alpha-Synuclein

Publication Title: 
Rejuvenation Research

A botanical extract (Regrapex-R) prepared from whole grape (Vitis vinifera) and Polygonum cuspidatum, which contains polyphenols, including flavans, anthocyanins, emodin, and resveratrol, exhibited dose-dependent scavenging effects on reactive oxygen species (ROS). The extract inhibited increases of ROS and protein carbonyl in isolated rat liver mitochondria following exposure to 2,2'-azobis (2-amidino propane) dihydrocholoride (AAPH), a potent lipid oxidant generator.

Author(s): 
Long, Jiangang
Gao, Hongxiang
Sun, Lijuan
Liu, Jiankang
Zhao-Wilson, Xi
Publication Title: 
PloS One

Induced pluripotent stem cell (iPSC) technology can be used to model human disorders, create cell-based models of human diseases, including neurodegenerative diseases, and in establishing therapeutic strategies. To detect subtle cellular abnormalities associated with common late-onset disease in iPSCs, valid control iPSCs derived from healthy donors free of serious late-onset diseases are necessary. Here, we report the generation of iPSCs from fibroblasts obtained immediately postmortem from centenarian donors (106- and 109-years-old) who were extremely healthy until an advanced age.

Author(s): 
Yagi, Takuya
Kosakai, Arifumi
Ito, Daisuke
Okada, Yohei
Akamatsu, Wado
Nihei, Yoshihiro
Nabetani, Akira
Ishikawa, Fuyuki
Arai, Yasumichi
Hirose, Nobuyoshi
Okano, Hideyuki
Suzuki, Norihiro
Publication Title: 
PloS One

Induced pluripotent stem cell (iPSC) technology can be used to model human disorders, create cell-based models of human diseases, including neurodegenerative diseases, and in establishing therapeutic strategies. To detect subtle cellular abnormalities associated with common late-onset disease in iPSCs, valid control iPSCs derived from healthy donors free of serious late-onset diseases are necessary. Here, we report the generation of iPSCs from fibroblasts obtained immediately postmortem from centenarian donors (106- and 109-years-old) who were extremely healthy until an advanced age.

Author(s): 
Yagi, Takuya
Kosakai, Arifumi
Ito, Daisuke
Okada, Yohei
Akamatsu, Wado
Nihei, Yoshihiro
Nabetani, Akira
Ishikawa, Fuyuki
Arai, Yasumichi
Hirose, Nobuyoshi
Okano, Hideyuki
Suzuki, Norihiro
Publication Title: 
Biochemical and Biophysical Research Communications

Multiple system atrophy is a neurodegenerative disease caused by abnormal ?-synuclein (?-syn) accumulation in oligodendrocytes and neurons. We previously demonstrated that transgenic (Tg) mice that selectively overexpressed human ?-syn in oligodendrocytes exhibited neuronal ?-syn accumulation. Microtubule ?-III tubulin binds to endogenous neuronal ?-syn to form an insoluble complex, leading to progressive neuronal degeneration. ?-Syn accumulation is increased in the presynaptic terminals of Tg mice neurons and may reduce neurotransmitter release.

Author(s): 
Ito, Hiroshi
Nakayama, Kimiko
Jin, Chenghua
Suzuki, Yasuyo
Yazawa, Ikuru
Publication Title: 
CNS & neurological disorders drug targets

The neural protein ?-synuclein aggregates both in vivo and in vitro to form insoluble fibrils that are involved in Parkinson's disease pathogenesis. We have generated ?-synuclein/fluorescent-protein fusion constructs overexpressed in muscle cells of the nematode, Caenorhabdtis elegans. Green Fluorescent Protein (GFP) variants, Cerulean (C) or Venus (V), were fused to the C-terminus of human ?-synuclein (S); the resultant fusion genes were designated SV and SC, plus a CV fusion as well as S, C and V singly. The aggregation behavior of the purified fusion proteins (expressed in E.

Author(s): 
Bodhicharla, Rakesh
Nagarajan, Archana
Winter, Jody
Adenle, Ademola
Nazir, Aamir
Brady, Declan
Vere, Kelly
Richens, Jo
O'Shea, Paul
Bell, David R.
de Pomerai, David
Publication Title: 
Neurotoxicity Research

?-Synuclein is the key aggregating protein in Parkinson's disease (PD), which is characterized by cytoplasmic protein inclusion bodies, termed Lewy bodies, thought to increase longevity of the host neuron by sequestering toxic soluble ?-synuclein oligomers. Previous post-mortem studies have shown relative sparing of neurons in PD that are positive for the Ca(2+) buffering protein, calbindin, and recent cell culture and in vitro studies have shown that ?-synuclein aggregation can be induced by Ca(2+).

Author(s): 
Follett, Jordan
Darlow, Bonnie
Wong, Mathew B.
Goodwin, Jacob
Pountney, Dean L.
Publication Title: 
CNS & neurological disorders drug targets

Aging, the major cause of several ailments has led to intense exploration of potential drugs that delay aging and its associated effects. We mined the information on traditional Indian medicines and identified an iridoid, 10-O-trans-p-Coumaroylcatalpol (OCC), a major ingredient of Premna integrifolia Linn. (syn: Premna serratifolia). OCC forms an important constituent of famous herbal formulation 'Dashmula', a ten herb formulation, commonly used for its various medicinal properties. Employing model system C.

Author(s): 
Shukla, Virendra
Phulara, Suresh C.
Yadav, Deepti
Tiwari, Sudeep
Kaur, Supinder
Gupta, M. M.
Nazir, Aamir
Pandey, Rakesh
Publication Title: 
Neuroreport

The aim of this study was to investigate whether the DNA methylation pattern within the alpha synuclein promoter region is altered in intoxicated and early abstinence patients with alcoholism undergoing alcohol withdrawal. We observed a significant increase of the alpha synuclein promoter DNA methylation in patients with alcoholism which was significantly associated with their elevated homocysteine levels. No significant differences of the promoter DNA methylation within a control gene (presenilin-1) in alcoholics and controls were found.

Author(s): 
Bˆnsch, Dominikus
Lenz, Bernd
Kornhuber, Johannes
Bleich, Stefan
Publication Title: 
Parkinsonism & Related Disorders

The identification of the p.A53T mutation in the SNCA gene encoding alpha-synuclein (alpha-syn), as causative of autosomal dominant Parkinson disease (PD) represented a fundamental milestone, which paved the way to the extremely prolific field of PD genetics. Despite being the oldest player in this field and only a rare cause of inherited PD, research on alpha-syn has remained incredibly active over nearly twenty decades, leading to identify alpha-syn aggregation as a key mechanism in PD pathogenesis.

Author(s): 
Petrucci, Simona
Ginevrino, Monia
Valente, Enza Maria
Publication Title: 
FEBS letters

Aggregation of α-synuclein is a pathological hallmark of sporadic or familial PD. However, the detailed molecular mechanism responsible for the aggregation of α-synuclein has not been properly explored. In the present study, we have identified a novel role of an anti-tumorigenic BTB/POZ domain containing protein-2 (BPOZ-2) in the regulation of α-synuclein accumulation in dopaminergic (DA) neurons. MPP(+), an etiological factor for PD, significantly downregulated the expression of BPOZ-2 ahead of α-synuclein upregulation.

Author(s): 
Roy, Avik
Pahan, Kalipada

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