کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4342497 | 1295871 | 2006 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cyclin-dependent kinase 5, Munc18a and Munc18-interacting protein 1/X11α protein up-regulation in Alzheimer's disease
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
NF-68PBSSDSAβNFTPBSTPAGESNAP25APPcdk5MMSEβ-Amyloid - β-آمیلوئیدNeuron loss - از دست دادن نورونpolyacrylamide gel electrophoresis - الکتروفورز ژل پلی آکریل آمیدNeurotransmission - انتقال عصبیAlzheimer’s disease - بیماری آلزایمرNeurofibrillary tangle - خلط نوروفیبریلاsodium dodecyl sulfate - سدیم دودسیل سولفاتcyclin-dependent kinase 5 - سیکلین وابسته به کیناز 5Occipital cortex - قشر OccipitalParietal cortex - قشر پاریتالPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریMini-Mental State Examination - معاینه دولتی مینی روانشناسیBrodmann’s area - منطقه برودمنMint - نعناwild type - نوع وحشیsynaptosomal-associated protein of 25 kDa - پروتئین مرتبط با سیناپتوزومال 25 کیلو دالتونamyloid precursor protein - پروتئین پیش ماده آمیلوئیNeuritic plaque - پلاک ملایمیβ-amyloid peptide - پپتید β-آمیلوئید
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Cyclin-dependent kinase 5, Munc18a and Munc18-interacting protein 1/X11α protein up-regulation in Alzheimer's disease Cyclin-dependent kinase 5, Munc18a and Munc18-interacting protein 1/X11α protein up-regulation in Alzheimer's disease](/preview/png/4342497.png)
چکیده انگلیسی
Besides formation of neurofibrillary tangles and neuron loss, the Alzheimer's disease brain is characterized by neuritic plaques consisting of β-amyloid peptide deposits and impaired neurotransmission. The proteins Munc18a, Munc18-interacting protein 1 and Munc18-interacting protein 2 mediate exocytosis and decrease β-amyloid peptide formation. Cyclin-dependent kinase 5 and its activator p35 disrupt Munc18a-syntaxin 1 binding, thereby promoting synaptic vesicle fusion during exocytosis. We investigated protein levels of the signaling pathway: p35, cyclin-dependent kinase 5, Munc18a, syntaxin 1A and 1B, Munc18-interacting protein 1 and Munc18-interacting protein 2 in Alzheimer's disease cortex and found that this pathway was up-regulated in the Alzheimer's disease parietal and occipital cortex. In the cortex of transgenic Tg2576 mice over-expressing human β-amyloid precursor protein with the Swedish mutation known to lead to familial Alzheimer's disease, which have substantial levels of β-amyloid peptide but lack neurofibrillary tangles and neuron loss, no alterations of protein levels were detected. These data suggest that the pathway is enhanced in dying or surviving neurons and might serve a protective role by compensating for decreased neurotransmission and decreasing β-amyloid peptide levels early during the progression of Alzheimer's disease.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 138, Issue 2, 2006, Pages 511-522
Journal: Neuroscience - Volume 138, Issue 2, 2006, Pages 511-522
نویسندگان
E.H. Jacobs, R.J. Williams, P.T. Francis,