Levels of alpha‐synuclein mRNA in sporadic Parkinson disease patients
Identifieur interne : 001271 ( Main/Exploration ); précédent : 001270; suivant : 001272Levels of alpha‐synuclein mRNA in sporadic Parkinson disease patients
Auteurs : Ornit Chiba-Falek [États-Unis] ; Grisel J. Lopez [États-Unis] ; Robert L. Nussbaum [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2006-10.
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Abstract
Lewy bodies, the pathological hallmark of Parkinson's disease (PD), consist largely of α‐synuclein, a 14.5‐kDa presynaptic neuronal protein implicated in familial PD. An increased copy number and elevated expression of wild‐type α‐synuclein (SNCA) has been shown to cause early‐onset familial PD. However, it is not clear whether increased α‐synuclein expression also plays a role in the pathogenesis of sporadic disease. In the current study, we analyzed the levels of SNCA‐mRNA in affected brains of sporadic PD patients. We compared the levels of steady state SNCA‐mRNA in 7 sporadic PD brain samples and 7 normal controls using real‐time polymerase chain reaction of RNA extracted from mid‐brain tissue, including the substantia nigra. Despite that there is neuronal loss in the substantia nigra of PD brains, overall the SNCA‐mRNA levels were increased in PD brains an average of nearly fourfold over normal control mid‐brain, although there was much greater variability in samples from PD patients compared to controls. Frontal cortex samples from selected individuals were also analyzed. SNCA‐mRNA levels were not significantly changed in PD frontal cortex compared to controls. These results suggest that elevated expression levels of SNCA‐mRNA are found in the affected regions of PD brain and support the hypothesis that increases in α‐synuclein expression is associated, among other factors, with the development of sporadic PD. © 2006 Movement Disorder Society
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DOI: 10.1002/mds.21007
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<front><div type="abstract" xml:lang="en">Lewy bodies, the pathological hallmark of Parkinson's disease (PD), consist largely of α‐synuclein, a 14.5‐kDa presynaptic neuronal protein implicated in familial PD. An increased copy number and elevated expression of wild‐type α‐synuclein (SNCA) has been shown to cause early‐onset familial PD. However, it is not clear whether increased α‐synuclein expression also plays a role in the pathogenesis of sporadic disease. In the current study, we analyzed the levels of SNCA‐mRNA in affected brains of sporadic PD patients. We compared the levels of steady state SNCA‐mRNA in 7 sporadic PD brain samples and 7 normal controls using real‐time polymerase chain reaction of RNA extracted from mid‐brain tissue, including the substantia nigra. Despite that there is neuronal loss in the substantia nigra of PD brains, overall the SNCA‐mRNA levels were increased in PD brains an average of nearly fourfold over normal control mid‐brain, although there was much greater variability in samples from PD patients compared to controls. Frontal cortex samples from selected individuals were also analyzed. SNCA‐mRNA levels were not significantly changed in PD frontal cortex compared to controls. These results suggest that elevated expression levels of SNCA‐mRNA are found in the affected regions of PD brain and support the hypothesis that increases in α‐synuclein expression is associated, among other factors, with the development of sporadic PD. © 2006 Movement Disorder Society</div>
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