3.235 ISOTHIOCYANATES PROTECT AGAINST DOPAMINERGIC CELL DEATH IN IN VITRO AND IN VIVO MODELS OF PARKINSON'S DISEASE

2012 ◽  
Vol 18 ◽  
pp. S212
Author(s):  
F. Morroni ◽  
P. Hrelia ◽  
C. Bolondi ◽  
G. Cantelli-Forti ◽  
A. Tarozzi
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Death ◽  
In Vivo Models ◽  
Dopaminergic Cell

scholarly journals Peripheral Inflammation Enhances Microglia Response and Nigral Dopaminergic Cell Death in an in vivo MPTP Model of Parkinson’s Disease

2018 ◽  
Vol 12 ◽  
Author(s):  
Irene García-Domínguez ◽  
Karolina Veselá ◽  
Juan García-Revilla ◽  
Alejandro Carrillo-Jiménez ◽  
María Angustias Roca-Ceballos ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Death ◽  
Peripheral Inflammation ◽  
Dopaminergic Cell ◽  
Mptp Model

scholarly journals Neuroprotection in Parkinson’s disease: facts and hopes

2019 ◽  
Vol 127 (5) ◽  
pp. 821-829 ◽  
Author(s):  
András Salamon ◽  
Dénes Zádori ◽  
László Szpisjak ◽  
Péter Klivényi ◽  
László Vécsei
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Loss ◽  
Substantia Nigra Pars Compacta ◽  
Neuroprotective Agents ◽  
Dopaminergic Cell ◽  
Pathological Mechanism ◽  
Positive Results

AbstractParkinson’s disease (PD) is the second most common neurodegenerative disease worldwide. Behind the symptoms there is a complex pathological mechanism which leads to a dopaminergic cell loss in the substantia nigra pars compacta. Despite the strong efforts, curative treatment has not been found yet. To prevent a further cell death, numerous molecules were tested in terms of neuroprotection in preclinical (in vitro, in vivo) and in clinical studies as well. The aim of this review article is to summarize our knowledge about the extensively tested neuroprotective agents (Search period: 1991–2019). We detail the underlying pathological mechanism and summarize the most important results of the completed animal and clinical trials. Although many positive results have been reported in the literature, there is still no evidence that any of them should be used in clinical practice (Cochrane analysis was performed). Therefore, further studies are needed to better understand the pathomechanism of PD and to find the optimal neuroprotective agent(s).

Clioquinol Protects Against Cell Death in Parkinson’s Disease Models In Vivo and In Vitro

2009 ◽  
pp. 431-442 ◽  
Author(s):  
Simon Wilkins ◽  
Colin L. Masters ◽  
Ashley I. Bush ◽  
Robert A. Cherny ◽  
David I. Finkelstein
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Death ◽  
Disease Models

scholarly journals Comparison of Adaptive Neuroprotective Mechanisms of Sulforaphane and its Interconversion Product Erucin in in Vitro and in Vivo Models of Parkinson’s Disease

2018 ◽  
Vol 66 (4) ◽  
pp. 856-865 ◽  
Author(s):  
Fabiana Morroni ◽  
Giulia Sita ◽  
Alice Djemil ◽  
Massimo D’Amico ◽  
Letizia Pruccoli ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
In Vivo Models

scholarly journals Ablation of RIP3 protects from dopaminergic neurodegeneration in experimental Parkinson’s disease

2019 ◽  
Vol 10 (11) ◽  
Author(s):  
Pedro A. Dionísio ◽  
Sara R. Oliveira ◽  
Maria M. Gaspar ◽  
Maria J. Gama ◽  
Margarida Castro-Caldas ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Death ◽  
Cultured Cells ◽  
Substantia Nigra Pars Compacta ◽  
Neuronal Cultures ◽  
Interacting Protein ◽  
Dopaminergic Neurodegeneration

Abstract Parkinson’s disease (PD) is driven by dopaminergic neurodegeneration in the substantia nigra pars compacta (SN) and striatum. Although apoptosis is considered the main neurodegenerative mechanism, other cell death pathways may be involved. In this regard, necroptosis is a regulated form of cell death dependent on receptor interacting protein 3 (RIP3), a protein also implicated in apoptosis and inflammation independently of its pro-necroptotic activity. Here, we explored the role of RIP3 genetic deletion in in vivo and in vitro PD models. Firstly, wild-type (Wt) and RIP3 knockout (RIP3ko) mice were injected intraperitoneally with MPTP (40 mg/kg, i.p.), and sacrificed after either 6 or 30 days. RIP3ko protected from dopaminergic neurodegeneration in the SN of MPTP-injected mice, but this effect was independent of necroptosis. In keeping with this, necrostatin-1s (10 mg/kg/day, i.p.) did not afford full neuroprotection. Moreover, MPTP led to DNA fragmentation, caspase-3 activation, lipid peroxidation and BAX expression in Wt mice, in the absence of caspase-8 cleavage, suggesting intrinsic apoptosis. This was mimicked in primary cortical neuronal cultures exposed to the active MPTP metabolite. RIP3 deficiency in cultured cells and in mouse brain abrogated all phenotypes. Curiously, astrogliosis was increased in the striatum of MPTP-injected Wt mice and further exacerbated in RIP3ko mice. This was accompanied by absence of microgliosis and reposition of glial cell line-derived neurotrophic factor (GDNF) levels in the striata of MPTP-injected RIP3ko mice when compared to MPTP-injected Wt mice, which in turn showed a massive GDNF decrease. RIP3ko primary mixed glial cultures also presented decreased expression of inflammation-related genes upon inflammatory stimulation. These findings hint at possible undescribed non-necroptotic roles for RIP3 in inflammation and MPTP-driven cell death, which can contribute to PD progression.

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