

A Review of the Effectiveness of Neuroimaging Modalities for the Detection of Traumatic Brain Injury

Amyot

Arciniegas

et al. 2015

Journal of Neurotrauma

183

147

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The incidence of traumatic brain injury (TBI) in the United States was 3.5 million cases in 2009, according to the Centers for Disease Control and Prevention. It is a contributing factor in 30.5% of injury-related deaths among civilians. Additionally, since 2000, more than 260,000 service members were diagnosed with TBI, with the vast majority classified as mild or concussive (76%). The objective assessment of TBI via imaging is a critical research gap, both in the military and civilian communities. In 2011, the Department of Defense (DoD) prepared a congressional report summarizing the effectiveness of seven neuroimaging modalities (computed tomography [CT], magnetic resonance imaging [MRI], transcranial Doppler [TCD], positron emission tomography, single photon emission computed tomography, electrophysiologic techniques [magnetoencephalography and electroencephalography], and functional near-infrared spectroscopy) to assess the spectrum of TBI from concussion to coma. For this report, neuroimaging experts identified the most relevant peer-reviewed publications and assessed the quality of the literature for each of these imaging technique in the clinical and research settings. Although CT, MRI, and TCD were determined to be the most useful modalities in the clinical setting, no single imaging modality proved sufficient for all patients due to the heterogeneity of TBI. All imaging modalities reviewed demonstrated the potential to emerge as part of future clinical care. This paper describes and updates the results of the DoD report and also expands on the use of angiography in patients with TBI.

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“…There have been significant recent advances in detecting and monitoring axonal injury and Aβ deposition in living TBI patients, using imaging techniques typically applied in clinical studies of aging, MCI, and AD: MRI of axonal injury and connectivity (diffuse tensor imaging (DTI) and high definition fiber tractography) (MacDonald et al, 2007, 2011; Presson et al, 2015) as well as amyloid PET (Eisenmenger et al, 2016; Gatson et al, 2016; Hong et al, 2014; Kawai et al, 2013; Mitsis et al, 2014; Scott et al, 2016). Several of these clinical analyses replicate data from histopathology studies.…”

Section: Role Of Aβ and Aging In Primary And Secondary Effects Of mentioning

confidence: 99%

Disordered APP metabolism and neurovasculature in trauma and aging: Combined risks for chronic neurodegenerative disorders

Ikonomović

Abrahamson

2017

Ageing Research Reviews

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Traumatic brain injury (TBI), advanced age, and cerebral vascular disease are factors conferring increased risk for late onset Alzheimer’s disease (AD). These conditions are also related pathologically through multiple interacting mechanisms. The hallmark pathology of AD consists of pathological aggregates of amyloid-β (Aβ) peptides and tau proteins. These molecules are also involved in neuropathology of several other chronic neurodegenerative diseases, and are under intense investigation in the aftermath of TBI as potential contributors to the risk for developing AD and chronic traumatic encephalopathy (CTE). The pathology of TBI is complex and dependent on injury severity, age-at-injury, and length of time between injury and neuropathological evaluation. In addition, the mechanisms influencing pathology and recovery after TBI likely involve genetic/epigenetic factors as well as additional disorders or comorbid states related to age and central and peripheral vascular health. In this regard, dysfunction of the aging neurovascular system could be an important link between TBI and chronic neurodegenerative diseases, either as a precipitating event or related to accumulation of AD-like pathology which is amplified in the context of aging. Thus with advanced age and vascular dysfunction, TBI can trigger self-propagating cycles of neuronal injury, pathological protein aggregation, and synaptic loss resulting in chronic neurodegenerative disease. In this review we discuss evidence supporting TBI and aging as dual, interacting risk factors for AD, and the role of Aβ and cerebral vascular dysfunction in this relationship. Evidence is discussed that Aβ is involved in cyto- and synapto-toxicity after severe TBI, and that its chronic effects are potentiated by aging and impaired cerebral vascular function. From a therapeutic perspective, we emphasize that in the fields of TBI- and aging-related neurodegeneration protective strategies should include preservation of neurovascular function.

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Detection of brain amyloid β deposition in patients with neuropsychological impairment after traumatic brain injury: PET evaluation using Pittsburgh Compound-B

Cited by 50 publications

References 25 publications

Chaperone-Mediated Autophagy after Traumatic Brain Injury

Chaperone-Mediated Autophagy after Traumatic Brain Injury

A Review of the Effectiveness of Neuroimaging Modalities for the Detection of Traumatic Brain Injury

Disordered APP metabolism and neurovasculature in trauma and aging: Combined risks for chronic neurodegenerative disorders

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