Citation: Molecular Neurodegeneration 2016 11:42
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Extracellular vesicles (EVs) act as key mediators of intercellular communication and are secreted and taken up by all cell types in the central nervous system (CNS). While detailed study of EV-based signaling ...
Citation: Molecular Neurodegeneration 2016 11:41
Citation: Molecular Neurodegeneration 2016 11:40
Induced pluripotent stem cells in Alzheimer’s disease: applications for disease modeling and cell-replacement therapy
Alzheimer's disease (AD) is the most common cause of dementia in those over the age of 65. While a numerous of disease-causing genes and risk factors have been identified, the exact etiological mechanisms of A...
Citation: Molecular Neurodegeneration 2016 11:39
Accumulation of amyloid-β by astrocytes result in enlarged endosomes and microvesicle-induced apoptosis of neurons
Despite the clear physical association between activated astrocytes and amyloid-β (Aβ) plaques, the importance of astrocytes and their therapeutic potential in Alzheimer’s disease remain elusive. Soluble Aβ ag...
Citation: Molecular Neurodegeneration 2016 11:38
Apolipoprotein E lipoprotein particles inhibit amyloid-β uptake through cell surface heparan sulphate proteoglycan
The accumulation, aggregation and deposition of amyloid-β (Aβ) peptides in the brain are central to the pathogenesis of Alzheimer’s disease (AD). Alzheimer’s disease risk increases significantly in individuals...
Citation: Molecular Neurodegeneration 2016 11:37
Targeting TDP-43 phosphorylation by Casein Kinase-1δ inhibitors: a novel strategy for the treatment of frontotemporal dementia
Mutations in the progranulin gene (GRN) are the most common cause of frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP). TDP-43 pathology is characterized by the hyperphosphorylation of the prote...
Citation: Molecular Neurodegeneration 2016 11:36
A multifunctional therapeutic approach to disease modification in multiple familial mouse models and a novel sporadic model of Alzheimer’s disease
Clinical failures singularly targeting amyloid-β pathology indicate a critical need for alternative Alzheimer’s disease (AD) therapeutic strategies. The mixed pathology reported in a large population of AD pat...
Citation: Molecular Neurodegeneration 2016 11:35
Ex vivo imaging of active caspase 3 by a FRET-based molecular probe demonstrates the cellular dynamics and localization of the protease in cerebellar granule cells and its regulation by the apoptosis-inhibiting protein survivin
Apoptosis takes place in naturally occurring neuronal death, but also in aging, neurodegenerative disorders, and traumatic brain injuries. Caspase 3 (Casp3) is the most important effector protease in apoptosis...
Citation: Molecular Neurodegeneration 2016 11:34
Tau mutant A152T, a risk factor for FTD/PSP, induces neuronal dysfunction and reduced lifespan independently of aggregation in a C. elegans Tauopathy model
A certain number of mutations in the Microtubule-Associated Protein Tau (MAPT) gene have been identified in individuals with high risk to develop neurodegenerative diseases, collectively called tauopathies. The m...
Citation: Molecular Neurodegeneration 2016 11:33
Tauopathy is characterized by neurofibrillary tangles composed of insoluble hyperphosphorylated tau protein. Currently, cellular models that mimic neurofibrillary tangles in vitro are lacking. Previous studies...
Citation: Molecular Neurodegeneration 2016 11:32
Biological pathways that significantly contribute to sporadic Alzheimer’s disease are largely unknown and cannot be observed directly. Cognitive symptoms appear only decades after the molecular disease onset, ...
Citation: Molecular Neurodegeneration 2016 11:31
In vitro and in vivo neuroprotective effects of cJun N-terminal kinase inhibitors on retinal ganglion cells
The c-Jun N-terminal kinase (JNK) signaling pathway plays an important role in neuronal pathophysiology. Using JNK inhibitors, we examined involvement of the JNK pathway in cultured rat retinal ganglion cell (...
