Accumulation of α-synuclein/NACP is a cytopathological feature common to Lewy body disease and multiple system atrophy

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NACP, a presynaptic protein, immunoreactivity in Lewy bodies in Parkinson's disease

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Hippocampal degeneration differentiates diffuse Lewy body disease (DLBD) from Alzheimer's disease

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Immunoreactivity profile of hippocampal CA2/3 neurites in diffuse Lewy body disease

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Cu/Zn superoxide dismutase-like immunoreactivity is present in Lewy bodies from Parkinson disease: a light and electron microscopic immunocytochemical study

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Ubiquitin-positive CA2/3 neurites in hippocampus coexist with cortical Lewy bodies

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Autosomal dominant diffuse Lewy body disease

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Hereditary dentatorubral-pallidoluysian atrophy: ubiquitinated filamentous inclusions in the cerebellar dentate nucleus neurons

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Tau immunoreactivity in glial cytoplasmic inclusions in multiple system atrophy

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Tau protein isoforms, phosphorylation and role in neurodegenerative disorders11These authors contributed equally to this work.

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The process of Lewy body formation, rather than simply α-synuclein fibrillization, is one of the major drivers of neurodegeneration

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Parkin ubiquitinates the α-synuclein–interacting protein, synphilin-1: implications for Lewy-body formation in Parkinson disease

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Subcellular Localization of Wild-Type and Parkinson's Disease-Associated Mutant α-Synuclein in Human and Transgenic Mouse Brain

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Stanley Fahn Lecture 2005: the staging procedure for the inclusion body pathology associated with sporadic Parkinson’s disease reconsidered

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The synaptic pathology of α-synuclein aggregation in dementia with Lewy bodies, Parkinson’s disease and Parkinson’s disease dementia

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α-Synuclein Membrane Interactions and Lipid Specificity

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Dityrosine Cross-linking Promotes Formation of Stable α-Synuclein Polymers

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The α‐Synucleinopathies: Parkinson's Disease, Dementia with Lewy Bodies, and Multiple System Atrophy

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Constitutive Phosphorylation of the Parkinson's Disease Associated α-Synuclein

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The Lewy body in Parkinson's disease: Molecules implicated in the formation and degradation of α‐synuclein aggregates

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Mutant and Wild Type Human α-Synucleins Assemble into Elongated Filaments with Distinct Morphologies in Vitro

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The Lewy Body in Parkinson’s Disease and Related Neurodegenerative Disorders

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Multiple system atrophy

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Membrane-bound α-Synuclein Has a High Aggregation Propensity and the Ability to Seed the Aggregation of the Cytosolic Form

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NACP/α-synuclein-positive filamentous inclusions in astrocytes and oligodendrocytes of Parkinson’s disease brains

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Oxidative Stress and Genetics in the Pathogenesis of Parkinson's Disease

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Evidence for Seeding of β-Amyloid by Intracerebral Infusion of Alzheimer Brain Extracts in β-Amyloid Precursor Protein-Transgenic Mice

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Multiple system atrophy: A primary oligodendrogliopathy

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Transcriptional profiles associated with aging and middle age-onset caloric restriction in mouse hearts

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Lewy-body formation is an aggresome-related process: a hypothesis

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Widespread Alterations of α-Synuclein in Multiple System Atrophy

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Golgi Fragmentation Occurs in the Cells with Prefibrillar α-Synuclein Aggregates and Precedes the Formation of Fibrillar Inclusion

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Morphogenesis of Lewy Bodies: Dissimilar Incorporation of α-Synuclein, Ubiquitin, and p62

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The relationship between oxidative/nitrative stress and pathological inclusions in Alzheimer’s and Parkinson’s diseases1,2 11Guest Editors: Mark A. Smith and George Perry 22This article is part of a series of reviews on “Causes and Consequences of Oxidative Stress in Alzheimer’s Disease.” The full list of papers may be found on the homepage of the journal.

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The structural differences between patient-derived α-synuclein strains dictate characteristics of Parkinson’s disease, multiple system atrophy and dementia with Lewy bodies

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Widespread Nitration of Pathological Inclusions in Neurodegenerative Synucleinopathies

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Lewy body–type degeneration in cardiac plexus in Parkinson’s and incidental Lewy body diseases

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