scholarly journals Correction to: Lewy body-like alpha-synuclein inclusions trigger reactive microgliosis prior to nigral degeneration

2018 ◽  
Vol 15 (1) ◽  
Author(s):  
Megan F. Duffy ◽  
Timothy J. Collier ◽  
Joseph R. Patterson ◽  
Christopher J. Kemp ◽  
Kelvin C. Luk ◽  
...  
Keyword(s):  
Lewy Body ◽  
Alpha Synuclein ◽  
Nigral Degeneration

scholarly journals Lewy body-like alpha-synuclein inclusions trigger reactive microgliosis prior to nigral degeneration

2018 ◽  
Vol 15 (1) ◽  
Author(s):  
Megan F. Duffy ◽  
Timothy J. Collier ◽  
Joseph R. Patterson ◽  
Christopher J. Kemp ◽  
Kelvin C. Luk ◽  
...  
Keyword(s):  
Lewy Body ◽  
Alpha Synuclein ◽  
Nigral Degeneration

scholarly journals Preclinical Detection of Alpha-Synuclein Seeding Activity in the Colon of a Transgenic Mouse Model of Synucleinopathy by RT-QuIC

Viruses ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 759
Author(s):  
Jung-Youn Han ◽  
Chaewon Shin ◽  
Young Pyo Choi
Keyword(s):  
Mouse Model ◽  
Transgenic Mice ◽  
Lewy Body ◽  
Dementia With Lewy Body ◽  
Transgenic Mouse Model ◽  
Alpha Synuclein ◽  
Gi Tract ◽  
Colon Tissue ◽  
Presymptomatic Stage ◽  
The Brain

In synucleinopathies such as Parkinson’s disease (PD) and dementia with Lewy body (DLB), pathological alpha-synuclein (α-syn) aggregates are found in the gastrointestinal (GI) tract as well as in the brain. In this study, using real-time quaking-induced conversion (RT-QuIC), we investigated the presence of α-syn seeding activity in the brain and colon tissue of G2-3 transgenic mice expressing human A53T α-syn. Here we show that pathological α-syn aggregates with seeding activity were present in the colon of G2-3 mice as early as 3 months old, which is in the presymptomatic stage prior to the observation of any neurological abnormalities. In contrast, α-syn seeding activity was not detectable in 3 month-old mouse brains and only identified at 6 months of age in one of three mice. In the symptomatic stage of 12 months of age, RT-QuIC seeding activity was consistently detectable in both the brain and colon of G2-3 mice. Our results indicate that the RT-QuIC assay can presymptomatically detect pathological α-syn aggregates in the colon of G2-3 mice several months prior to their detection in brain tissue.

scholarly journals Lewy‐body Like Inclusions in Human Midbrain Organoid Carrying Glucocerebrosidase and Alpha Synuclein Mutations

2021 ◽  
Author(s):  
Junghyun Jo ◽  
Lin Yang ◽  
Hoang‐Dai Tran ◽  
Weonjin Yu ◽  
Alfred Xuyang Sun ◽  
...  
Keyword(s):  
Lewy Body ◽  
Alpha Synuclein

scholarly journals Alpha-synuclein alters the faecal viromes of rats in a gut-initiated model of Parkinson’s disease

2021 ◽  
Author(s):  
S. R. Stockdale ◽  
L. A. Draper ◽  
S. M. O’Donovan ◽  
W. Barton ◽  
O. O’Sullivan ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nervous System ◽  
Lewy Body ◽  
Neurological Disorder ◽  
Alpha Synuclein ◽  
Observational Period ◽  
Β Diversity ◽  
Potential Trigger ◽  
The Brain

AbstractParkinson’s disease (PD) is a chronic neurological disorder associated with the misfolding of alpha-synuclein (α-syn) into Lewy body aggregates within nerve cells that contribute to their neurodegeneration. Recent evidence suggests α-syn aggregation may begin in the gut and travel to the brain along the vagus nerve, with microbes a potential trigger initiating the misfolding of α-syn. However, changes in the gut virome in response to α-syn alterations have not been investigated. In this study, we show longitudinal changes in the faecal virome of rats administered either monomeric or preformed fibrils (PFF) of α-syn directly into their enteric nervous system. Differential changes in rat viromes were observed when comparing monomeric and PFF α-syn. The virome β-diversity changes after α-syn treatment were compounded by the addition of LPS as an adjunct. Changes in the diversity of rat faecal viromes were observed after one month and did not resolve within the study’s five month observational period. Overall, these results suggest that microbiome alterations associated with PD may, partially, be reactive to host α-syn associated changes.