Citation: Molecular Neurodegeneration 2016 11:30
Resequencing analysis of five Mendelian genes and the top genes from genome-wide association studies in Parkinson’s Disease
Most sequencing studies in Parkinson’s disease (PD) have focused on either a particular gene, primarily in familial and early onset PD samples, or on screening single variants in sporadic PD cases. To date, th...
Citation: Molecular Neurodegeneration 2016 11:29
MicroRNA-7 targets Nod-like receptor protein 3 inflammasome to modulate neuroinflammation in the pathogenesis of Parkinson’s disease
α-Synuclein (α-Syn), a pathological hallmark of Parkinson’s disease (PD), has been recognized to induce the production of interleukin-1β in a process that depends, at least in vitro, on nod-like receptor prote...
Citation: Molecular Neurodegeneration 2016 11:28
Manifestation of Huntington’s disease pathology in human induced pluripotent stem cell-derived neurons
Huntington’s disease (HD) is an incurable hereditary neurodegenerative disorder, which manifests itself as a loss of GABAergic medium spiny (GABA MS) neurons in the striatum and caused by an expansion of the C...
Citation: Molecular Neurodegeneration 2016 11:27
Inhibition of the classical pathway of the complement cascade prevents early dendritic and synaptic degeneration in glaucoma
Glaucoma is a complex, multifactorial disease characterised by the loss of retinal ganglion cells and their axons leading to a decrease in visual function. The earliest events that damage retinal ganglion cell...
Citation: Molecular Neurodegeneration 2016 11:26
Pioglitazone ameliorates the phenotype of a novel Parkinson’s disease mouse model by reducing neuroinflammation
Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by motor and non-motor symptoms. The cause of the motor symptoms is the loss of dopaminergic neurons in the substantia nigra with...
Citation: Molecular Neurodegeneration 2016 11:25
C1q propagates microglial activation and neurodegeneration in the visual axis following retinal ischemia/reperfusion injury
C1q represents the initiating protein of the classical complement cascade, however recent findings indicate pathway independent roles such as developmental pruning of retinal ganglion cell (RGC) axons. Further...
Citation: Molecular Neurodegeneration 2016 11:24
Interleukin-1 beta (IL-1β) and its key regulator, the inflammasome, are suspected to play a role in the neuroinflammation observed in Alzheimer’s disease (AD); no conclusive data are nevertheless available in ...
Citation: Molecular Neurodegeneration 2016 11:23
Vitamin D interacts with Esr1 and Igf1 to regulate molecular pathways relevant to Alzheimer’s disease
Increasing evidence suggests a potential therapeutic benefit of vitamin D supplementation against Alzheimer’s disease (AD). Although studies have shown improvements in cognitive performance and decreases in ma...
Citation: Molecular Neurodegeneration 2016 11:22
Frontotemporal dementia: insights into the biological underpinnings of disease through gene co-expression network analysis
In frontotemporal dementia (FTD) there is a critical lack in the understanding of biological and molecular mechanisms involved in disease pathogenesis. The heterogeneous genetic features associated with FTD su...
Citation: Molecular Neurodegeneration 2016 11:21
Citation: Molecular Neurodegeneration 2016 11:20
Generation of aggregation prone N-terminally truncated amyloid β peptides by meprin β depends on the sequence specificity at the cleavage site
The metalloprotease meprin β cleaves the Alzheimer’s Disease (AD) relevant amyloid precursor protein (APP) as a β-secretase reminiscent of BACE-1, however, predominantly generating N-terminally truncated Aβ2-x...
Citation: Molecular Neurodegeneration 2016 11:19
Activation of zebrafish Src family kinases by the prion protein is an amyloid-β-sensitive signal that prevents the endocytosis and degradation of E-cadherin/β-catenin complexes in vivo
Prions and amyloid-β (Aβ) oligomers trigger neurodegeneration by hijacking a poorly understood cellular signal mediated by the prion protein (PrP) at the plasma membrane. In early zebrafish embryos, PrP-1-depe...
