| P50 | author | Johannes Burtscher | Q60369717 |
| | Graham Knott | Q50285827 |
| P2093 | author name string | Hilal A Lashuel | |
| | Marion Leleu | |
| | Anne-Laure Mahul-Mellier | |
| | Fabien Kuttler | |
| | Marie Croisier | |
| | Niran Maharjan | |
| | Laura Weerens | |
| P2860 | cites work | Heterogeneity of nigral and cortical Lewy bodies differentiated by amplified triple-labeling for alpha-synuclein, ubiquitin, and thiazin red. | Q30870225 |
| | Localization of phosphorylated ERK/MAP kinases to mitochondria and autophagosomes in Lewy body diseases | Q31030866 |
| | Anatomic and disease specificity of NADH CoQ1 reductase (complex I) deficiency in Parkinson's disease | Q33789328 |
| | Parkinson's disease-implicated kinases in the brain; insights into disease pathogenesis | Q33797449 |
| | Aggregation promoting C-terminal truncation of alpha-synuclein is a normal cellular process and is enhanced by the familial Parkinson's disease-linked mutations | Q33836384 |
| | Critical role of truncated α-synuclein and aggregates in Parkinson's disease and incidental Lewy body disease | Q33894382 |
| | The novel Parkinson's disease linked mutation G51D attenuates in vitro aggregation and membrane binding of α-synuclein, and enhances its secretion and nuclear localization in cells. | Q33991720 |
| | Comparison of the behavioural and histological characteristics of the 6-OHDA and α-synuclein rat models of Parkinson's disease | Q34186437 |
| | Mitochondria, oxidative damage, and inflammation in Parkinson's disease | Q34212155 |
| | Endocannabinoid signaling and synaptic function | Q34304094 |
| | Lewy bodies | Q34478663 |
| | Mechanistic approaches to Parkinson's disease pathogenesis. | Q34984539 |
| | Convergence of heat shock protein 90 with ubiquitin in filamentous alpha-synuclein inclusions of alpha-synucleinopathies | Q35088093 |
| | Addition of exogenous α-synuclein preformed fibrils to primary neuronal cultures to seed recruitment of endogenous α-synuclein to Lewy body and Lewy neurite-like aggregates. | Q35215169 |
| | Mitochondrial Dysfunction and α-Synuclein Synaptic Pathology in Parkinson's Disease: Who's on First? | Q35412397 |
| | Cytoplasmic aggregates of phosphorylated extracellular signal-regulated protein kinases in Lewy body diseases | Q35748184 |
| | Aggregation of alpha-synuclein in Lewy bodies of sporadic Parkinson's disease and dementia with Lewy bodies. | Q35764504 |
| | Lewy-body formation is an aggresome-related process: a hypothesis | Q35840040 |
| | Mitochondrial DNA Depletion in Respiratory Chain-Deficient Parkinson Disease Neurons. | Q35852144 |
| | Aggregation of αSynuclein promotes progressive in vivo neurotoxicity in adult rat dopaminergic neurons | Q35863939 |
| | Contrasting features of ERK1/2 activity and synapsin I phosphorylation at the ERK1/2-dependent site in the rat brain in status epilepticus induced by kainic acid in vivo | Q36260373 |
| | Synchrotron FTIR micro-spectroscopy for structural analysis of Lewy bodies in the brain of Parkinson's disease patients. | Q36333500 |
| | Induction of de novo α-synuclein fibrillization in a neuronal model for Parkinson's disease | Q36607413 |
| | Lewy body-like α-synuclein aggregates resist degradation and impair macroautophagy | Q36873680 |
| | Proteomic identification of novel proteins associated with Lewy bodies | Q37146740 |
| | Aggregates assembled from overexpression of wild-type alpha-synuclein are not toxic to human neuronal cells | Q37401007 |
| | The Synucleinopathies: Twenty Years On. | Q37693375 |
| | Viral vector-mediated overexpression of α-synuclein as a progressive model of Parkinson's disease | Q37796011 |
| | Neuropathology underlying clinical variability in patients with synucleinopathies | Q37896515 |
| | The Lewy body in Parkinson's disease and related neurodegenerative disorders | Q38012653 |
| | Modeling Lewy pathology propagation in Parkinson's disease | Q38164894 |
| | Synthetic alpha-synuclein fibrils cause mitochondrial impairment and selective dopamine neurodegeneration in part via iNOS-mediated nitric oxide production. | Q50630062 |
| | A comparative electron microscopic study of reactive, degenerating, regenerating, and dystrophic axons | Q51211462 |
| | Mechanisms of α-Synuclein Induced Synaptopathy in Parkinson's Disease. | Q52363911 |
| | α-Synuclein fibril-induced paradoxical structural and functional defects in hippocampal neurons. | Q53827082 |
| | Role of Mitogen Activated Protein Kinase Signaling in Parkinson's Disease | Q57065048 |
| | Quality Over Quantity: Advantages of Using Alpha-Synuclein Preformed Fibril Triggered Synucleinopathy to Model Idiopathic Parkinson's Disease | Q58764665 |
| | Pathogenic alpha-synuclein aggregates preferentially bind to mitochondria and affect cellular respiration | Q64091665 |
| | In situ and in vitro study of colocalization and segregation of alpha-synuclein, ubiquitin, and lipids in Lewy bodies | Q64764806 |
| | The A53T alpha-synuclein mutation increases iron-dependent aggregation and toxicity | Q64777142 |
| | Heterogeneity in α-synuclein subtypes and their expression in cortical brain tissue lysates from Lewy body diseases and Alzheimer's disease | Q64819923 |
