scholarly journals Effect of the pituitary adenylate cyclase-activating polypeptide on the autophagic activation observed in in vitro and in vivo models of Parkinson's disease

2016 ◽  
Vol 1862 (4) ◽  
pp. 688-695 ◽  
Author(s):  
Asma Lamine-Ajili ◽  
Ahmed M. Fahmy ◽  
Myriam Létourneau ◽  
David Chatenet ◽  
Patrick Labonté ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Adenylate Cyclase ◽  
In Vivo Models ◽  
Pituitary Adenylate Cyclase

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 Neuroprotective Effect of the Marine-Derived Compound 11-Dehydrosinulariolide through DJ-1-Related Pathway in In Vitro and In Vivo Models of Parkinson’s Disease

Marine Drugs ◽  
2016 ◽  
Vol 14 (10) ◽  
pp. 187 ◽  
Author(s):  
Chien-Wei Feng ◽  
Han-Chun Hung ◽  
Shi-Ying Huang ◽  
Chun-Hong Chen ◽  
Yun-Ru Chen ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neuroprotective Effect ◽  
In Vivo Models ◽  
Related Pathway

scholarly journals Disruption of Mitochondrial Homeostasis: The Role of PINK1 in Parkinson’s Disease

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 3022
Author(s):  
Maria Vizziello ◽  
Linda Borellini ◽  
Giulia Franco ◽  
Gianluca Ardolino
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopaminergic Neurons ◽  
Gene Mutations ◽  
Neuronal Population ◽  
In Vivo Models ◽  
Mitochondrial Homeostasis

The progressive reduction of the dopaminergic neurons of the substantia nigra is the fundamental process underlying Parkinson’s disease (PD), while the mechanism of susceptibility of this specific neuronal population is largely unclear. Disturbances in mitochondrial function have been recognized as one of the main pathways in sporadic PD since the finding of respiratory chain impairment in animal models of PD. Studies on genetic forms of PD have provided new insight on the role of mitochondrial bioenergetics, homeostasis, and autophagy. PINK1 (PTEN-induced putative kinase 1) gene mutations, although rare, are the second most common cause of recessively inherited early-onset PD, after Parkin gene mutations. Our knowledge of PINK1 and Parkin function has increased dramatically in the last years, with the discovery that a process called mitophagy, which plays a key role in the maintenance of mitochondrial health, is mediated by the PINK1/Parkin pathway. In vitro and in vivo models have been developed, supporting the role of PINK1 in synaptic transmission, particularly affecting dopaminergic neurons. It is of paramount importance to further define the role of PINK1 in mitophagy and mitochondrial homeostasis in PD pathogenesis in order to delineate novel therapeutic targets.

scholarly journals Preclinical Investigation in Neuroprotective Effects of the GPR55 Ligand VCE-006.1 in Experimental Models of Parkinson’s Disease and Amyotrophic Lateral Sclerosis

Molecules ◽  
2021 ◽  
Vol 26 (24) ◽  
pp. 7643
Author(s):  
Sonia Burgaz ◽  
Concepción García ◽  
Claudia Gonzalo-Consuegra ◽  
Marta Gómez-Almería ◽  
Francisco Ruiz-Pino ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Amyotrophic Lateral Sclerosis ◽  
Neuroprotective Effects ◽  
In Vivo Models ◽  
Bv2 Cells ◽  
Lateral Sclerosis ◽  
Glial Reactivity

