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https://www.readbyqxmd.com/read/29050387/temporal-lobe-networks-supporting-the-comprehension-of-spoken-words
#1
Leonardo Bonilha, Argye E Hillis, Gregory Hickok, Dirk B den Ouden, Chris Rorden, Julius Fridriksson
Auditory word comprehension is a cognitive process that involves the transformation of auditory signals into abstract concepts. Traditional lesion-based studies of stroke survivors with aphasia have suggested that neocortical regions adjacent to auditory cortex are primarily responsible for word comprehension. However, recent primary progressive aphasia and normal neurophysiological studies have challenged this concept, suggesting that the left temporal pole is crucial for word comprehension. Due to its vasculature, the temporal pole is not commonly completely lesioned in stroke survivors and this heterogeneity may have prevented its identification in lesion-based studies of auditory comprehension...
September 1, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/29050191/-the-ocular-involvement-in-the-transthyretin-related-familial-amyloid-polyneuropathy
#2
H Y Lin, R P Dai
Transthyretin (TTR)-related familial amyloid polyneuropathy (FAP), which is caused by mutant TTR, is a rare but fatal autosomal dominant disease. TTR is synthesized by the liver (95%) , the choroid plexus of the brain and the retinal pigment epithelium. FAP leads to peripheral neuropathy, and the main ocular manifestations are vitreous opacity (yellowish cotton-like), secondary glaucoma and keratoconjunctivitis sicca. Liver transplantation has proven to be the most effective treatment for TTR-FAP. Nowadays, tafamidis is the only drug approved for TTR-FAP (early stage)...
October 11, 2017: [Zhonghua Yan Ke za Zhi] Chinese Journal of Ophthalmology
https://www.readbyqxmd.com/read/29050158/-ct-perfusion-analysis-on-the-association-of-permeability-surface-with-hematoma-and-edema-volume-in-acute-spontaneous-putaminal-and-thalamic-hematoma
#3
H L Xu, J C Wang, Y Zhang, S L Liu, W W He, X T Qin, G Q Cao, Y J Yang, Q C Zhuge, W J Chen
Objective: To discuss the correlation of permeability surface (PS) with hematoma and edema volume in acute spontaneous putaminal and thalamic hematoma using CT perfusion imaging. Methods: A total of 48 acute spontaneous putaminal and thalamic hemorrhage patients were enrolled in this study during October 2015 and December 2016 at the First Affiliated Hospital of Wenzhou Medical University. At the image slice with maximum size of hematoma, PS was measured by drawing various regions of interest (ROI) including"hot spots", perihematomal regions, outward regions, hemisphere regions and contralateral mirror regions...
October 10, 2017: Zhonghua Yi Xue za Zhi [Chinese medical journal]
https://www.readbyqxmd.com/read/29049987/isoflavones-induce-bex2-dependent-autophagy-to-prevent-atr-induced-neurotoxicity-in-sh-sy5y-cells
#4
Peng Li, Kun Ma, Hao-Yu Wu, Yan-Ping Wu, Bai-Xiang Li
BACKGROUND/AIMS: Atrazine (ATR) is a broad-spectrum herbicide in wide use around the world. However, ATR is neurotoxic and can cause cell death in dopaminergic neurons, leading to neurodegenerative disorders. Autophagy is the basic cellular catabolic process involving the degradation of proteins and damaged organelles. Studies have shown that certain plant compounds can induce autophagy and prevent neuronal cell death. This prompted us to investigate plant compounds that might reduce the neurotoxic effects of ATR...
October 19, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29049976/sodium-valproate-enhances-doxorubicin-induced-cognitive-dysfunction-in-wistar-rats
#5
Thaneshwar Verma, Sanchari Basu Mallik, G V Ramalingayya, Pawan G Nayak, Anoop Kishore, K Sreedhara R Pai, Krishnadas Nandakumar
BACKGROUND: Increasing number of scientific reports have highlighted the role of histone acetylation/deacetylation in neurodegenerative conditions, including chemotherapy-induced cognitive dysfunction (also known as chemobrain). Multiple sources state that increased activity of histone deacetylases (HDACs) play a detrimental role in chemobrain. In the present study, sodium valproate, a well-known HDAC inhibitor, was explored for its neuroprotective potential against chemobrain development...
