Showing papers in "Neurochemistry International in 2017"

TL;DR: HMSC-generated exosomes significantly improve functional recovery in rats after TBI, at least in part, by promoting endogenous angiogenesis and neurogenesis and reducing neuroinflammation.

TL;DR: An updated mechanistic overview ofMitophagy pathways is provided and potential translational applications of mitophagy‐inducing compounds, such as NAD+ precursors and urolithins are highlighted.

TL;DR: This review will discuss ferroptosis and other cell death pathways implicated in PD neurodegeneration, with a focus on the potential to therapeutically target these pathways to slow the progression of this disease.

TL;DR: Recent work is examined that examines the ability of NSCs to provide trophic support to disease‐effected neuronal populations and synapses in models of neurodegeneration and some of key challenges that remain before NSC‐based therapies for neurodegenersative diseases can be translated toward potential clinical testing.

TL;DR: The current understanding of epidemiology, diagnoses, mechanisms, risk factors, and treatments of PSE are discussed.

TL;DR: Treatments manipulating aspects of reactive astrogliosis can enhance neuronal plasticity following stroke and benefit from a more complete characterization of the specific responses of peri-infarct astrocytes to stroke as well as a better understanding of the influence of other factors including age, sex, comorbidities and reperfusion of the ischemic tissue.

TL;DR: How the ‘pro‐apoptotic’ Bcl‐2 family proteins, Bax and Bok, physiologically expressed in the nervous system, regulate such ‘non‐APoptotic/daytime’ functions are discussed.

TL;DR: Overall, this study demonstrated that omega‐3 fatty acids and vitamin E co‐supplementation in people with PD had favorable effects on UPDRS, hs‐CRP, TAC, GSH and markers of insulin metabolism.

TL;DR: The novel findings show that activation of AMPK‐dependent signaling by resveratrol rescues A&bgr;‐mediated neurotoxicity in hNSCs, and provides evidence supporting a neuroprotective role for AMPK activating drugs in A &b Gr;‐related diseases such as AD.

TL;DR: All relevant neurochemical research, including the intriguing link with (prodromal) dementia, several biomarker opportunities, the latest therapeutic strategies to enhance NE signaling, and, finally, some overarching comments and perspectives for future research are discussed.

TL;DR: Recent developments in the “oligomer hypothesis” are discussed, including research findings regarding the pathogenesis of AD, suggesting that pre‐fibrillar forms (oligomers of A&bgr;) are more deleterious than are extracellular fibril forms.

TL;DR: The current progress in the understanding of the role of ncRNAs in initiation and progression of secondary neuronal damage and their application as biomarkers after acute CNS injuries is highlighted.

TL;DR: Explorations of a key factor that underlies the bidirectional interactions between diabetes and AD, "Factor X", could lead to the development of a potential therapeutic target for neurodegeneration.

TL;DR: It is reported that expression of the mitochondrial isoform of SIRT3 is altered in muscle from the G93A‐SOD1 mice during progression of disease; this alteration influences mitochondrial metabolism, which may be relevant for the well known energetic alterations taking place in ALS patients.

TL;DR: Through cell‐specific upregulation of these enzymes, LIF and other Akt‐inducing factors have the potential to protect multiple cell types against damage from ROS during the early and late phases of ischemic damage.

TL;DR: Potential application of this chemokine/receptor interaction axis for the expansion of future anti-glioma therapies as well is discussed.

TL;DR: A systematic examination of A&bgr; PTM and the analysis of the toxicity that they induced may help create essential biomarkers to more precisely stage AD pathology, design countermeasures and gauge the impacts of interventions.

TL;DR: Many processes that govern mitochondrial structure and function in health and disease are discussed, and how Bcl‐2 family proteins integrate into some of these processes are discussed.

TL;DR: How PMNs are attracted to the site of injury and their tasks within the inflamed brain tissue and the periphery are described and new therapeutic applications could emerge from this new knowledge on the action and interaction of PMNs following cerebral ischemia.

TL;DR: Agomelatine treatment protects the brain from cerebral I/R injury by suppressing apoptosis and agomel atine has antioxidant properties, suggesting it may be a potential candidate for treating ischemic stroke.

TL;DR: Preliminary evidence suggests that oxytocin might be the ideal candidate as a target for reducing the severity of pain, and a summary of the total literature related to the effects of Oxytocin on pain modulation in both animals and humans is presented.

TL;DR: Treatment with resveratrol for four weeks restored the core and associated symptoms of autistic phenotype by suppressing oxidative‐nitrosative stress, mitochondrial dysfunction, TNF‐&agr; and MMP‐9 expression in PPA induced ASD in rats.

TL;DR: The temporal linkage of these post‐TBI events suggests a possible neuroprotective therapeutic window of as much as 12–24 h and a surprisingly delayed peak in secondary injury, suggest that the therapeutic window and needed treatment duration for certain antioxidant treatment strategies following CCI‐T BI in rodents may be longer than previously believed.

TL;DR: The pathologic and clinical aspects of ischemic stroke are described in this review, where a non‐exhaustive list of biomarkers that interrogate different aspects ofIschemic strokes such as oxidative damage, inflammation, thrombus formation, cardiac function and brain injury are described.

TL;DR: The obtained results suggest that hiPSC‐derived mixed neuronal/glial culture could be a valuable in vitro human model for the establishment of neuronal specific assays in order to link Nrf2 pathway activation (biomarker of oxidative stress) with additional neuronal specific readouts that could be applied to in vitro neurotoxicity evaluation.

TL;DR: Current knowledge about the architecture and functions of the ER‐mitochondria contact sites, and the consequences of their alteration in different neurodegenerative disorders are summarized.

TL;DR: The present study showed a putative therapeutic role of CeO2NPs in the treatment of 6‐OHDA‐induced Parkinsonian rats, and suggested their antioxidant and antiapoptotic effects as possible mechanisms for elevated striatal dopamine level and improved motor performance.

TL;DR: The controlled release of growth factor hydrogel based scaffolds, targeted delivery to the brain and glysominoglycan chemistry that enhance the half life and selectivity of the growth factors are highlighted.

TL;DR: It is demonstrated that melatonin is protective against NP‐induced neurotoxicity and cognitive alteration and the potential use of melatonin as a nutraceutical is emphasized.

TL;DR: Findings support a protective role of miR‐132 in a mouse model of ICH, providing new opportunities for therapeutic intervention.