Zobrazeno 1 - 10 of 105 pro vyhledávání: '"genetics [alpha-Synuclein]"'
1
miR-101a-3p Impairs Synaptic Plasticity and Contributes to Synucleinopathy
Autor: Mary Xylaki, Isabel Paiva, Mohammed Al-Azzani, Ellen Gerhardt, Gaurav Jain, Md Rezaul Islam, Eftychia Vasili, Zinah Wassouf, Julia M. Schulze-Hentrich, André Fischer, Tiago Fleming Outeiro
Publikováno v: Journal of Parkinson's Disease : JPD
Journal of Parkinson's Disease 13(2), 179-196 (2023). doi:10.3233/JPD-225055
Background:Synucleinopathies are disorders characterized by the abnormal accumulation of α-synuclein (aSyn). Synaptic compromise is observed in synucleinopathies parallel to aSyn aggregation and is accompanied by transcript deregulation.Objective:We
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::179995a601cf57d2d0eab04219b18be8
https://doi.org/10.3233/jpd-225055
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2
Acid ceramidase involved in pathogenic cascade leading to accumulation of α-synuclein in iPSC model of GBA1-associated Parkinson’s disease
Autor: Manoj Kumar, Manasa P Srikanth, Michela Deleidi, Penelope J Hallett, Ole Isacson, Ricardo A Feldman
Publikováno v: Human molecular genetics 32(11), 1888-1900 (2023). doi:10.1093/hmg/ddad025
Bi-allelic mutations in GBA1, the gene that encodes β-glucocerebrosidase (GCase), cause Gaucher disease (GD), whereas mono-allelic mutations do not cause overt pathology. Yet mono- or bi-allelic GBA1 mutations are the highest known risk factor for P
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0e623d80d2d569f3311782fe53a2d787
https://doi.org/10.1093/hmg/ddad025
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3
Inflammation promotes synucleinopathy propagation
Autor: Tae-Kyung Kim, Eun-Jin Bae, Byung Chul Jung, Minsun Choi, Soo Jean Shin, Sung Jun Park, Jeong Tae Kim, Min Kyo Jung, Ayse Ulusoy, Mi-Young Song, Jun Sung Lee, He-Jin Lee, Donato A. Di Monte, Seung-Jae Lee
Publikováno v: Experimental & molecular medicine 54(12), 2148-2161 (2022). doi:10.1038/s12276-022-00895-w
The clinical progression of neurodegenerative diseases correlates with the spread of proteinopathy in the brain. The current understanding of the mechanism of proteinopathy spread is far from complete. Here, we propose that inflammation is fundamenta
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::37e379b9c198ff4f5969aaf652911957
https://doi.org/10.1038/s12276-022-00895-w
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4
Failure of diet-induced transcriptional adaptations in alpha-synuclein transgenic mice
Autor: Alexander Kilzheimer, Thomas Hentrich, Carola Rotermund, Philipp J Kahle, Julia M Schulze-Hentrich
Publikováno v: Human molecular genetics 32(3), 450-461 (2023). doi:10.1093/hmg/ddac205
Nutritional influences have been discussed as potential modulators of Parkinson’s disease (PD) pathology through various epidemiological and physiological studies. In animal models, a high-fat diet (HFD) with greater intake of lipid-derived calorie
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ea1796898c93b59fc865d9cb30511ebb
https://doi.org/10.1093/hmg/ddac205
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5
α-Synuclein conformers reveal link to clinical heterogeneity of α-synucleinopathies
Autor: Matthias Schmitz, Niccolò Candelise, Sezgi Canaslan, Hermann C. Altmeppen, Jakob Matschke, Markus Glatzel, Neelam Younas, Saima Zafar, Peter Hermann, Inga Zerr
Publikováno v: Translational neurodegeneration 12(1), 12 (2023). doi:10.1186/s40035-023-00342-4
α-Synucleinopathies, such as Parkinson’s disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy, are a class of neurodegenerative diseases exhibiting intracellular inclusions of misfolded α-synuclein (αSyn), referred to as Lew
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0a4c5cc481b8016769c70689b2aaa440
https://doi.org/10.1186/s40035-023-00342-4
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7
Non-SUMOylated alternative spliced isoforms of alpha-synuclein are more aggregation-prone and toxic
Autor: Kambiz Hassanzadeh, Castrese Morrone, Keivan Akhtari, Ellen Gerhardt, Ludovica Zaccagnini, Tiago Fleming Outeiro, Marco Feligioni
Publikováno v: Mechanisms of ageing and development 209, 111759 (2023). doi:10.1016/j.mad.2022.111759
The exon skipping of α-Synuclein (α-Syn), the main constituent of the abnormal protein aggregation in Lewy bodies of Parkinson's disease (PD), forms four isoforms. In contrast to the full length α-Syn (α-Syn 140), little is known about the splice
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c6ca16c86426562edccb2cadf5a7c7f2
https://pub.dzne.de/record/169127
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10
Intracranial administration of alpha-synuclein fibrils in A30P-synuclein transgenic mice causes robust synucleinopathy and microglial induction
Autor: Philipp J. Kahle, Renee C Gentzel, Lei Ma, Jacob Marcus, Sean M. Smith, Dawn Toolan, Joel B. Schachter, Sarah Jinn
Publikováno v: Neurobiology of aging 106, 12-25 (2021). doi:10.1016/j.neurobiolaging.2021.05.012
Synucleinopathies are neurodegenerative disorders involving pathological alpha-synuclein (αSyn) protein, including dementia with Lewy bodies, multiple system atrophy and Parkinson's disease (PD). Current in vivo models of synucleinopathy include tra
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::cd63ea6b0e4145e8f82abc6da25eeae2
https://doi.org/10.1016/j.neurobiolaging.2021.05.012
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