scholarly journals Characterization of Polyethylene Glycol-Polyethyleneimine as a Vector for Alpha-Synuclein siRNA Delivery to PC12 Cells for Parkinson's Disease

2013 ◽  
Vol 20 (1) ◽  
pp. 76-85 ◽  
Author(s):  
Yun-Yun Liu ◽  
Xing-Yi Yang ◽  
Zhong Li ◽  
Zhong-Lin Liu ◽  
Du Cheng ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Polyethylene Glycol ◽  
Pc12 Cells ◽  
Sirna Delivery ◽  
Alpha Synuclein

scholarly journals Single Molecule FRET Characterization of Oligomers from Alpha-Synuclein Early Onset Parkinson's Disease Mutants

2014 ◽  
Vol 106 (2) ◽  
pp. 269a ◽  
Author(s):  
Laura Tosatto ◽  
Mathew H. Horrocks ◽  
Cremades Nunilo ◽  
Tim Guilliams ◽  
Mauro Dalla Serra ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Single Molecule ◽  
Early Onset ◽  
Alpha Synuclein ◽  
Single Molecule Fret ◽  
Early Onset Parkinson’S Disease

scholarly journals Novel Immunotherapeutic Approaches to Target Alpha-Synuclein and Related Neuroinflammation in Parkinson’s Disease

Cells ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 105 ◽  
Author(s):  
Maria Zella ◽  
Judith Metzdorf ◽  
Friederike Ostendorf ◽  
Fabian Maass ◽  
Siegfried Muhlack ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Glial Cell ◽  
Dopaminergic Neurons ◽  
Basic Research ◽  
Alpha Synuclein ◽  
Models Of Disease ◽  
Novel Therapeutic Strategies ◽  
Lymphocyte Populations

The etiology of Parkinson’s disease (PD) is significantly influenced by disease-causing changes in the protein alpha-Synuclein (aSyn). It can trigger and promote intracellular stress and thereby impair the function of dopaminergic neurons. However, these damage mechanisms do not only extend to neuronal cells, but also affect most glial cell populations, such as astroglia and microglia, but also T lymphocytes, which can no longer maintain the homeostatic CNS milieu because they produce neuroinflammatory responses to aSyn pathology. Through precise neuropathological examination, molecular characterization of biomaterials, and the use of PET technology, it has been clearly demonstrated that neuroinflammation is involved in human PD. In this review, we provide an in-depth overview of the pathomechanisms that aSyn elicits in models of disease and focus on the affected glial cell and lymphocyte populations and their interaction with pathogenic aSyn species. The interplay between aSyn and glial cells is analyzed both in the basic research setting and in the context of human neuropathology. Ultimately, a strong rationale builds up to therapeutically reduce the burden of pathological aSyn in the CNS. The current antibody-based approaches to lower the amount of aSyn and thereby alleviate neuroinflammatory responses is finally discussed as novel therapeutic strategies for PD.

A Characterization of Misfolded Alpha‐Synuclein in Parkinson’s Disease

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Daniel Shannon ◽  
John-Paul Bugada ◽  
Ethan Collins ◽  
Ellie Fischer ◽  
Delaney Hellard ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Alpha Synuclein

scholarly journals Transcriptome deregulation of peripheral monocytes in GBA-related Parkinson's disease

2021 ◽  
Author(s):  
Giulietta Maria Riboldi ◽  
Ricardo A Vialle ◽  
Elisa Navarro ◽  
Evan Udine ◽  
Katia de Paiva Lopes ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Membrane Trafficking ◽  
Whole Blood ◽  
Differential Expression Analysis ◽  
Enrichment Analysis ◽  
Alpha Synuclein ◽  
Ultrastructural Characterization ◽  
Gba Gene

