Dopamine depletion impairs precursor cell proliferation in Parkinson disease

2004 ◽  
Vol 7 (7) ◽  
pp. 726-735 ◽  
Author(s):  
Günter U Höglinger ◽  
Pamela Rizk ◽  
Marie P Muriel ◽  
Charles Duyckaerts ◽  
Wolfgang H Oertel ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Parkinson Disease ◽  
Precursor Cell ◽  
Dopamine Depletion

Patterns of striatal dopamine depletion in early Parkinson disease

Neurology ◽  
2020 ◽  
Vol 95 (3) ◽  
pp. e280-e290 ◽  
Author(s):  
Seok Jong Chung ◽  
Hye Sun Lee ◽  
Han Soo Yoo ◽  
Yang Hyun Lee ◽  
Phil Hyu Lee ◽  
...  
Keyword(s):  
Factor Analysis ◽  
Parkinson Disease ◽  
Cox Regression ◽  
Early Stage ◽  
Freezing Of Gait ◽  
Striatal Dopamine ◽  
Dopamine Depletion ◽  
Wearing Off ◽  
Striatal Dopamine Depletion ◽  
Selective Dopamine

ObjectiveTo investigate whether the patterns of striatal dopamine depletion on dopamine transporter (DAT) scans could provide information on the long-term prognosis in Parkinson disease (PD).MethodsWe enrolled 205 drug-naive patients with early-stage PD, who underwent 18F-FP-CIT PET scans at initial assessment and received PD medications for 3 or more years. After quantifying the DAT availability in each striatal subregion, factor analysis was conducted to simplify the identification of striatal dopamine depletion patterns and to yield 4 striatal subregion factors. We assessed the effect of these factors on the development of levodopa-induced dyskinesia (LID), wearing-off, freezing of gait (FOG), and dementia during the follow-up period (6.84 ± 1.80 years).ResultsThe 4 factors indicated which striatal subregions were relatively preserved: factor 1 (caudate), factor 2 (more-affected sensorimotor striatum), factor 3 (less-affected sensorimotor striatum), and factor 4 (anterior putamen). Cox regression analyses using the composite scores of these striatal subregion factors as covariates demonstrated that selective dopamine depletion in the sensorimotor striatum was associated with a higher risk for developing LID. Selective dopamine loss in the putamen, particularly in the anterior putamen, was associated with early development of wearing-off. Selective involvement of the anterior putamen was associated with a higher risk for dementia conversion. However, the patterns of striatal dopamine depletion did not affect the risk of FOG.ConclusionsThese findings suggested that the patterns of striatal dopaminergic denervation, which were estimated by the equation derived from the factor analysis, have a prognostic implication in patients with early-stage PD.

scholarly journals Oncogenes - the basics

2018 ◽  
Vol 3 (4) ◽  
pp. 35-37
Author(s):  
Arnab Ghosh ◽  
Diasma Ghartimagar ◽  
Sushma Thapa
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Dna Repair ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Normal Cell ◽  
Tumor Formation ◽  
Precursor Cell ◽  
Single Precursor ◽  
Normal Cell Cycle

Normal cell cycle and cell proliferation are regulated by several genes which can be broadly classified into 4 groups viz, proto-oncogenes, tumor suppressor genes, genes regulating apoptosis and genes involved in DNA repair. These genes may be defective due to different factors. The defective genes may lead to production of abnormal proteins which may lead to disruption of the normal cell cycle and proliferation. A single precursor cell with defective gene proliferates surpassing the normal physiologic regulatory process and leads to tumor formation, so, traditionally,it is said that “tumors are clonal”.

scholarly journals Nox4 Promotes Neural Stem/Precursor Cell Proliferation and Neurogenesis in the Hippocampus and Restores Memory Function Following Trimethyltin-Induced Injury

Neuroscience ◽  
2019 ◽  
Vol 398 ◽  
pp. 193-205 ◽  
Author(s):  
Yoji Yoshikawa ◽  
Tetsuro Ago ◽  
Junya Kuroda ◽  
Yoshinobu Wakisaka ◽  
Masaki Tachibana ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Memory Function ◽  
Precursor Cell

Corrigendum to “Neuropeptide Y is important for basal and seizure-induced precursor cell proliferation in the hippocampus” [Neurobiol. Dis. 26/1 (2007) 174–188]

2013 ◽  
Vol 49 ◽  
pp. 199
Author(s):  
Owain W. Howell ◽  
Sharmalene Silva ◽  
Helen E. Scharfman ◽  
Alexander A. Sosunov ◽  
Malik Zaben ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Neuropeptide Y ◽  
Precursor Cell

scholarly journals Stabilized β-Catenin Functions through TCF/LEF Proteins and the Notch/RBP-Jκ Complex To Promote Proliferation and Suppress Differentiation of Neural Precursor Cells

2008 ◽  
Vol 28 (24) ◽  
pp. 7427-7441 ◽  
Author(s):  
Takeshi Shimizu ◽  
Tetsushi Kagawa ◽  
Toshihiro Inoue ◽  
Aya Nonaka ◽  
Shinji Takada ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Neuronal Differentiation ◽  
Glycogen Synthase ◽  
Precursor Cells ◽  
Precursor Cell ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Self Renewal ◽  
Fgf Receptor ◽  
Proliferation And Differentiation

ABSTRACT The proliferation and differentiation of neural precursor cells are mutually exclusive during brain development. Despite its importance for precursor cell self renewal, the molecular linkage between these two events has remained unclear. Fibroblast growth factor 2 (FGF2) promotes neural precursor cell proliferation and concurrently inhibits their differentiation, suggesting a cross talk between proliferation and differentiation signaling pathways downstream of the FGF receptor. We demonstrate that FGF2 signaling through phosphatidylinositol 3 kinase activation inactivates glycogen synthase kinase 3β (GSK3β) and leads to the accumulation of β-catenin in a manner different from that in the Wnt canonical pathway. The nuclear accumulated β-catenin leads to cell proliferation by activating LEF/TCF transcription factors and concurrently inhibits neuronal differentiation by potentiating the Notch1-RBP-Jκ signaling pathway. β-Catenin and the Notch1 intracellular domain form a molecular complex with the promoter region of the antineurogenic hes1 gene, allowing its expression. This signaling interplay is especially essential for neural stem cell maintenance, since the misexpression of dominant-active GSK3β completely inhibits the self renewal of neurosphere-forming stem cells and prompts their neuronal differentiation. Thus, the GSK3β/β-catenin signaling axis regulated by FGF and Wnt signals plays a pivotal role in the maintenance of neural stem/precursor cells by linking the cell proliferation to the inhibition of differentiation.

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