Accumulation of amyloid in cognitive impairment after mild traumatic brain injury

Yang, Shung Tai; Hsiao, Ing‐Tsung; Hsieh, Chia-Ju; Chiang, Yung Hsiao; Yen, Tzu Chen; Chiu, Wen Ta; Lin, Kun-Ju; Hu, Chaur Jong

doi:10.1016/j.jns.2014.12.032

Cited by 49 publications

(43 citation statements)

References 37 publications

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“…Such findings demonstrate the long-term consequences of a single TBI event [145]. Another study where TBI patients underwent minimental state examination, apolipoprotein E genotyping, and amyloid-PET found an increase of amyloid accumulation and allele frequency of APOE4 in the mild TBI patients with cognitive impairment [146]. In transgenic mice models of AD, several studies have investigated A β after experimental brain injury in transgenic mice, reporting both increased and decreased plaque loads [147, 148].…”

Section: Tbi As a Risk Factor For Neurological Disease: Role Of Nmmentioning

confidence: 99%

Role of NMDA Receptor-Mediated Glutamatergic Signaling in Chronic and Acute Neuropathologies

2016

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N-Methyl-D-aspartate receptors (NMDARs) have two opposing roles in the brain. On the one hand, NMDARs control critical events in the formation and development of synaptic organization and synaptic plasticity. On the other hand, the overactivation of NMDARs can promote neuronal death in neuropathological conditions. Ca2+ influx acts as a primary modulator after NMDAR channel activation. An imbalance in Ca2+ homeostasis is associated with several neurological diseases including schizophrenia, Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. These chronic conditions have a lengthy progression depending on internal and external factors. External factors such as acute episodes of brain damage are associated with an earlier onset of several of these chronic mental conditions. Here, we will review some of the current evidence of how traumatic brain injury can hasten the onset of several neurological conditions, focusing on the role of NMDAR distribution and the functional consequences in calcium homeostasis associated with synaptic dysfunction and neuronal death present in this group of chronic diseases.

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Section: Tbi As a Risk Factor For Neurological Disease: Role Of Nmmentioning

confidence: 99%

Role of NMDA Receptor-Mediated Glutamatergic Signaling in Chronic and Acute Neuropathologies

2016

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“…In TBI patients with cognitive impairment, increase in the accumulation of amyloid and allele frequency of APOE4 was observed (Walker et al, 2012;Yang et al, 2015). Also, β-secretase, presenilin 1, and caspase 3 accumulate up to 6 months after injury (Chen et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective properties of mitochondria-targeted antioxidants of the SkQ-type

Isaev

Stelmashook

Генрихс

et al. 2016

Reviews in the Neurosciences

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AbstractIn 2008, using a model of compression brain ischemia, we presented the first evidence that mitochondria-targeted antioxidants of the SkQ family, i.e. SkQR1 [10-(6′-plastoquinonyl)decylrhodamine], have a neuroprotective action. It was shown that intraperitoneal injections of SkQR1 (0.5–1 μmol/kg) 1 day before ischemia significantly decreased the damaged brain area. Later, we studied in more detail the anti-ischemic action of this antioxidant in a model of experimental focal ischemia provoked by unilateral intravascular occlusion of the middle cerebral artery. The neuroprotective action of SkQ family compounds (SkQR1, SkQ1, SkQTR1, SkQT1) was manifested through the decrease in trauma-induced neurological deficit in animals and prevention of amyloid-β-induced impairment of long-term potentiation in rat hippocampal slices. At present, most neurophysiologists suppose that long-term potentiation underlies cellular mechanisms of memory and learning. They consider inhibition of this process by amyloid-β1-42 as an in vitro model of memory disturbance in Alzheimer’s disease. Further development of the above studies revealed that mitochondria-targeted antioxidants could retard accumulation of hyperphosphorylated τ-protein, as well as amyloid-β1-42, and its precursor APP in the brain, which are involved in developing neurodegenerative processes in Alzheimer’s disease.

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“…More promising is the demonstration of amyloid deposition by compounds such as Pittsburgh compound B (PiB) and F-Florbetapir [101,102]. Aβ plaques appear acutely after injury and deposition in the cortical gray matter and striatum of patients following injury and may persist even after a single injury [103].…”

Section: Do Damaged Axons Contribute To Development Of Dementia?mentioning

confidence: 99%

“…Aβ plaques appear acutely after injury and deposition in the cortical gray matter and striatum of patients following injury and may persist even after a single injury [103]. Using F-Flobetapri, Yang et al demonstrated greater amyloid deposition in patients who had sustained mTBI with cognitive impairment as compared to those without cognitive impairment and uninjured controls, suggesting that Aβ accumulation does in fact play a significant role in the development of mTBI symptomatology [102]. Being able to quantify these pathological changes will significantly aid in many aspects of concussion management.…”

Section: Do Damaged Axons Contribute To Development Of Dementia?mentioning

confidence: 99%

The Pathophysiology of Concussion

Choe

2016

Curr Pain Headache Rep

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Concussion is a significant issue in medicine and the media today. With growing interest on the long-term effects of sports participation, it is important to understand what occurs in the brain after an impact of any degree. While some of the basic pathophysiology has been elucidated, much is still unknown about what happens in the brain after traumatic brain injury, particularly with milder injuries where no damage can be seen at the structural level on standard neuroimaging. Understanding the chain of events from a cellular level using studies investigating more severe injuries can help to drive research efforts in understanding the symptomatology that is seen in the acute phase after concussion, as well as point to mechanisms that may underlie persistent post-concussive symptoms. This review discusses the basic neuropathology that occurs after traumatic brain injury at the cellular level. We also present the pathology of chronic traumatic encephalopathy and its similarities to other neurodegenerative diseases. We conclude with recent imaging and biomarker findings looking at changes that may occur after repeated subconcussive blows, which may help to guide efforts in understanding if cumulative subconcussive mechanical forces upon the brain are detrimental in the long term or if concussive symptoms mark the threshold for brain injury.

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Accumulation of amyloid in cognitive impairment after mild traumatic brain injury

Cited by 49 publications

References 37 publications

Role of NMDA Receptor-Mediated Glutamatergic Signaling in Chronic and Acute Neuropathologies

Role of NMDA Receptor-Mediated Glutamatergic Signaling in Chronic and Acute Neuropathologies

Neuroprotective properties of mitochondria-targeted antioxidants of the SkQ-type

The Pathophysiology of Concussion

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