Citation: Molecular Neurodegeneration 2016 11:18
Automated longitudinal monitoring of in vivo protein aggregation in neurodegenerative disease C. elegans models
While many biological studies can be performed on cell-based systems, the investigation of molecular pathways related to complex human dysfunctions – e.g. neurodegenerative diseases – often requires long-term ...
Citation: Molecular Neurodegeneration 2016 11:17
Alzheimer disease (AD) and other tauopathies develop cerebral intracellular inclusions of hyperphosphorylated tau. Epidemiological and experimental evidence suggests a clear link between type 2 diabetes mellit...
Citation: Molecular Neurodegeneration 2016 11:16
Citation: Molecular Neurodegeneration 2016 11:15
A unique feature of the pathological change after spinal cord injury (SCI) is the progressive enlargement of lesion area, which usually results in cavity formation and is accompanied by reactive astrogliosis a...
Citation: Molecular Neurodegeneration 2016 11:14
Parkinson’s disease (PD) is a motor disease associated with the degeneration of dopaminergic neurons of the substantia nigra pars compacta. p53 is a major neuronal pro-apoptotic factor that is at the center of gr...
Citation: Molecular Neurodegeneration 2016 11:13
Deep brain stimulation-associated brain tissue imprints: a new in vivo approach to biological research in human Parkinson’s disease
Deep brain stimulation (DBS) of the subthalamic nucleus (STN) or the internal segment of the globus pallidus (GPi) has been established as a highly effective symptomatic therapy for Parkinson’s disease (PD). A...
Citation: Molecular Neurodegeneration 2016 11:12
A Fluorescent Oligothiophene-Bis-Triazine ligand interacts with PrP fibrils and detects SDS-resistant oligomers in human prion diseases
Prion diseases are characterized by the accumulation in the central nervous system of an abnormally folded isoform of the prion protein, named PrPSc. Aggregation of PrPSc into oligomers and fibrils is critically ...
Citation: Molecular Neurodegeneration 2016 11:11
A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) proteoglycanases are specialized in the degradation of chondroitin sulfate proteoglycans and participate in mechanisms mediating neuropla...
Citation: Molecular Neurodegeneration 2016 11:10
Heparan sulfate proteoglycans mediate Aβ-induced oxidative stress and hypercontractility in cultured vascular smooth muscle cells
Substantial evidence suggests that amyloid-β (Aβ) species induce oxidative stress and cerebrovascular (CV) dysfunction in Alzheimer’s disease (AD), potentially contributing to the progressive dementia of this ...
Citation: Molecular Neurodegeneration 2016 11:9
Directly converted patient-specific induced neurons mirror the neuropathology of FUS with disrupted nuclear localization in amyotrophic lateral sclerosis
Mutations in the fused in sarcoma (FUS) gene have been linked to amyotrophic lateral sclerosis (ALS). ALS patients with FUS mutations exhibit neuronal cytoplasmic mislocalization of the mutant FUS protein. ALS pa...
Citation: Molecular Neurodegeneration 2016 11:8
Despite decades of intensive research, to date, there is no accepted diagnosis for Parkinson’s disease (PD) based on biochemical analysis of blood or CSF. However, neurodegeneration in the brains of PD patient...
Citation: Molecular Neurodegeneration 2016 11:7
Novel (Hetero)arylalkenyl propargylamine compounds are protective in toxin-induced models of Parkinson’s disease
Mitochondrial dysfunction, oxidative stress and their interplay are core pathological features of Parkinson’s disease. In dopaminergic neurons, monoamines and their metabolites provide an additional source of ...
Citation: Molecular Neurodegeneration 2016 11:6
LRRK2 phosphorylates pre-synaptic N-ethylmaleimide sensitive fusion (NSF) protein enhancing its ATPase activity and SNARE complex disassembling rate
Lrrk2, a gene linked to Parkinson’s disease, encodes a large scaffolding protein with kinase and GTPase activities implicated in vesicle and cytoskeletal-related processes. At the pres...
