کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6019236 | 1186547 | 2011 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Interaction between α-synuclein and tau in Parkinson's disease
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کلمات کلیدی
NFTAβαsynDATPDDGSK-3βTauopathiesIFGα-synuclein - α-سینوکلینβ-Amyloid - β-آمیلوئیدDopamine transporter - انتقال دهنده دوپامینLewy bodies - بدن لویLewy body - بدن لویAlzheimer disease - بیماری آلزایمرAlzheimer's disease - بیماری آلزایمرParkinson's disease - بیماری پارکینسونParkinson's disease with dementia - بیماری پارکینسون با زوال عقلHyperphosphorylated tau - تئو هیپرفسفیریل شدهNeurodegeneration - تولید نوروژنیکtyrosine hydroxylase - تیروزین هیدروکسیلازNeurofibrillary tangle - خلط نوروفیبریلاTau - خود راpTau - صinferior frontal gyrus - قارچ پیشانی پایین ترSynucleinopathies - هموئینوپاتی هاTau protein - پروتئین تاو
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Interaction between α-synuclein and tau in Parkinson's disease Interaction between α-synuclein and tau in Parkinson's disease](/preview/png/6019236.png)
چکیده انگلیسی
Recent neurochemical studies in postmortem brains of patients with Parkinson's disease (PD), PD with dementia (PDD) and age-matched controls revealed significant decrease of tyrosine hydroxylase (TH) and dopamine transporter (DAT) in striatum, confirming previous studies indicating substantial loss of dopaminergic neurons and terminals. Insoluble α-synuclein (αSyn) was significantly increased in both striata and inferior frontal gyrus (IFG), more severe in PDD, probably related to Lewy body (LB) burden discussed as one cause of dementia in PD. Parkin levels frequently related to recessive and young-onset PD were unchanged, suggesting no link to sporadic PD. Novel and most interesting data showed elevated tauopathy in striata of both PD and PDD, associated with increased levels of phosphorylated GSK-3β and reduced 20S proteasomal subunits but - despite increased cortical αSyn - unchanged pTau in IFG, related to increased pGSK-3β and decreased 19S proteasome subunits. These data, recently confirmed in PDGF-αSyn transgenic mice (Haggerty et al., submitted) suggest tauopathy in PD and PDD restricted to the dopaminergic nigrostriatal system and in various animal models of PD show topographic differences from a global tauopathy in Alzheimer's disease (AD) (and other tauopathies). Although some of these data are at variance to current neuropathologic findings in PD and PDD, they confirm frequently discussed correlations/overlaps between AD and PD/PDD and synergistic effects of αSyn, pTau, β-amyloid, and other pathologic proteins, suggesting a dualism or triad of neurodegeneration, the basic molecular pathogenesis remains to be elucidated.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Neurology - Volume 227, Issue 1, January 2011, Pages 13-18
Journal: Experimental Neurology - Volume 227, Issue 1, January 2011, Pages 13-18
نویسندگان
Kurt A. Jellinger,