کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6279687 | 1615081 | 2016 | 19 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Effects of different isoforms of apoE on aggregation of the 뱉synuclein protein implicated in Parkinson's disease
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کلمات کلیدی
TRFAβLBSα-synuclein - α-سینوکلینβ-Amyloid - β-آمیلوئیدapolipoprotein E - آپولیپوپروتئین ELewy bodies - بدن لویLewy body - بدن لویThT - بلهParkinson’s disease - بیماری پارکینسونAggregation - تجمعsubstantia nigra - توده سیاهThioflavin T - تیوفلاوین TTime-resolved fluorescence - فلورسانس حل شده در زمانCerebrospinal fluid - مایع مغزی نخاعیCSF - مایع مغزی نخاعی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Parkinson's disease is a progressive brain disorder due to the degeneration of dopaminergic neurons in the substantia nigra. The accumulation of aggregated forms of α-synuclein protein into Lewy bodies is one of the characteristic features of this disease although the pathological role of any such protein deposits in causing neurodegeneration remains elusive. Here, the effects of different apolipoprotein E isoforms (apoE2, apoE3, apoE4) on the aggregation of α-synuclein in vitro were examined using thioflavin T assays and also an immunoassay to detect the formation of multimeric forms. Our results revealed that the aggregation of α-synuclein is influenced by apoE concentration. At low concentrations of apoE (<15 nM), all of the isoforms were able to increase the aggregation of α-synuclein (50 μM), with apoE4 showing the greatest stimulatory effect. This is in contrast to a higher concentration (>15 nM) of these isoforms, where a decrease in the aggregation of α-synuclein was noted. The data show that exceptionally low levels of apoE may seed α-syn aggregation, which could potentially lead to the pathogenesis of αâsynuclein-induced neurodegeneration. On the other hand, higher levels of apoE could potentially lower the degree of α-synuclein aggregation and confer protection. The differential effects noted with apoE4 could explain why this particular isoform results in an earlier age of onset for Parkinson's disease.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 618, 8 April 2016, Pages 146-151
Journal: Neuroscience Letters - Volume 618, 8 April 2016, Pages 146-151
نویسندگان
Fatemeh Nouri Emamzadeh, Harmesh Aojula, Patrick C. McHugh, David Allsop,