Citation: Molecular Neurodegeneration 2016 11:1
Alzheimer’s disease-like APP processing in wild-type mice identifies synaptic defects as initial steps of disease progression
Alzheimer’s disease (AD) is the most frequent form of dementia in the elderly and no effective treatment is currently available. The mechanisms triggering AD onset and progression are still imperfectly dissect...
Citation: Molecular Neurodegeneration 2016 11:5
The novel RAGE interactor PRAK is associated with autophagy signaling in Alzheimer’s disease pathogenesis
The receptor for advanced glycation end products (RAGE) has been found to interact with amyloid β (Aβ). Although RAGE does not have any kinase motifs in its cytosolic domain, the interaction between RAGE and A...
Citation: Molecular Neurodegeneration 2016 11:4
The discovery that heterozygous missense mutations in the gene encoding triggering receptor expressed on myeloid cells 2 (TREM2) are risk factors for Alzheimer’s disease (AD), with only the apolipoprotein E (A...
Citation: Molecular Neurodegeneration 2016 11:3
Apolipoprotein E (ApoE) is a major cholesterol carrier and plays an important role in maintaining lipid homeostasis both in the periphery and brain. Human APOE gene is polymorphic at two single nucleotides (rs429...
Citation: Molecular Neurodegeneration 2016 11:2
Beclin 1 regulates neuronal transforming growth factor-β signaling by mediating recycling of the type I receptor ALK5
Beclin 1 is a key regulator of multiple trafficking pathways, including autophagy and receptor recycling in yeast and microglia. Decreased beclin 1 levels in the CNS result in neurodegeneration, an effect attr...
Citation: Molecular Neurodegeneration 2015 10:69
Tau missorting and spastin-induced microtubule disruption in neurodegeneration: Alzheimer Disease and Hereditary Spastic Paraplegia
In Alzheimer Disease (AD), the mechanistic connection of the two major pathological hallmarks, namely deposition of Amyloid-beta (Aβ) in the form of extracellular plaques, and the pathological changes of the i...
Citation: Molecular Neurodegeneration 2015 10:68
Although the genetic cause for Huntington’s disease (HD) has been known for over 20 years, the mechanisms that cause the neurotoxicity and behavioral symptoms of this disease are not well understood. One hypot...
Citation: Molecular Neurodegeneration 2015 10:67
Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS) are both neurodegenerative diseases leading to impaired execution of movement. α-Synuclein plays a central role in the pathogenesis of PD wherea...
Citation: Molecular Neurodegeneration 2015 10:66
Loss of Munc18-1 long splice variant in GABAergic terminals is associated with cognitive decline and increased risk of dementia in a community sample
Presynaptic terminals contribute to cognitive reserve, balancing the effects of age-related pathologies on cognitive function in the elderly. The presynaptic protein Munc18-1, alternatively spliced into long (...
Citation: Molecular Neurodegeneration 2015 10:65
Identification of novel CSF biomarkers for neurodegeneration and their validation by a high-throughput multiplexed targeted proteomic assay
Currently there are no effective treatments for many neurodegenerative diseases. Reliable biomarkers for identifying and stratifying these diseases will be important in the development of future novel therapie...
Citation: Molecular Neurodegeneration 2015 10:64
Loss of parkin promotes lipid rafts-dependent endocytosis through accumulating caveolin-1: implications for Parkinson’s disease
Parkinson’s disease (PD) is characterized by progressive loss of midbrain dopaminergic neurons, resulting in motor dysfunctions. While most PD is sporadic in nature, a significant subset can be linked to eithe...
Citation: Molecular Neurodegeneration 2015 10:63
Is L-methionine a trigger factor for Alzheimer’s-like neurodegeneration?: Changes in Aβ oligomers, tau phosphorylation, synaptic proteins, Wnt signaling and behavioral impairment in wild-type mice
L-methionine, the principal sulfur-containing amino acid in proteins, plays critical roles in cell physiology as an antioxidant and in the breakdown of fats and heavy metals. Previous studies suggesting the us...
Citation: Molecular Neurodegeneration 2015 10:62
- ISSN: 1750-1326 (electronic)