Neurological research
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Brain-derived neurotrophic factor (BDNF) is a member of neurotrophins family that plays a pivotal role in memory and learning. Brain-derived neurotrophic factor mediates health benefits of physical activity both in humans and animals. The nerve damage and cognitive impairment in diabetic rats are thought to be the result of reduced BDNF levels. The purpose of this study was to examine the effect of short- and long-term moderate forced exercise on BDNF levels in the hippocampus of type 1 diabetic rats. ⋯ It was shown that spatial memory was improved by the exercise protocol, while the BDNF levels did not change significantly in any group. As a BDNF secretion in the brain is dependent on running paradigm factor, the protocol chosen might not be intensive or long enough to increase the BDNF levels. Exercise may improve spatial memory in type 1 diabetic rats in a way that BDNF is not included.
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Neurological research · Mar 2015
TDP-43 modification in the hSOD1(G93A) amyotrophic lateral sclerosis mouse model.
Amyotrophic lateral sclerosis (ALS) is an adult onset disease that produces gradual motor neuron cell death in the spinal cord (SP). Recently, transactive response DNA-binding protein 43 kDa (TDP-43), a critical component of insoluble ubiquitinated inclusions, has received attention in the treatment of neurodegenerative disorders, including frontotemporal lobar degeneration (FTLD) and ALS. TDP-43 modifications, including hyperphosphorylation, truncation, and ubiquitination, have been reported in the pathogenesis of neurodegenerative diseases (NDs). ⋯ The protein expression level of HO-1 related to oxidative stress was increased in the SP of hSOD1(G93A) Tg relative to non-Tg. We show that an increase of TDP-43 modification, including phosphorylation or truncation, associates with dysfunctional iron homeostasis and an increase in oxidative stress in the SP of symptomatic hSOD1(G93A) Tg. These findings suggest that modified TDP-43 may be involved in motor neuron death in the SP of a SOD1(G93A)-expressing familial ALS (fALS) animal model.
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Neurological research · Feb 2015
ReviewCurrent evidence of temozolomide and bevacizumab in treatment of gliomas.
This review article summarizes in vitro, in vivo, and clinical evidence pertaining to temozolomide (TMZ) and bevacizumab (BEV) efficacy and mechanism of action in gliomas. ⋯ Our collected data support the addition of radiotherapy, BEV, and other targeted agents to TMZ treatment, indicating prolonged survival duration in newly diagnosed patients. However, the optimal regimen for treating high-grade glioma cannot be concluded without more clinical trials.
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Neurological research · Feb 2015
Quantitative analysis of early postoperative cerebral blood flow contributes to the prediction and diagnosis of cerebral hyperperfusion syndrome after revascularization surgery for moyamoya disease.
Cerebral hyperperfusion syndrome (HPS) is a potential complication of extracranial-intracranial (EC-IC) bypass for moyamoya disease; however, the pathological threshold of the early cerebral blood flow (CBF) increases after EC-IC bypass has yet to be determined. The purpose of this study is to evaluate the predictive and diagnostic values of early quantitative CBF analysis for the detection of HPS after EC-IC bypass for moyamoya disease. ⋯ Quantitative analysis of early postoperative CBF is useful for predicting and diagnosing HPS after revascularization surgery for moyamoya disease.
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Neurological research · Jan 2015
Multicenter StudyPreexisting dual antiplatelet treatment increases the risk of post-thrombolysis intracranial hemorrhage in Chinese stroke patients.
Previous studies have shown conflicting results on the use of antiplatelet (AP) agent and its risk of symptomatic intracerebral hemorrhage (sICH) following thrombolysis for acute ischemic stroke. Our study was to explore the safety of intravenous (IV) thrombolysis in Chinese stroke patients who were on AP prior to stroke. ⋯ The risk of developing sICH is low when thrombolysis is given to patients who are on ASA alone. However, there is potential increased risk of sICH if a patient is on dual AP treatment.