October 16, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29048371/znt3-gene-deletion-reduces-colchicine-induced-dentate-granule-cell-degeneration
#6
Bo Young Choi, Dae Ki Hong, Sang Won Suh
Our previous study demonstrated that colchicine-induced dentate granule cell death is caused by blocking axonal flow and the accumulation of intracellular zinc. Zinc is concentrated in the synaptic vesicles via zinc transporter 3 (ZnT3), which facilitates zinc transport from the cytosol into the synaptic vesicles. The aim of the present study was to identify the role of ZnT3 gene deletion on colchicine-induced dentate granule cell death. The present study used young (3-5 months) mice of the wild-type (WT) or the ZnT3(-)(/)(-) genotype...
October 19, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29047291/recurrent-moderate-hypoglycemia-exacerbates-oxidative-damage-and-neuronal-death-leading-to-cognitive-dysfunction-after-the-hypoglycemic-coma
#7
Gabriela Languren, Teresa Montiel, Leticia Ramírez-Lugo, Israela Balderas, Gustavo Sánchez-Chávez, Francisco Sotres-Bayón, Federico Bermúdez-Rattoni, Lourdes Massieu
Moderate recurrent hypoglycemia (RH) is frequent in Type 1 diabetes mellitus (TIDM) patients who are under intensive insulin therapy increasing the risk for severe hypoglycemia (SH). The consequences of RH are not well understood and its repercussions on neuronal damage and cognitive function after a subsequent episode of SH have been poorly investigated. In the current study, we have addressed this question and observed that previous RH during seven consecutive days exacerbated oxidative damage and neuronal death induced by a subsequent episode of SH accompanied by a short period of coma, in the parietal cortex, the striatum and mainly in the hippocampus...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/29046700/cerebral-ischemic-injury-decreases-%C3%AE-synuclein-expression-in-brain-tissue-and-glutamate-exposed-ht22-cells
#8
Phil-Ok Koh
α-Synuclein is abundantly expressed in neuronal tissue, plays an essential role in the pathogenesis of neurodegenerative disorders, and exerts a neuroprotective effect against oxidative stress. Cerebral ischemia causes severe neurological disorders and neuronal dysfunction. In this study, we examined α-synuclein expression in middle cerebral artery occlusion (MCAO)-induced cerebral ischemic injury and neuronal cells damaged by glutamate treatment. MCAO surgical operation was performed on male Sprague-Dawley rats, and brain samples were isolated 24 hours after MCAO...
September 2017: Laboratory Animal Research
https://www.readbyqxmd.com/read/29046694/hyperglycemia-exacerbates-downregulation-of-dynamin-like-protein-1-in-ischemic-cerebral-injury
#9
Dong-Ju Park, Myeong-Ok Kim, Phil-Ok Koh
Ischemic stroke is one of the leading causes of adult disability and death. Hyperglycemia is associated with an increased risk of stroke and poor outcomes after brain injury. Dynamin-like protein I (DLP-1) regulates mitochondrial fission and promotes mitochondrial dynamics. Neurodegenerative diseases are associated with mitochondrial dysfunction, and the downregulation of DLP-1 has been previously identified in a stroke animal model. Here, we investigated the changes in DLP-1 protein expression in an animal model of focal cerebral ischemia with induced hyperglycemia...
September 2017: Laboratory Animal Research
https://www.readbyqxmd.com/read/29046426/phosphorylation-of-connexin-43-induced-by-traumatic-brain-injury-promotes-exosome-release
#10
Wei Chen, Yijun Guo, Wenjin Yang, Lei Chen, Dabin Ren, Chenxing Wu, Bin He, Ping Zheng, Wusong Tong
Traumatic brain injury (TBI) caused by the external force leads to the neuronal dysfunction and even death. TBI has been reported to significantly increase the phosphorylation of glial gap junction protein connexin 43 (Cx43), which in turn propagates damages into surrounding brain tissues. However, the neuroprotective and anti-apoptosis effects of glia-derived exosomes have also been implicated in recent studies. Therefore, we detected whether TBI-induced phosphorylation of Cx43 would promote exosome release in rat brain...
October 18, 2017: Journal of Neurophysiology
https://www.readbyqxmd.com/read/29046153/potential-therapeutics-for-vascular-cognitive-impairment-and-dementia
#11
Miao-Kun Sun
As the human lifespan increases, the number of people affected by age-related dementia is growing at an epidemic pace. Vascular pathology dramatically affects cognitive profiles, resulting in dementia and cognitive impairment. While vascular dementia itself constitutes a medical challenge, hypoperfusion/vascular risk factors enhance amyloid toxicity and other memory-damaging factors and hasten Alzheimer's disease (AD) and other memory disorders' progression, as well as negatively affect treatment outcome. Few therapeutic options are, however, currently available to improve the prognosis of patients with vascular dementia and cognitive impairment, mixed AD dementia with vascular pathology, or other memory disorders...