Background: Genetic mutations in the beta-glucocerebrosidase (GCase), GBA gene, represent the major genetic risk factor for Parkinson's disease (PD). The function of the GBA gene is at the crossroads between the endo-lysosomal pathway and the immune response, two important mechanisms involved in the pathogenesis of PD. However, modifiers of GBA penetrance have not yet been fully elucidated. Methods: we characterized the transcriptomic profiles of circulating monocytes and whole blood in a population of patients with PD and healthy controls (CTRL) with (PD/GBA and CTRL/GBA) and without GBA variants (iPD and CTRL) (monocytes: n = 56 iPD, 66 CTRL, 23 PD/GBA, 13 CTRL/GBA; whole blood: n = 616 iPD, 362 CTRLs, 127 PD/GBA, 165 CTRL/GBA). Differential expression analysis, pathways enrichment analysis, and outliers detections were performed. Ultrastructural characterization of isolated CD14+ monocytes in the four groups was also performed through electron microscopy. Results: We observed hundreds of differentially expressed genes and dysregulated pathways when comparing manifesting and non-manifesting GBA mutation carriers. Specifically, when compared to idiopathic PD, GBA-PD showed dysregulation in genes involved in alpha-synuclein degradation, aging and amyloid processing (i.e. SNCA, LMNA). Gene-based outlier analysis confirmed the involvement of lysosomal, membrane trafficking, and mitochondrial processing in manifesting compared to nonmanifesting GBA-carriers, as also observed at the ultrastructural levels. Conclusions: Overall, our transcriptomic analysis of primary monocytes identified gene targets and biological processes that can help in understanding the pathogenic mechanisms associated with GBA mutations in the context of PD.

scholarly journals Mitochondria-mitochondria interaction networks show altered topological patterns in Parkinson’s disease

2020 ◽  
Author(s):  
Massimiliano Zanin ◽  
Bruno F. R. Santos ◽  
Paul M.A. Antony ◽  
Clara Berenguer-Escuder ◽  
Simone B. Larsen ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopaminergic Neurons ◽  
Point Mutations ◽  
Alpha Synuclein ◽  
Interaction Networks ◽  
Scale Free ◽  
Midbrain Dopaminergic Neurons ◽  
Machine Learning Approach

SUMMARYMitochondrial dysfunction is linked to pathogenesis of Parkinson’s disease (PD). However, individual-mitochondria-based analyses do not show a uniform feature in PD patients. Since mitochondria interact with each other, we hypothesize that PD-related features might exist in topological patterns of mitochondria-mitochondria interaction networks (MINs). Here we showed that MINs form non-classical scale-free supernetworks in colonic ganglia both from healthy controls and PD patients, however, altered topological patterns are observed in PD patients. These patterns highly correlate with PD clinical scores and a machine-learning approach based on the MIN features accurately distinguish between patients and controls with an area-under-curve value of 0.989. The MINs of midbrain dopaminergic neurons (mDANs) derived from several genetic PD patients also display specific changes. CRISPR/CAS9-based genome correction of alpha-synuclein point mutations reverses the changes in MINs of mDANs. Our MIN network analysis opens a new dimension for a deeper characterization of various complex diseases with mitochondrial dysregulation.

Formulation and Characterization of Microcapsules Encapsulating PC12 Cells as a Prospective Treatment Approach for Parkinson’s Disease

2021 ◽  
Vol 22 (4) ◽  
Author(s):  
Devyani J. Joshi ◽  
Neha M. Chitre ◽  
Amit Bansal ◽  
Kevin S. Murnane ◽  
Martin J. D’Souza
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Pc12 Cells ◽  
Treatment Approach

scholarly journals Longitudinal follow-up and characterization of a robust rat model for Parkinson's disease based on overexpression of alpha-synuclein with adeno-associated viral vectors

2015 ◽  
Vol 36 (3) ◽  
pp. 1543-1558 ◽  
Author(s):  
Anke Van der Perren ◽  
Jaan Toelen ◽  
Cindy Casteels ◽  
Francesca Macchi ◽  
Anne-Sophie Van Rompuy ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Rat Model ◽  
Viral Vectors ◽  
Alpha Synuclein
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