Showing papers in "Experimental Neurology in 2017"

TL;DR: It is concluded that alpha-synuclein remains one of the most compelling therapeutic targets for Parkinson's disease, and related synucleinopathies, and that the multitude of approaches being tested provides hope for the future.

TL;DR: Insight is provided into VNS‐evoked phasic neural activity in multiple neural structures and may be useful in guiding the selection of VNS parameters to enhance clinical efficacy.

TL;DR: Progress in optic nerve regeneration holds promise not only for visual restoration but also for improving outcome after injury to other parts of the mature CNS.

TL;DR: The evidence for the role of the best known and other possible compensatory mechanisms in PD are reviewed and the possibility that, although beneficial in practical terms, compensation could also play a deleterious role in disease progression is discussed.

TL;DR: A unique molecular program, a regenerative transcriptome, underlies post‐stroke axonal sprouting, which induces the formation of new connections in brain and spinal cord and mediate some aspects of motor recovery.

TL;DR: Four key areas must be considered for achieving neuroprotection with L RRK2 kinase inhibitors in PD: identification of patient populations most likely to benefit from LRRK2Kinase inhibitors, prioritization of superior LRRk2 small molecule inhibitors based on open disclosures of drug performance, incorporation of biomarkers and empirical measures of LRR kynase inhibition in clinical trials, and utilization of appropriate efficacy measures guided in part by rigorous pre-clinical modeling.

TL;DR: A review of the recent literature on the pharmacological modulation of the AMPK system as a potential molecular target in the management of neurodegenerative diseases is offered.

TL;DR: Treadmill exercise increased SIRT‐1 level, which subsequently resulted in increased ADAM‐10 level by down‐regulation of ROCK‐1 and upregulation of RAR&bgr;, ultimately facilitating the non‐amyloidogenic pathway.

TL;DR: Clear differences in the inflammatory expression profiles between microglia and macrophages 72 h post‐ischemia are shown which may shape repair and pro‐regenerative mechanisms after stroke.

TL;DR: In this paper, the main antioxidant found in plasma as well as the end product of purine metabolism in humans, has emerged as a promising potential neuroprotectant with advantages that distinguish it from previously tested antioxidant agents.

TL;DR: It is shown that emotion‐related networks can be identified and modulated in individual patients and that stimulation in cingulate and amygdala changes patients' performance in ways that are linked to the task's emotional content.

TL;DR: In vitro data supported the hypothesis that P2X7R/NLRP3 pathway plays a vital role in caspase‐3 dependent neuronal apoptosis after ischemic stroke and in vitro data also supported that P 2X7 R/NL RP3 pathway triggers neurons apoptosis.

TL;DR: The ability of paclitaxel to arrest their growth accounts for the selective vulnerability of sensory neurons to pac litaxel neurotoxicity, and local effects of microtubule hyperstabilization on the distal‐most portion of the axon are pointed to as an early mediator ofpaclitaxe neurotoxicity.

TL;DR: These findings implicate brain PPAR&ggr;2 among the mechanisms by which the ketogenic diet reduces seizures and strongly support the development of PPAR &ggR;2 as a therapeutic target for severe, refractory epilepsy.

TL;DR: Rat models of complete and partial injuries are the most frequently used models for analysis of the cellular and molecular processes of nerve regeneration and axon sprouting and make important contributions to knowledge of the degenerative and regenerative processes that occur after the peripheral nerve injuries.

TL;DR: This review outlines the linkage between Ca2+ entry through Cav1 channels, mitochondrial oxidant stress and cPD pathogenesis and summarizes considerations that went into the design and execution of the ongoing Phase 3 clinical trial with an inhibitor of these channels - isradipine.

TL;DR: The results suggest that TUDCA is a promising agent to limit ROS‐mediated damage, in different models of PD acting, at least in part, through modulation of the Nrf2 signaling pathway.

TL;DR: Surgical intervention alone does not provide satisfactory nerve repair results and roadblocks to recovery after nerve injury remain unsolved, so as to develop new strategies to improve functional regeneration for these life changing injuries.

TL;DR: The majority of adult axon regeneration studies have focused on the optic nerve or spinal axons of the teleosts goldfish and zebrafish, which have been productive models for identifying genes associated with axon regenerate, cellular mechanisms of circuit reestablishment, and the basis of functional recovery.

TL;DR: Cerebrovascular dysfunction is supported as a fundamental underlying process in AD pathology after an impairment in the neurovascular coupling along aging in the 3xTg‐AD mice which preceded obvious cognitive decline.

TL;DR: Findings reveal that the Wnt/β-catenin signaling is a potential target for prevention of AD and sodium selenate may be developed as a new drug for AD treatment.

TL;DR: It is found that NLRP3 inflammasome and subsequent pro‐inflammatory cytokines were activated in human brains after TBI and G protein‐coupled receptor 40 (GPR40) was observed to be involved in this anti‐inflammation.

TL;DR: It is demonstrated that tauopathy disrupts normal circadian clock function both at the behavioral and molecular levels, which may be attributed to the t Tauopathy‐induced neuropathology in the SCN.

TL;DR: Direct measurement of elevated striatal extracellular acetylcholine (ACh) in a knock‐in mouse model of human DYT1 dystonia is provided, confirming a striatal hypercholinergic state and evidence that a switch in D2R polarity results from a change in coupling from the preferred Gi/o pathway to non‐canonical &bgr;‐arrestin signaling.

TL;DR: The role of MIF in neurological disorders appears to be diverse with both beneficial and adversary effects, and its modulation is rather complex and it is regulated by different proteins, either on a molecular or protein level.

TL;DR: It is reported that single TBI using CHIMERA induces injury dose‐ and time‐dependent changes in behavioral and neurological deficits, axonal damage, white matter tract microgliosis and astrogliosis and it is shown that linear head kinematics are the most robust predictors of duration of unconsciousness, severity of Neurological deficits,white matter injury, and microglia following single T BI.

TL;DR: It is demonstrated that ROS contribute to SE‐induced cytokine production and antioxidant treatment may offer a novel approach to control neuroinflammation in epilepsy.

TL;DR: Understanding how aberrancy in these common processes leads to neurodegeneration has provided the field with numerous targets that may be therapeutically relevant to the development of disease-modifying treatments.

TL;DR: A brief review of several well-studied models of respiratory plasticity, including plasticity initiated by inactivity in the respiratory system, intermittent and sustained hypoxia, and traumatic injury to the spinal cord are discussed.

TL;DR: The protein levels of classical complement proteins (C1q‐C3) along with other phagocytosis signaling molecules in human epilepsy are determined to suggest that aberrantPhagocytic signaling occurs in human refractory epilepsy.