دورية أكاديمية

Alpha-synuclein and beta-amyloid different targets, same players: calcium, free radicals and mitochondria in the mechanism of neurodegeneration

التفاصيل البيبلوغرافية
العنوان: Alpha-synuclein and beta-amyloid different targets, same players: calcium, free radicals and mitochondria in the mechanism of neurodegeneration
المؤلفون: Angelova, PR, Abramov, AY
المصدر: Biochemical and Biophysical Research Communications , 483 (4) pp. 1110-1115. (2017)
بيانات النشر: ACADEMIC PRESS INC ELSEVIER SCIENCE
سنة النشر: 2017
المجموعة: University College London: UCL Discovery
مصطلحات موضوعية: Science & Technology, Life Sciences & Biomedicine, Biochemistry & Molecular Biology, Biophysics, PERMEABILITY TRANSITION PORE, COMPLEX I DEFICIENCY, PARKINSONS-DISEASE, ALZHEIMERS-DISEASE, OXIDATIVE STRESS, ION CHANNELS, VESICLE PERMEABILIZATION, INDUCED NEUROTOXICITY, LIPID-PEROXIDATION, PRECURSOR PROTEIN
الوصف: Two of the most devastating neurodegenerative diseases are consequences out of misfolding and aggregation of key proteins-alpha synuclein and beta-amyloid. Although the primary targets for the two proteins are different, they both share a common mechanism that involves formation of pore-like structure on the plasma membrane, consequent dysregulation of calcium homeostasis, mitochondrial dysfunction and oxidative damage. The combined effect of all this factors ultimately leads to neuronal cell death. Whereas beta amyloid acts on the astrocytic plasma membrane, exhibiting a tight dependence to the membrane cholesterol content, alpha–synuclein does not distinguish between type of membrane or cell. Additionally, oligomeric forms of both proteins produce reactive oxygen species through different mechanisms: beta-amyloid through activation of the NADPH oxidase and alpha-synuclein through non-enzymatic way. Finally, both peptides in oligomeric form induce mitochondrial depolarisation through calcium overload and free radical production that ultimately lead to opening of the mitochondrial permeability transition pore and trigger cell death.
نوع الوثيقة: article in journal/newspaper
وصف الملف: text
اللغة: English
العلاقة: https://discovery.ucl.ac.uk/id/eprint/1508935/1/Abramov_Angelova%252C%20Abramov-BBRC.pdfTest; https://discovery.ucl.ac.uk/id/eprint/1508935Test/
الإتاحة: https://discovery.ucl.ac.uk/id/eprint/1508935/1/Abramov_Angelova%252C%20Abramov-BBRC.pdfTest
https://discovery.ucl.ac.uk/id/eprint/1508935Test/
حقوق: open
رقم الانضمام: edsbas.CDCBF0F1
قاعدة البيانات: BASE