Cannabinoids act as pleiotropic compounds exerting, among others, a broad-spectrum of neuroprotective effects. These effects have been investigated in the last years in different preclinical models of neurodegeneration, with the cannabinoid type-1 (CB1) and type-2 (CB2) receptors concentrating an important part of this research. However, the issue has also been extended to additional targets that are also active for cannabinoids, such as the orphan G-protein receptor 55 (GPR55). In the present study, we investigated the neuroprotective potential of VCE-006.1, a chromenopyrazole derivative with biased orthosteric and positive allosteric modulator activity at GPR55, in murine models of two neurodegenerative diseases. First, we proved that VCE-006.1 alone could induce ERK1/2 activation and calcium mobilization, as well as increase cAMP response but only in the presence of lysophosphatidyl inositol. Next, we investigated this compound administered chronically in two neurotoxin-based models of Parkinson’s disease (PD), as well as in some cell-based models. VCE-006.1 was active in reversing the motor defects caused by 6-hydroxydopamine (6-OHDA) in the pole and the cylinder rearing tests, as well as the losses in tyrosine hydroxylase-containing neurons and the elevated glial reactivity detected in the substantia nigra. Similar cytoprotective effects were found in vitro in SH-SY5Y cells exposed to 6-OHDA. We also investigated VCE-006.1 in LPS-lesioned mice with similar beneficial effects, except against glial reactivity and associated inflammatory events, which remained unaltered, a fact confirmed in BV2 cells treated with LPS and VCE-006.1. We also analyzed GPR55 in these in vivo models with no changes in its gene expression, although GPR55 was down-regulated in BV2 cells treated with LPS, which may explain the lack of efficacy of VCE-006.1 in such an assay. Furthermore, we investigated VCE-006.1 in two genetic models of amyotrophic lateral sclerosis (ALS), mutant SOD1, or TDP-43 transgenic mice. Neither the neurological decline nor the deteriorated rotarod performance were prevented with this compound, and the same happened with the elevated microglial and astroglial reactivities, albeit modest spinal motor neuron preservation was achieved in both models. We also analyzed GPR55 in these in vivo models and found no changes in both TDP-43 transgenic and mSOD1 mice. Therefore, our findings support the view that targeting the GPR55 may afford neuroprotection in experimental PD, but not in ALS, thus stressing the specificities for the development of cannabinoid-based therapies in the different neurodegenerative disorders.

Implications of VIP and PACAP in Parkinson’s disease: what do we know so far?

2020 ◽  
Vol 27 ◽  
Author(s):  
Filipe Resende Oliveira de Souza ◽  
Fabiola Mara Ribeiro ◽  
Patricia Maria d' Almeida Lima
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Vasoactive Intestinal Peptide ◽  
In Vitro Models ◽  
Cytokines And Chemokines ◽  
Pituitary Adenylate Cyclase ◽  
Key Factor

Background: Parkinson’s disease is one of the most common neurodegenerative disorders and, although its etiology remains not yet fully understood, neuroinflammation has been pointed as a key factor for the progres-sion of the disease. Vasoactive intestinal peptide and pituitary adenilate-cyclase activating polypeptide are two neuropeptides that exhibit antiinflammatory and neuroprotective properties, modulating the production of cyto-kines and chemokines and the behaviour of immune cells. However, the role of chemokines and cytokines modu-lated by the endogenous receptors of the peptides vary according to the stage of the disease. Methods: Overview of the relationship between some cytokines and chemokines with vasoactive intestinal peptide, pituitary adenylate cyclase activating polypeptide and their endogenous receptors in the context of Parkinson’s disease neuroinflammation and oxidative stress, as well as the modulation of microglial cells by the peptides in this context. Results: The two peptides exhibit neuroprotective and antiinflammatory properties in models of Parkinson’s dis-ease, as they ameliorate cognitive functions, decrease the levels of neuroinflammation and promote dopaminergic neuronal survival. The peptides have been tested in a variety of in vivo and in vitro models of Parkinson’s disease, demonstrating potential for therapeutic application. Conclusion: More studies are needed to stablish the clinical use of vasoactive intestinal peptide and pituitary ade-nylate cyclase activating polypeptide as safe candidates for treating Parkinson’s disease, as the use of the peptides in different stages of the disease could produce different results concerning effectiveness.

EPO-Dependent Activation of PI3K/Akt/FoxO3a Signalling Mediates Neuroprotection in In Vitro and In Vivo Models of Parkinson’s Disease

2014 ◽  
Vol 53 (1) ◽  
pp. 117-124 ◽  
Author(s):  
Yu Jia ◽  
Shi-Jing Mo ◽  
Qi-Qi Feng ◽  
Ma-Li Zhan ◽  
Li-Si OuYang ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
In Vivo Models
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