Articles
Page 18 of 27
-
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P52
-
Mechanism of tau transfer: insights from cell culture and animal models
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P50 -
Differential pathways for the interleukin-1β production activated by chromogranin A and Aβ in microglia
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P48 -
Phosphorylation of hnRNP K controls cytosolic accumulation of TDP-43
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P46 -
Role of ROS in Aβ42 mediated cell surface P-selectin expression and actin polymerization
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P44 -
Exposure to the saturated free fatty acid palmitate alters microglia inflammatory response
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P42 -
Bexarotene treatment does not clear β-Amyloid in an AD mouse model and Beagle dogs
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P40 -
Neuronal MHC-I display in T-cell mediated neurodegeneration
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P38 -
Harnessing endogenous pathways and metabolites to treat or prevent neurodegenerative disease
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):O36 -
Identification of proteins potentially involved in the formation of Lafora bodies, a hallmark of Lafora disease
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P36 -
Excitotoxicity increases the release of 24S-hydroxycholesterol via CYP46A1 activation
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):O32 -
Peripheral inflammation increases PKR activation, Tau phosphorylation and amyloid β production in wild-type mice
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P32 -
Genetic modulation of soluble Aβ rescues cognitive and synaptic impairment in a mouse model of AD
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):O30 -
Glutathion-S-Transferases (GSTs) and Parkinson’s disease in a MPTP-induced C57BL/6 mouse model
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P30 -
Identification of potent inhibitors of microtubule affinity regulating kinase for inhibition of tau hyperphosphorylation
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P28 -
Mechanisms of Aβ induced synaptic toxicity
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):O26 -
Cytoprotective functions of amyloid precursor protein family members in stress signaling and aging
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P26 -
The transcription factor XBP-1 in neurodegenerative diseases
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):O24 -
Regulation of Fe65 during neuronal differentiation
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P24 -
A novel mechanism underlying pathogenesis of Down syndrome
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):O23 -
Secretases: potential and roadblocks on the way to therapy
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):O22 -
FcgRIIb mediates amyloid-β neurotoxicity and memory impairment in a model of Alzheimer’s disease
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P22 -
O-GlcNAcylation increases non-amyloidogenic processing of the amyloid-β precursor protein (APP)
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P21 -
Vascular hypothesis of Alzheimer’s disease: role of apoE and apoE receptors
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):O20 -
Regulation of key proteins in Alzheimer’s disease molecular pathogenesis by ubiquilin-1
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P20 -
Super-resolution fluorescence imaging of intracellular mutant huntingtin protein reveals a population of fibrillar aggregates co-existing with compact perinuclear inclusion bodies
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):O18 -
Serum from Parkinson’s disease patients presents excess of protein halogenation and nitrosylation, with anomalous nitrosylation of serum α-synuclein as potentially etiological factor
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P18 -
Novel non-carbohydrate O-GlcNAcase inhibitors with CNS drug properties as potential treatment for Alzheimer’s disease and tauopathies
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):O17 -
A cell-based model of pathological tau uptake and propagation
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P17 -
Designing nanoparticles for delivery of neurotrophic proteins
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):O16 -
Altered expression of antioxidant enzymes and autophagic proteins in transglutaminase 2 knockout mice
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P15 -
Expanded G4C2 repeats linked to C9ORF72ALS and FTD form length-dependent RNA foci, sequester RNA binding proteins and are neurotoxic
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):O14 -
The dishomeostasis of metal ions plays an important role for the cognitive impartment
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P13 -
Genetic analysis of neurodegeneration.. the end game
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):O12 -
Function and dysfunction of presenilin in Alzheimer’s disease
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):O11 -
Posterior cortical atrophy: correlation between clinical, neuropsychological, magnetic resonance and positron emission tomography Imaging
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P11 -
CYP2E1 and Parkinson’s disease in a MPTP-induced C57BL/6 mouse model
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P9 -
Neurochemical changes in animal models of Parkinson’s disease
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P7 -
BACE1, the Alzheimer’s beta-secretase enzyme, in health and disease
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):O7 -
RAGE targeted strategies for Alzheimer’s amyloid β peptide induced blood brain barrier dysfunctions
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P5 -
The biological function of β-secretase
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):O5 -
dld-1 suppression attenuates the detrimental effects of amyloid beta deposition in a Caenorhabditis elegansmodel of Alzheimer’s disease
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P3 -
Functional genetics – an approach to mechanisms in Alzheimer’s disease
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):O3 -
Methylene blue decreases brain mitochondrial ABAD and amyloid beta levels protecting mitochondrial functions in LPS-mouse model
Citation: Molecular Neurodegeneration 2013 8(Suppl 1):P1 -
Rapamycin increases survival in ALS mice lacking mature lymphocytes
Amyotrophic Lateral Sclerosis (ALS) is a devastating progressive neurodegenerative disease. Disease pathophysiology is complex and not yet fully understood, but is proposed to include the accumulation of misfo...
Citation: Molecular Neurodegeneration 2013 8:31 -
Amyotrophic lateral sclerosis-linked FUS/TLS alters stress granule assembly and dynamics
Amyotrophic lateral sclerosis (ALS)-linked fused in sarcoma/translocated in liposarcoma (FUS/TLS or FUS) is concentrated within cytoplasmic stress granules under conditions of induced stress. Since only the mu...
Citation: Molecular Neurodegeneration 2013 8:30 -
S-Nitrosylation of parkin as a novel regulator of p53-mediated neuronal cell death in sporadic Parkinson’s disease
Mutations in the gene encoding parkin, a neuroprotective protein with dual functions as an E3 ubiquitin ligase and transcriptional repressor of p53, are linked to familial forms of Parkinson’s disease (PD). We...
Citation: Molecular Neurodegeneration 2013 8:29 -
Genetics of amyotrophic lateral sclerosis: an update
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder involving both upper motor neurons (UMN) and lower motor neurons (LMN). Enormous research has been done in the past few decades i...
Citation: Molecular Neurodegeneration 2013 8:28 -
Autophagy is involved in oligodendroglial precursor-mediated clearance of amyloid peptide
Accumulation of β-amyloid peptides is an important hallmark of Alzheimer’s disease (AD). Tremendous efforts have been directed to elucidate the mechanisms of β-amyloid peptides degradation and develop strategi...
Citation: Molecular Neurodegeneration 2013 8:27 -
Erratum to: treatment with bexarotene, a compound that increases apolipoprotein-E, provides no cognitive benefit in mutant APP/PS1 mice
Citation: Molecular Neurodegeneration 2013 8:26
Follow
- ISSN: 1750-1326 (electronic)