کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5736148 | 1613187 | 2017 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Sleep in Alzheimer's Disease-Beyond Amyloid
ترجمه فارسی عنوان
خواب در بیماری آلزایمر - فراتر از آمیلوئید
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کلمات کلیدی
VLPOEDSDLBNFTSCNLDTSWSREMNREMMPBNBMPAGbvFTDPSPCBDvPAGPPTPLMDAβVentral periaqueductal grayRBDTMNAPPFTDPFZsld - SldAlpha-synuclein - آلفا سینوئولینamyloid β - آمیلوئید βPeriodic limb movement disorder - اختلال حرکتی اندام دوره ایREM sleep behavior disorder - اختلال خواب خواب REMElectroencephalography - الکتروانسافالوگرافیAlzheimer's disease - بیماری آلزایمرrapid eye movement - حرکت سریع چشمnon-rapid eye movement - حرکت سریع چشم نیستNeurofibrillary tangle - خلط نوروفیبریلاexcessive daytime sleepiness - خواب آلودگی بیش از حد در طول روزslow wave sleep - خواب کم آهستهTau - خود راCorticobasal degeneration - دژنراسیون کورتیزوبازالDorsal raphé - رفسنجی پشتیhtau - زمانDLB, Dementia with Lewy bodies - زوال عقل با اجسام لوییfrontotemporal dementia - فراموشی پیشانی گیجگاهی، انحطاط پیشانی گیجگاهیProgressive supranuclear palsy - فلج پیشرونده ی فوق هسته ایlocus coeruleus - لوکوس سیرولئوسPeriaqueductal gray matter - ماده خاکستری پرایاکوداکتinterstitial fluid - مایع بینابینیCerebrospinal fluid - مایع مغزی نخاعیCSF - مایع مغزی نخاعیEEG - نوار مغزیISF - نیروهای امنیتی عراقVentrolateral preoptic nucleus - هسته preoptic Ventrolateralpedunculopontine tegmental nucleus - هسته تمثالی pedunculopontineTuberomammillary nucleus - هسته سلول های بنیادیmedial parabrachial nucleus - هسته پاراباژیالی Medialnucleus basalis of Meynert - هسته پایه Meynertlaterodorsal tegmental nucleus - هسته چرکین زاSuprachiasmatic nucleus - هستههای سوپراکیاسماتیکlateral hypothalamus - هیپوتالاموس جانبیamyloid precursor protein - پروتئین پیش ماده آمیلوئیbasal forebrain - پیشانی پایه
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب رفتاری
چکیده انگلیسی
Sleep disorders are prevalent in Alzheimer's disease (AD) and a major cause of institutionalization. Like AD pathology, sleep abnormalities can appear years before cognitive decline and may be predictive of dementia. A bidirectional relationship between sleep and amyloid β (Aβ) has been well established with disturbed sleep and increased wakefulness leading to increased Aβ production and decreased Aβ clearance; whereas Aβ deposition is associated with increased wakefulness and sleep disturbances. Aβ fluctuates with the sleep-wake cycle and is higher during wakefulness and lower during sleep. This fluctuation is lost with Aβ deposition, likely due to its sequestration into amyloid plaques. As such, Aβ is believed to play a significant role in the development of sleep disturbances in the preclinical and clinical phases of AD. In addition to Aβ, the influence of tau AD pathology is likely important to the sleep disturbances observed in AD. Abnormal tau is the earliest observable AD-like pathology in the brain with abnormal tau phosphorylation in many sleep regulating regions such as the locus coeruleus, dorsal raphe, tuberomammillary nucleus, parabrachial nucleus, and basal forebrain prior to the appearance of amyloid or cortical tau pathology. Furthermore, human tau mouse models exhibit AD-like sleep disturbances and sleep changes are common in other tauopathies including frontotemporal dementia and progressive supranuclear palsy. Together these observations suggest that tau pathology can induce sleep disturbances and may play a large role in the sleep disruption seen in AD. To elucidate the relationship between sleep and AD it will be necessary to not only understand the role of amyloid but also tau and how these two pathologies, together with comorbid pathology such as alpha-synuclein, interact and affect sleep regulation in the brain.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Sleep and Circadian Rhythms - Volume 2, January 2017, Pages 4-14
Journal: Neurobiology of Sleep and Circadian Rhythms - Volume 2, January 2017, Pages 4-14
نویسندگان
Jerrah K. Holth, Tirth K. Patel, David M. Holtzman,