Time to move beyond nigrostriatal dopamine deficiency in Parkinson's disease

2004 ◽  
Vol 55 (6) ◽  
pp. 761-765 ◽  
Author(s):  
Anthony E. Lang ◽  
Jos� A. Obeso
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nigrostriatal Dopamine

scholarly journals Functional Crosstalk between CB and TRPV1 Receptors Protects Nigrostriatal Dopaminergic Neurons in the MPTP Model of Parkinson’s Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Rayul Wi ◽  
Young Cheul Chung ◽  
Byung Kwan Jin ◽  
Lihua Duan
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Significant Loss ◽  
Glial Activation ◽  
Dopamine Neurons ◽  
Pcr Analysis ◽  
Beneficial Effects ◽  
Nigrostriatal Dopamine ◽  
Nigrostriatal Dopamine Neurons

The present study examined whether crosstalk between cannabinoid (CB) and transient potential receptor vanilloid type 1 (TRPV1) could contribute to the survival of nigrostriatal dopamine neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson’s disease (PD). MPTP induced a significant loss of nigrostriatal dopamine neurons and glial activation in the substantia nigra (SN) and striatum (STR) as visualized by tyrosine hydroxylase (TH) or macrophage antigen complex-1 (MAC-1) or glial fibrillary acidic protein (GFAP) immunocytochemistry, respectively. RT-PCR analysis shows the upregulation of inducible nitric oxide synthase, interleukin-1β, and tumor necrosis factor-α in microglia in the SN in vivo, indicating the activation of the inflammatory system. By contrast, treatment with capsaicin (a specific TRPV1 agonist) increased the survival of dopamine neurons in the SN and their fibers and dopamine levels in the STR in MPTP mice. Capsaicin neuroprotection is accompanied by inhibiting MPTP-induced glial activation and production of inflammatory cytokines. Treatment with AM251 and AM630 (CB1/2 antagonists) abolished capsaicin-induced beneficial effects, indicating the existence of a functional crosstalk between CB and TRPV1. Moreover, treatment with anandamide (an endogenous agonist for both CB and TRVP1) rescued nigrostriatal dopamine neurons and reduced gliosis-derived neuroinflammatory responses in MPTP mice. These results suggest that the cannabinoid and vanilloid system may be beneficial for the treatment of neurodegenerative diseases, such as PD, that are associated with neuroinflammation.

Nigrostriatal dopamine transporter availability in early Parkinson's disease

2018 ◽  
Vol 33 (4) ◽  
pp. 592-599 ◽  
Author(s):  
Patrik Fazio ◽  
Per Svenningsson ◽  
Zsolt Cselényi ◽  
Christer Halldin ◽  
Lars Farde ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopamine Transporter ◽  
Nigrostriatal Dopamine ◽  
Early Parkinson’S Disease

scholarly journals Four Copies of SNCA Responsible for Autosomal Dominant Parkinson’s Disease in Two Italian Siblings

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Rosangela Ferese ◽  
Nicola Modugno ◽  
Rosa Campopiano ◽  
Marco Santilli ◽  
Stefania Zampatti ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Genetic Analysis ◽  
Psychiatric Symptoms ◽  
Alpha Synuclein ◽  
Genomic Region ◽  
Comparative Genomic ◽  
Nigrostriatal Dopamine ◽  
First Time ◽  
Dependent Probe

Background. Parkinson’s disease (PD) is mostly characterized by alpha-synuclein (SNCA) aggregation and loss of nigrostriatal dopamine-containing neurons. In this study a novel SNCA multiplication is described in two siblings affected by severe parkinsonism featuring early onset dyskinesia, psychiatric symptoms, and cognitive deterioration. Methods. SNCA dosage was performed using High-Density Comparative Genomic Hybridization Array (CGH-Array), Multiple Ligation Dependent Probe Amplification (MLPA), and Quantitative PCR (qPCR). Genetic analysis was associated with clinical evaluation. Results. Genetic analysis of siblings showed for the first time a 351 Kb triplication containing SNCA gene along with 6 exons of MMRN1 gene in 4q22.1 and a duplication of 1,29 Mb of a genomic region flanking the triplication. Conclusions. The identification of this family indicates a novel mechanism of SNCA gene multiplication, which confirms the genomic instability in this region and provides data on the genotype-phenotype correlation in PD patients.

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