Differential expression of alpha-synuclein, parkin, and synphilin-1 isoforms in Lewy body disease

Neurogenetics ◽  
2008 ◽  
Vol 9 (3) ◽  
pp. 163-172 ◽  
Author(s):  
Katrin Beyer ◽  
Montserrat Domingo-Sàbat ◽  
Jordi Humbert ◽  
Cristina Carrato ◽  
Isidro Ferrer ◽  
...  
Keyword(s):  
Differential Expression ◽  
Lewy Body ◽  
Lewy Body Disease ◽  
Alpha Synuclein

scholarly journals Alpha-synuclein biology in Lewy body diseases

2014 ◽  
Vol 6 (5-8) ◽  
Author(s):  
Woojin Scott Kim ◽  
Katarina Kågedal ◽  
Glenda M Halliday
Keyword(s):  
Lewy Body ◽  
Alpha Synuclein ◽  
Lewy Body Diseases

scholarly journals Alpha-Synuclein Post-translational Modifications: Implications for Pathogenesis of Lewy Body Disorders

2021 ◽  
Vol 13 ◽  
Author(s):  
Nelson de Oliveira Manzanza ◽  
Lucia Sedlackova ◽  
Raj N. Kalaria
Keyword(s):  
Neurodegenerative Diseases ◽  
Lewy Body ◽  
Clinical Symptoms ◽  
Lewy Bodies ◽  
Alpha Synuclein ◽  
Lewy Neurites ◽  
Post Translational Modifications ◽  
Age Related ◽  
Neurodegenerative Dementias

Lewy Body Disorders (LBDs) lie within the spectrum of age-related neurodegenerative diseases now frequently categorized as the synucleinopathies. LBDs are considered to be among the second most common form of neurodegenerative dementias after Alzheimer's disease. They are progressive conditions with variable clinical symptoms embodied within specific cognitive and behavioral disorders. There are currently no effective treatments for LBDs. LBDs are histopathologically characterized by the presence of abnormal neuronal inclusions commonly known as Lewy Bodies (LBs) and extracellular Lewy Neurites (LNs). The inclusions predominantly comprise aggregates of alpha-synuclein (aSyn). It has been proposed that post-translational modifications (PTMs) such as aSyn phosphorylation, ubiquitination SUMOylation, Nitration, o-GlcNacylation, and Truncation play important roles in the formation of toxic forms of the protein, which consequently facilitates the formation of these inclusions. This review focuses on the role of different PTMs in aSyn in the pathogenesis of LBDs. We highlight how these PTMs interact with aSyn to promote misfolding and aggregation and interplay with cell membranes leading to the potential functional and pathogenic consequences detected so far, and their involvement in the development of LBDs.

scholarly journals An analytical solution simulating growth of Lewy bodies

2021 ◽  
Author(s):  
Ivan A Kuznetsov ◽  
Andrey V Kuznetsov
Keyword(s):  
Analytical Solution ◽  
Analytical Solutions ◽  
Minimal Model ◽  
Lewy Body ◽  
Lewy Bodies ◽  
Alpha Synuclein ◽  
The Core ◽  
Spherical Core ◽  
Intracellular Organelles

This paper reports a minimal model simulating the growth of a Lewy body (LB). The LB is assumed to consist of a central spherical core, which is composed of membrane fragments and various dysfunctional intracellular organelles, and a halo, which is composed of alpha-synuclein fibrils. Membrane fragments and alpha-synuclein monomers are assumed to be produced in the soma at constant rates. The growth of the core and the halo are simulated by the Finke-Watzky model. Analytical solutions describing the growth of the core and the halo are obtained.

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