Dopaminergic Cell

2020 ◽  
Author(s):  
Keyword(s):  
Author(s):  
Jamila Zaiter ◽  
Achraf Hibot ◽  
Abderrafia Hafid ◽  
Mostafa Khouili ◽  
Claudia M.B. Neves ◽  
...  

2001 ◽  
Vol 7 (3) ◽  
pp. 273-281 ◽  
Author(s):  
D Beitner-Johnson ◽  
K Seta ◽  
Y Yuan ◽  
H.-W Kim ◽  
R.T Rust ◽  
...  

Author(s):  
Irene García-Domínguez ◽  
Karolina Veselá ◽  
Juan García-Revilla ◽  
Alejandro Carrillo-Jiménez ◽  
María Angustias Roca-Ceballos ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Deok-Sang Hwang ◽  
Hyo Geun Kim ◽  
Jun-Bock Jang ◽  
Myung Sook Oh

Dangguijakyak-san (DJS), a famous traditional Korean multiherbal medicine, has been used to treat gynecological and neuro-associated disease. Recent studies demonstrated that DJS has multiple bioactivities including neuroprotection. In the present study, we were to investigate the effect of DJS and its mechanism in anin vitroandin vivomodel of Parkinson’s disease (PD). In primary mesencephalic culture system, DJS attenuated the dopaminergic cell damage induced by 1-methyl-4-phenylpyridine toxicity, and it inhibited production of inflammatory factors such as tumor necrosis factorα(TNF-α), nitric oxide (NO), and activation of microglial cells. Then, we confirmed the effect of DJS in a mouse PD model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). In the pole test, DJS at 50 mg/kg/day for 5 days showed increase of motor activity showing shortened time to turn and locomotor activity compared with the MPTP only treated mice. In addition, DJS significantly protected nigrostriatal dopaminergic neuron from MPTP stress. Moreover, DJS showed inhibition of gliosis in the substantia nigra pars compacta. These results have therapeutic implications for DJS in the treatment of PD via anti-inflammatory effects.


Author(s):  
Alexey Kuznetsov ◽  
Boris Gutkin

Biomolecules ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 93
Author(s):  
Victor Blokhin ◽  
Maria Shupik ◽  
Ulyana Gutner ◽  
Ekaterina Pavlova ◽  
Albert T. Lebedev ◽  
...  

Parkinson’s disease (PD) is a neurodegenerative disease incurable due to late diagnosis and treatment. Therefore, one of the priorities of neurology is to study the mechanisms of PD pathogenesis at the preclinical and early clinical stages. Given the important role of sphingolipids in the pathogenesis of neurodegenerative diseases, we aimed to analyze the gene expression of key sphingolipid metabolism enzymes (ASAH1, ASAH2, CERS1, CERS3, CERS5, GBA1, SMPD1, SMPD2, UGCG) and the content of 32 sphingolipids (subspecies of ceramides, sphingomyelins, monohexosylceramides and sphinganine, sphingosine, and sphingosine-1-phosphate) in the nigrostriatal system in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse models of the preclinical and clinical stages of PD. It has been shown that in PD models, the expression of five of the nine studied genes (CERS1, CERS5, ASAH1, ASAH2, and GBA1) increases but only in the substantia nigra (SN) containing dopaminergic cell bodies. Changes in the expression of enzyme genes were accompanied by an increase in the content of 7 of the 32 studied sphingolipids. Such findings suggest these genes as attractive candidates for diagnostic purposes for preclinical and clinical stages of PD.


2017 ◽  
Vol 7 (8) ◽  
pp. 562 ◽  
Author(s):  
B. Grimmig ◽  
L. Daly ◽  
C. Hudson ◽  
K.R. Nash ◽  
P.C. Bickford

Background: Astaxanthin (AXT) is a natural carotenoid with diverse biological activities. Although it is best known as a potent antioxidant, recent work suggests additional mechanisms of action that have the potential to oppose the ongoing pathophysiology of Parkinson’s disease (PD). For example, AXT has a putative role in modulating microglial activity and preserving mitochondrial function, thereby implicating this compound as a neuroprotective agent. Both oxidative stress and inflammation are involved in the progression of many neurodegenerative diseases. Therefore, we examined the efficacy for AXT to reduced neurotoxicity in a toxic model of PD in mice. Methods: In this study, we used a 4-week dietary supplementation of algae derived AXT to reduce 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced dopaminergic cell death.Results: AXT treated mice were protected against the loss of tyrosine hydroxylase (TH) staining in the substantia nigra (SN) after MPTP exposure compared to the control diet. This effect of preserved TH immunoreactivity was also observed in the striatum. Furthermore, AXT administration was able to interrupt the neuroinflammatory process known to contribute to neurodegeneration in this model.Conclusions: We demonstrate that AXT neuroprotection was associated with attenuated microglial activation as indicated by reduced immunohistochemical detection of IBA-1 in the SN and striatum of AXT treated mice. Altogether, these studies suggest that AXT has neuroprotective property in the central nervous system against MPTP neurodegeneration.Keywords: Astaxanthin, Neuroprotection, Neurodegeneration, Neuroinflammation, Parkinson’s disease


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