| | ɑ-Synuclein strains and seeding in Parkinson's disease, incidental Lewy body disease, dementia with Lewy bodies and multiple system atrophy: similarities and differences | Q64877664 |
| | Identification of a highly neurotoxic α-synuclein species inducing mitochondrial damage and mitophagy in Parkinson's disease | Q64976796 |
| | α-Synuclein Aggregation Monitored by Thioflavin T Fluorescence Assay. | Q65002554 |
| | Parkinson's disease: the presence of Lewy bodies in Auerbach's and Meissner's plexuses | Q69846956 |
| | Lewy bodies | Q69991514 |
| | alpha-Synuclein immunoreactivity in dementia with Lewy bodies: morphological staging and comparison with ubiquitin immunostaining | Q73727325 |
| | Three-layered structure shared between Lewy bodies and lewy neurites-three-dimensional reconstruction of triple-labeled sections | Q81032677 |
| | Axonal transport dysfunction in neurodegenerative diseases: the "holy grail" for developing disease modifying therapies? | Q88582188 |
| | Transmission of α-synuclein seeds in neurodegenerative disease: recent developments | Q91559574 |
| | α-Synuclein (αSyn) Preformed Fibrils Induce Endogenous αSyn Aggregation, Compromise Synaptic Activity and Enhance Synapse Loss in Cultured Excitatory Hippocampal Neurons | Q91623616 |
| | α-Synuclein aggregation at low concentrations | Q92078465 |
| | Lewy pathology in Parkinson's disease consists of crowded organelles and lipid membranes | Q93001087 |
| | Review: Parkinson's disease: from synaptic loss to connectome dysfunction. | Q38650395 |
| | Constitutive ERK MAPK activity regulates macrophage ATP production and mitochondrial integrity | Q38804893 |
| | Ultrastructure of Lewy bodies in the stellate ganglion | Q39987734 |
| | Mitochondrial complex I deficiency in Parkinson's disease. | Q40868964 |
| | In vitro aggregation assays for the characterization of α-synuclein prion-like properties. | Q41821396 |
| | Brain alpha-synuclein accumulation in multiple system atrophy, Parkinson's disease and progressive supranuclear palsy: a comparative investigation | Q43244813 |
| | Sphingomyelin in Lewy inclusion bodies in Parkinson's disease | Q43441611 |
| | MAPK/Erk-dependent phosphorylation of synapsin mediates formation of functional synapses and short-term homosynaptic plasticity. | Q43997175 |
| | Phosphorylation does not prompt, nor prevent, the formation of alpha-synuclein toxic species in a rat model of Parkinson's disease | Q46202469 |
| | Electron microscopy of Lewy bodies in the amygdala-parahippocampal region. Comparison with inclusion bodies in the MPTP-treated squirrel monkey | Q46269170 |
| | Phosphorylation of Ser-129 is the dominant pathological modification of alpha-synuclein in familial and sporadic Lewy body disease | Q46593989 |
| | Morphogenesis of Lewy bodies: dissimilar incorporation of alpha-synuclein, ubiquitin, and p62. | Q47300849 |
| | Distinct α-Synuclein strains and implications for heterogeneity among α-Synucleinopathies | Q48019506 |
| | Unbiased Proteomics of Early Lewy Body Formation Model Implicates Active Microtubule Affinity-Regulating Kinases (MARKs) in Synucleinopathies | Q48124425 |
| | Proteomic identification of novel proteins in cortical lewy bodies | Q48227693 |
| | The Lewy body in Parkinson's disease. | Q48254020 |
| | Presynaptic alpha-synuclein aggregates, not Lewy bodies, cause neurodegeneration in dementia with Lewy bodies. | Q48279657 |
| | Accumulation of alpha-synuclein/NACP is a cytopathological feature common to Lewy body disease and multiple system atrophy | Q48342277 |
| | An early cytoplasmic change before Lewy body maturation: an ultrastructural study of the substantia nigra from an autopsy case of juvenile parkinsonism | Q48352469 |
| | Novel antibodies to synuclein show abundant striatal pathology in Lewy body diseases | Q48494226 |
| | Selective dendritic degeneration of medium spiny neurons in dementia with Lewy bodies. | Q48527481 |
| | Hippocampal degeneration differentiates diffuse Lewy body disease (DLBD) from Alzheimer's disease: Light and electron microscopic immunocytochemistry of CA2-3 neurites specific to DLBD | Q48669050 |
| | Lewy bodies in parkinsonism share components with intraneuronal protein bodies of normal brains | Q48821685 |
| | Depletion of 26S proteasomes in mouse brain neurons causes neurodegeneration and Lewy-like inclusions resembling human pale bodies. | Q48971205 |
| | Concentric hyalin intraneuronal inclusions of Lewy type in the brains of elderly persons (50 incidental cases): relationship to parkinsonism | Q49024553 |
| P275 | copyright license | Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International | Q24082749 |
| P6216 | copyright status | copyrighted | Q50423863 |
| P433 | issue | 9 | |
| P921 | main subject | neurodegeneration | Q1755122 |
| P304 | page(s) | 4971-4982 | |
| P577 | publication date | 2020-02-19 | |
| P1433 | published in | Proceedings of the National Academy of Sciences of the United States of America | Q1146531 |
| P1476 | title | The process of Lewy body formation, rather than simply α-synuclein fibrillization, is one of the major drivers of neurodegeneration | |
| P478 | volume | 117 | |