دورية أكاديمية

Mechanisms by which autophagy regulates memory capacity in ageing

التفاصيل البيبلوغرافية
العنوان: Mechanisms by which autophagy regulates memory capacity in ageing
المؤلفون: De Risi M., Torromino G., Tufano M., Moriceau S., Pignataro A., Rivagorda M., Carrano N., Middei S., Settembre C., Ammassari-Teule M., Gardoni F., Mele A., Oury F., De Leonibus E.
المساهمون: M. De Risi, G. Torromino, M. Tufano, S. Moriceau, A. Pignataro, M. Rivagorda, N. Carrano, S. Middei, C. Settembre, M. Ammassari-Teule, F. Gardoni, A. Mele, F. Oury, E. De Leonibus
بيانات النشر: Wiley Blackwell Publishing
سنة النشر: 2020
المجموعة: The University of Milan: Archivio Istituzionale della Ricerca (AIR)
مصطلحات موضوعية: ageing, alpha-synuclein, amyloid fibril, autophagy, GluA1, mild cognitive impairment, Spermidine, Settore BIO/14 - Farmacologia
الوصف: Autophagy agonists have been proposed to slow down neurodegeneration. Spermidine, a polyamine that acts as an autophagy agonist, is currently under clinical trial for the treatment of age-related memory decline. How Spermidine and other autophagy agonists regulate memory and synaptic plasticity is under investigation. We set up a novel mouse model of mild cognitive impairment (MCI), in which middle-aged (12-month-old) mice exhibit impaired memory capacity, lysosomes engulfed with amyloid fibrils (β-amyloid and α-synuclein) and impaired task-induced GluA1 hippocampal post-translation modifications. Subchronic treatment with Spermidine as well as the autophagy agonist TAT-Beclin 1 rescued memory capacity and GluA1 post-translational modifications by favouring the autophagy/lysosomal-mediated degradation of amyloid fibrils. These findings provide new mechanistic evidence on the therapeutic relevance of autophagy enhancers which, by improving the degradation of misfolded proteins, slow down age-related memory decline.
نوع الوثيقة: article in journal/newspaper
اللغة: English
العلاقة: info:eu-repo/semantics/altIdentifier/pmid/32729663; info:eu-repo/semantics/altIdentifier/wos/WOS:000553553200001; volume:19; issue:9; numberofpages:15; journal:AGING CELL; http://hdl.handle.net/2434/787385Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85088790610
DOI: 10.1111/acel.13189
الإتاحة: https://doi.org/10.1111/acel.13189Test
http://hdl.handle.net/2434/787385Test
حقوق: info:eu-repo/semantics/openAccess
رقم الانضمام: edsbas.1FE52662
قاعدة البيانات: BASE