دورية أكاديمية

A Focus on the Beneficial Effects of Alpha Synuclein and a Re-appraisal of Synucleinopathies

التفاصيل البيبلوغرافية
العنوان: A Focus on the Beneficial Effects of Alpha Synuclein and a Re-appraisal of Synucleinopathies
المؤلفون: Larisa Ryskalin, Carla L. Busceti, Fiona Limanaqi, Francesca Biagioni, Stefano Gambardella, Francesco Fornai
المساهمون: L. Ryskalin, C.L. Busceti, F. Limanaqi, F. Biagioni, S. Gambardella, F. Fornai
بيانات النشر: Bentham Science Publishers
سنة النشر: 2018
المجموعة: The University of Milan: Archivio Istituzionale della Ricerca (AIR)
مصطلحات موضوعية: Alpha synuclein, synucleinopathie, alpha synuclein aggregate, loss-of-function, co-chaperonine, neurodegeneration, neuroprotection, Settore BIO/13 - Biologia Applicata, Settore BIO/16 - Anatomia Umana
الوصف: Alpha synuclein (α-syn) belongs to a class of proteins which are commonly considered to play a detrimental role in neuronal survival. This assumption is based on the occurrence of a severe neuronal degeneration in patients carrying a multiplication of the α-syn gene (SNCA) and in a variety of experimental models, where overexpression of α-syn leads to cell death and neurological impairment. In these conditions, a higher amount of normally structured α-syn produces a damage, which is even worse compared with that produced by α-syn owing an abnormal structure (as occurring following point gene mutations). In line with this, knocking out the expression of α-syn is reported to protect from specific neurotoxins such as 1-methyl, 4-phenyl 1,2,3,6-tetrahydropyridine (MPTP). In the present review we briefly discuss these well-known detrimental effects but we focus on findings showing that, in specific conditions α-syn is beneficial for cell survival. This occurs during methamphetamine intoxication which is counteracted by endogenous α-syn. Similarly, the dysfunction of the chaperone cysteine-string protein-alpha leads to cell pathology which is counteracted by over-expressing α-syn. In line with this, an increased expression of α-syn protects against oxidative damage produced by dopamine. Remarkably, when the lack of α-syn is combined with a depletion of β- and γ- synucleins, alterations in brain structure and function occur. This review tries to balance the evidence showing a beneficial effect with the bulk of data reporting a detrimental effect of endogenous α-syn. The specific role of α-syn as a chaperone protein is discussed to explain such a dual effect.
نوع الوثيقة: article in journal/newspaper
اللغة: English
العلاقة: info:eu-repo/semantics/altIdentifier/pmid/29150919; info:eu-repo/semantics/altIdentifier/wos/WOS:000430104200007; volume:19; issue:6; firstpage:598; lastpage:611; numberofpages:14; journal:CURRENT PROTEIN & PEPTIDE SCIENCE; https://hdl.handle.net/2434/995038Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85046751466
DOI: 10.2174/1389203718666171117110028
الإتاحة: https://doi.org/10.2174/1389203718666171117110028Test
https://hdl.handle.net/2434/995038Test
حقوق: info:eu-repo/semantics/openAccess
رقم الانضمام: edsbas.2D85BD06
قاعدة البيانات: BASE