Showing papers in "Neurobiology of Disease in 2016"

TL;DR: The present work shows that ferroptosis is an important cell death pathway for dopaminergic neurons in Parkinson's disease, and is the first to emphasize the importance of ferroPTosis dysregulation in PD.

TL;DR: It is shown that CSF-derived Aβ40 co-localizes with existing endogenous vascular and parenchymal amyloid-β plaques, and thus, may contribute to the progression of both cerebral amyloids angiopathy andparenchylal Aβ accumulation.

TL;DR: The central actors of mitochondrial fusion and fission are presented and the role of mitochondrial dynamics in neuronal physiology and pathophysiology is reviewed and particular emphasis is placed on DRP1,MFN1-2, and OPA1 as well as on GDAP1, a protein of the mitochondrial outer membrane preferentially expressed in neurons.

TL;DR: Fast-spiking, inhibitory interneurons - prototype is the parvalbumin-positive (PV+) basket cell - generate action potentials at high frequency and synchronize the activity of numerous excitatory principal neurons, such as pyramidal cells, during fast network oscillations by rhythmic inhibition.

TL;DR: An overview of the most recent advances in astrocytic Ca(2+) signaling, spatial, and temporal dynamics of the morphology and proliferation of reactiveAstrocytes as well as signaling pathways involved in the reactive astrogliosis after ischemic stroke based on results from experimental studies performed in various animal models.

TL;DR: This review will highlight AS-dependent alterations of glial function and their impact on neuronal vulnerability thereby providing a detailed summary on the multifaceted role of glia in ASP.

TL;DR: Astroglia contribute to neurodegenerative processes seen in amyotrophic lateral sclerosis, Alzheimer's and Huntington's diseases, and play a role in major neuropsychiatric disorders, ranging from schizophrenia to depression, as well as in addictive disorders.

TL;DR: An overview of the cellular, molecular and genetic bases of brain development with an emphasis on the major mechanisms associated with landmarks of normal neural development in the embryonic stage and early postnatal life is provided.

TL;DR: Restoring CuATSM treatment could rescue these mice after they became symptomatic, providing a means to start and stop disease progression, and it is hoped that familial SOD ALS patients could respond to CuAT SM treatment similarly to the CCSxSOD mice.

TL;DR: It is concluded that soluble Aβ oligomers at the low nanomolar levels present in AD brain increase neuronal excitability by disrupting glutamatergic/GABAergic balance, thereby impairing synaptic plasticity.

TL;DR: It is shown that this reaction can be serially propagated to produce increasing amounts of phosphorylated TDP-43 pathology, and that aggregates can spread from cell to cell in an analogous fashion to that seen in the prion diseases.

TL;DR: Histological examination of the EYFP expression revealed that, in addition to orthodromic and antidromic effects, stimulation of cortico-subthalamic neurons may cause wide-spread increased glutamatergic activity due to collaterals that project to areas of the thalamus and other brain regions.

TL;DR: It is demonstrated that exercise training reduces extracellular soluble Aβ in the brains of Tg2576 mice in a dose-dependent manner through an up-regulation of Aβ clearance.

TL;DR: This study reveals the first evidence for hypothermia mediated regulation on inflammatory factor expression, microglia polarization, migration and indicates that the anti-inflammatory effect is an important mechanism underlying the brain protective effects of a TH therapy.

TL;DR: Cerebral amyloid angiopathy and microvascular inflammation occur in 5xFAD mice concomitantly to parenchymal plaque deposition, and the prospect of cerebrovascular pharmacology in AD is discussed.

TL;DR: Evidence is provided of a novel mechanism of microRNA-210 in a neonatal HI brain injury model, and a potential therapeutic approach of miR-210 inhibition in the treatment of neonatal HIE is suggested.

TL;DR: The current evidence for mHtt-induced abnormalities in mitochondrial dynamics and quality control is reviewed, with a particular focus on brain and neuronal data pertaining to striatal vulnerability.

TL;DR: The roles of NPY in the pathological mechanisms of neurodegenerative disorders are focused on, highlighting NPY as a neuroprotective agent, as a neural stem cell proliferativeAgent, as an agent that increases trophic support and as an inhibitor of excitotoxicity and neuroinflammation.

TL;DR: ERP habituation is established as a translation relevant, physiological pre-clinical marker of auditory processing deficits in FXS and abnormal MMP-9 regulation is a mechanism underlying auditory hypersensitivity inFXS.

TL;DR: Two features of subthalamic LFPs that have been proposed as specific parkinsonian biomarkers, beta power and coupling of beta phase to HFO amplitude, were also present in isolated dystonia, including focal dystonias, casting doubt on the utility of these metrics as disease-specific diagnostic biomarkers.

TL;DR: Diagnosis of newborns suffering from hypoxic–ischaemic encephalopathy with hypothermia and various add-on therapies including erythropoietin, xenon, topiramate, melatonin and stem cells are explored.

TL;DR: Administration of NMN at a proper dosage has a strong protective effect against ischemic brain injury and significantly improved the neurological outcome.

TL;DR: It is suggested that the cortical representation of rest tremor is distinct from that of voluntary movement, and support a model in which tremor acts to decrease beta band synchronization within the basal ganglia-cortical loop.

TL;DR: Impairment of the ALP and mitochondria dysfunction are common pathogenic themes between GD and PD and probably explain why GBA mutations increase the risk of developing PD that is very similar to sporadic forms of the disease.

TL;DR: Chronic HF DBS exerts long-term plasticity in the sensorimotor network, which may contribute to a lack of progression in underlying motor disability in PD.

TL;DR: Old 5xFAD astrocytes show impairment in support of neuronal growth in co-culture and neurotoxicity concomitant with an elevation in IL-6 expression, and that expression of scavenger receptor B1 is reduced in adult old 5xfad astroCytes.

TL;DR: In this article, a model of conditional monocyte/macrophage depletion was used to study the contribution of these myeloid cells to brain lesion progression after ischemia, and their influence on the ischemic inflammatory environment.

TL;DR: In this paper, the effect of mitochondrial dysfunction restricted to parvalbumin interneurons has been directly addressed in vivo by generating conditional knockout mice with a progressive decline in oxidative phosphorylation.

TL;DR: This work focuses on how the susceptibility of the highly organized neocortex and hippocampus may be due to their laminar organization, which involves the tight regulation, both temporally and spatially, of gene expression, specialized progenitor cells, the migration of neurons over large distances and a birthdate-specific layering of neurons.

TL;DR: This study systematically investigated whether PKCδ contributes to the heightened microglial activation response following exposure to major proinflammatory stressors, including α-synuclein, tumor necrosis factor α (TNFα), and lipopolysaccharide (LPS).