October 16, 2017: Current Neuropharmacology
https://www.readbyqxmd.com/read/29045497/ceftriaxone-and-n-acetylcysteine-induced-brain-tolerance-to-ischemia-influence-on-glutamate-levels-in-focal-cerebral-ischemia
#12
Weronika Krzyżanowska, Bartosz Pomierny, Beata Bystrowska, Lucyna Pomierny-Chamioło, Małgorzata Filip, Bogusława Budziszewska, Joanna Pera
One of the major players in the pathophysiology of cerebral ischemia is disrupted homeostasis of glutamatergic neurotransmission, resulting in elevated extracellular glutamate (Glu) concentrations and excitotoxicity-related cell death. In the brain, Glu concentrations are regulated by Glu transporters, including Glu transporter-1 (GLT-1) and cystine/Glu antiporter (system xc-). Modulation of these transporters by administration of ceftriaxone (CEF, 200 mg/kg, i.p.) or N-acetylcysteine (NAC, 150 mg/kg, i.p.) for 5 days before focal cerebral ischemia may induce brain tolerance to ischemia by significantly limiting stroke-related damage and normalizing Glu concentrations...
2017: PloS One
https://www.readbyqxmd.com/read/29044654/animal-models-of-neuroinflammation-secondary-to-acute-insults-originated-outside-the-brain
#13
REVIEW
Mike Yoshio Hamasaki, Marcel Cerqueira César Machado, Fabiano Pinheiro da Silva
The term "neuroinflammation" has been widely used to describe a series of acute or chronic conditions that cause inflammation in the central nervous system (CNS). Neurological damage can be a consequence of direct local injury or, secondary, of systemic or even distant inflammatory processes. In this respect, animal models have been developed to better understand the pathophysiology and, possibly, to evaluate more effective methods of treatment for these disorders. Animal models that promote alterations in blood-brain barrier permeability-the activation of microglia or astrocytes, modifications in neuropeptide expression, oxidative stress, increased apoptosis, release of inflammatory mediators, leukocyte infiltration, and brain edema-are likely to involve neuroinflammation and therefore can serve as useful models for human inflammatory CNS injury...
October 16, 2017: Journal of Neuroscience Research
https://www.readbyqxmd.com/read/29042874/serum-neuron-specific-enolase-is-increased-in-pediatric-acute-encephalitis-syndrome
#14
Dian Pratamastuti, Prastiya Indra Gunawan, Darto Saharso
PURPOSE: This study aimed to investigate whether serum neuron-specific enolase (NSE) was expressed in acute encephalitis syndrome (AES) that causes neuronal damage in children. METHODS: This prospective observational study was conducted in the pediatric neurology ward of Soetomo Hospital. Cases of AES with ages ranging from 1 month to 12 years were included. Cases that were categorized as simple and complex febrile seizures constituted the non-AES group. Blood was collected for the measurement of NSE within 24 hours of hemodynamic stabilization...
September 2017: Korean Journal of Pediatrics
https://www.readbyqxmd.com/read/29042526/-differential-diagnosis-of-immune-mediated-encephalopathies-neurological-symptoms-of-diffuse-brain-damage-a-new-concept
#15
Yoshimitsu Maki, Hiroshi Takashima
In recent years, incidence of autoimmune encephalopathies has increased. The diagnosis of the severe form of autoimmune encephalopathy is not difficult; however, milder forms can be misdiagnosed as general encephalopathies. We often treat Hashimoto's encephalopathy, which has diverse clinical symptoms and is often misdiagnosed as a psychosomatic disease. We have found that the neurological findings and symptoms of patients with Hashimoto's encephalopathy are similar to those of psychogenic diseases, such as giveway weakness and atypical sensory disorder...
