کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8842168 | 1615350 | 2018 | 146 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The interactions of p53 with tau and AÃ as potential therapeutic targets for Alzheimer's disease
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کلمات کلیدی
I2PP2AAICDGSK-3βCBPpKaAPPNFTGAP-43RNSβ-site APP cleaving enzyme 1PP2AAβBACE1BIN1HEK 293PHFp53JnkHIPK2c-Jun N-terminal kinase - C-Jun N-terminal kinaseERK1/2 - ERK1 / 2MAPKs - MAPK هاMdm2 - MDM2Mitogen activated protein kinases - Mitogen فعال پروتئین کینازp53 upregulated modulator of apoptosis - modulator modulator آپوپتوزی p53ROS - ROSamyloid β peptides - β پپتیدهای آمیلوئیدApoe - آپوapolipoprotein E - آپولیپوپروتئین ENeuronal apoptosis - آپوپتوز عصبیAlzheimer’s disease - بیماری آلزایمرAlzheimer's disease - بیماری آلزایمرlong-term potentiation - تقویت درازمدتLTP - تقویت طولانی مدت یا LTP Oxidative stress - تنش اکسیداتیوTau - خود راAmyloid precursor protein intracellular domain - دامنه داخل سلولی پروتئین پیش ماده آمیلوئیدPaired helical filaments - رشته های مارپیچ دوزی شدهhuman embryonic kidney 293 cells - سلول های انسانی جنینی انسان 293Transcriptional activation - فعال سازی رونویسیLow-density lipoprotein - لیپوپروتئین کم چگالی یا الدیال LDL - لیپوپروتئین کم چگالی(کلسترول بد)neurofibrillary tangles - مگس های نوروفیبریلیالmap - نقشهPresenilin - پرنسیلینCREB-binding protein - پروتئین اتصال CREBprotein phosphatase 2A - پروتئین فسفاتاز 2Agrowth-associated protein 43 - پروتئین مرتبط با رشد 43microtubule-associated protein - پروتئین مرتبط با میکروتوبولprotein kinase A - پروتئین کیناز Abridging integrator 1 - پل مونتاژ 1PUMA - پوماGlycogen synthase kinase-3β - گلیکوزین سنتاز کیناز 3βreactive nitrogen species - گونه های واکنش پذیر نیتروژنReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: The interactions of p53 with tau and AÃ as potential therapeutic targets for Alzheimer's disease The interactions of p53 with tau and AÃ as potential therapeutic targets for Alzheimer's disease](/preview/png/8842168.png)
چکیده انگلیسی
Alzheimer's disease (AD), the most common progressive neurodegenerative disorder, is characterized by severe cognitive decline and personality changes as a result of synaptic and neuronal loss. The defining clinicopathological hallmarks of the disease are deposits of amyloid precursor protein (APP)-derived amyloid-β peptides (Aβ) in the brain parenchyma, and intracellular aggregates of truncated and hyperphosphorylated tau protein in neurofibrillary tangles (NFT). At the cellular and molecular levels, many intertwined pathological mechanisms that relate Aβ and tau pathology with a transcription factor p53 have been revealed. p53 is activated in response to various stressors that threaten genomic stability. Depending on damage severity, it promotes neuronal death or survival, predominantly via transcription-dependent mechanisms that affect expression of apoptosis-related target genes. Levels of p53 are enhanced in the AD brain and maintain sustained tau hyperphosphorylation, whereas intracellular Aβ directly contributes to p53 pool and promotes downstream p53 effects. The review summarizes the role of p53 in neuronal function, discusses the interactions of p53, tau, and Aβ in the normal brain and during the progression of AD pathology, and considers the impact of the most prominent hereditary risk factors of AD on p53/tau/Aβ interactions. A better understanding of this intricate interplay would provide deeper insight into AD pathology and might offer some novel therapeutic targets for the improvement of treatment options. In this regard, drugs and natural compounds targeting the p53 pathway are of growing interest in neuroprotection as they may represent promising therapeutic approaches in the prevention of oxidative stress-dependent pathological processes underlying AD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Progress in Neurobiology - Volume 168, September 2018, Pages 104-127
Journal: Progress in Neurobiology - Volume 168, September 2018, Pages 104-127
نویسندگان
Maja JazvinÅ¡Äak Jembrek, Neda Slade, Patrick R. Hof, Goran Å imiÄ,