دورية أكاديمية
أعرض في EDS

Mitochondria, Amyloid β, and Alzheimer's Disease.

التفاصيل البيبلوغرافية
العنوان: Mitochondria, Amyloid β, and Alzheimer's Disease.
المؤلفون: Readnower RD; Spinal Cord & Brain Injury Research Center, University of Kentucky, Lexington, KY 40536, USA., Sauerbeck AD, Sullivan PG
المصدر: International journal of Alzheimer's disease [Int J Alzheimers Dis] 2011 Mar 22; Vol. 2011, pp. 104545. Date of Electronic Publication: 2011 Mar 22.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Hindawi Country of Publication: United States NLM ID: 101525141 Publication Model: Electronic Cited Medium: Internet ISSN: 2090-0252 (Electronic) NLM ISO Abbreviation: Int J Alzheimers Dis Subsets: PubMed not MEDLINE
أسماء مطبوعة: Publication: 2011- : New York : Hindawi
Original Publication: London, England ; New York, NY : SAGE-Hindawi Access to Research,
مستخلص: Hypometabolism is a hallmark of Alzheimer's disease (AD) and implicates a mitochondrial role in the neuropathology associated with AD. Mitochondrial amyloid-beta (Aβ) accumulation precedes extracellular Aβ deposition. In addition to increasing oxidative stress, Aβ has been shown to directly inhibit mitochondrial enzymes. Inhibition of mitochondrial enzymes as a result of oxidative damage or Aβ interaction perpetuates oxidative stress and leads to a hypometabolic state. Additionally, Aβ has also been shown to interact with cyclophilin D, a component of the mitochondrial permeability transition pore, which may promote cell death. Therefore, ample evidence exists indicating that the mitochondrion plays a vital role in the pathophysiology observed in AD.
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تواريخ الأحداث: Date Created: 20110507 Date Completed: 20110714 Latest Revision: 20211020
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC3087417
DOI: 10.4061/2011/104545
PMID: 21547208
قاعدة البيانات: MEDLINE
الوصف
تدمد:2090-0252
DOI:10.4061/2011/104545