October 2017: Brain and Nerve, Shinkei Kenkyū No Shinpo
https://www.readbyqxmd.com/read/29042514/neuron-specific-methylome-analysis-reveals-epigenetic-regulation-and-tau-related-dysfunction-of-brca1-in-alzheimer-s-disease
#16
Tatsuo Mano, Kenichi Nagata, Takashi Nonaka, Airi Tarutani, Tomohiro Imamura, Tadafumi Hashimoto, Taro Bannai, Kagari Koshi-Mano, Takeyuki Tsuchida, Ryo Ohtomo, Junko Takahashi-Fujigasaki, Satoshi Yamashita, Yasumasa Ohyagi, Ryo Yamasaki, Shoji Tsuji, Akira Tamaoka, Takeshi Ikeuchi, Takaomi C Saido, Takeshi Iwatsubo, Toshikazu Ushijima, Shigeo Murayama, Masato Hasegawa, Atsushi Iwata
Alzheimer's disease (AD) is a chronic neurodegenerative disease characterized by pathology of accumulated amyloid β (Aβ) and phosphorylated tau proteins in the brain. Postmortem degradation and cellular complexity within the brain have limited approaches to molecularly define the causal relationship between pathological features and neuronal dysfunction in AD. To overcome these limitations, we analyzed the neuron-specific DNA methylome of postmortem brain samples from AD patients, which allowed differentially hypomethylated region of the BRCA1 promoter to be identified...
October 17, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29042259/widespread-optogenetic-expression-in-macaque-cortex-obtained-with-mr-guided-convection-enhanced-delivery-ced-of-aav-vector-to-the-thalamus
#17
Azadeh Yazdan-Shahmorad, Nan Tian, Viktor Kharazia, Lluis Samaranch, Adrian Kells, John Bringas, Jiwei He, Krystof Bankiewicz, Philip N Sabes
BACKGROUND: In non-human primate (NHP) optogenetics, infecting large cortical areas with viral vectors is often a difficult and time-consuming task. Previous work has shown that parenchymal delivery of adeno-associated virus (AAV) in the thalamus by convection-enhanced delivery (CED) can lead to large-scale transduction via axonal transport in distal areas including cortex. We used this approach to obtain widespread cortical expression of light-sensitive ion channels. NEW METHOD: AAV vectors co-expressing channelrhodopsin-2 (ChR2) and yellow fluorescent protein (YFP) genes were infused into thalamus of three rhesus macaques under MR-guided CED...
October 14, 2017: Journal of Neuroscience Methods
https://www.readbyqxmd.com/read/29042248/the-antidepressant-and-anxiolytic-like-effects-of-fluoxetine-and-clozapine-in-chronically-isolated-rats-involve-inhibition-of-hippocampal-tnf-%C3%AE
#18
Nevena Todorović, Dragana Filipović
Brain oxidative stress and neuroinflammation are implicated in psychiatric disorders. Thus, it is important to investigate the effects of individual psychotropic agents on antioxidative defense and proinflammatory mediators in brain regions associated with these disorders. Psychosocial stress is recognized as a threat to mental health, and the hippocampus is a primary target of stress-related damage. Chronic social isolation (CSIS) is a mild psychosocial stress used to model the pathophysiology of depression...
October 14, 2017: Pharmacology, Biochemistry, and Behavior
https://www.readbyqxmd.com/read/29041864/targets-of-therapy-in-progressive-ms
#19
Hans Lassmann
Highly effective anti-inflammatory therapies have so far been developed for patients with relapsing/remitting multiple sclerosis, which also show some benefits in the early progressive stage of the disease. However, treatment options for patients, who have entered the progressive phase, are still limited. Disease starts as an inflammatory process, which induces focal demyelinating lesions in the gray and white matter. This stage of the disease dominates in the relapsing phase, extends into the early stages of progressive disease, and can be targeted by current anti-inflammatory treatments...
October 2017: Multiple Sclerosis: Clinical and Laboratory Research
https://www.readbyqxmd.com/read/29040306/micheliolide-suppresses-lps-induced-neuroinflammatory-responses
#20
Zhaomeng Sun, Guodong Li, Tanjun Tong, Jun Chen
Microglia-involved neuroinflammation is thought to promote brain damage in various neurodegenerative disorders. Thus, inhibition of microglial over-activation may have a therapeutic benefit for the treatment of neurodegenerative disorders. Micheliolide (MCL) is a sesquiterpene lactone which inhibits various inflammatory response. However, whether MCL can inhibit neuroinflammation caused by LPS-activated BV2 microglia has not yet been explored. In this study, we demonstrated that treatment of BV2 cells with MCL significantly repressed LPS-stimulated nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression, as well as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and nitric oxide (NO) induction...
2017: PloS One
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