Emerging pathways to neurodegeneration: Dissecting the critical molecular mechanisms in Alzheimer’s disease, Parkinson’s disease - 16/02/19
pages | 13 |
Iconographies | 9 |
Vidéos | 0 |
Autres | 0 |
Graphical abstract |
Highlights |
• | The pathways to the development of Alzheimer’s and Parkinson’s disease share similarities, though the specific components or proteins involved may differ. |
• | This review highlights, insights regarding ubiquitin-proteasome system, aberrant alternative splicing of exons, dysfunctional mitochondria role in neurodegeneration and improves the understanding of the common mechanism. |
• | This discussion is particularly relevant, given the strong relationship between major pathways and neurodegeneration, and the pressing need to improve the mechanisms contributing to biomarker screening. |
Abstract |
Neurodegenerative diseases are usually sporadic in nature and commonly influenced by a wide range of genetic, life style and environmental factors. A unifying feature of Alzheimer’s disease (AD) and Parkinson’s disease (PD) is the abnormal accumulation and processing of mutant or damaged intra and extracellular proteins; this leads to neuronal vulnerability and dysfunction in the brain. Through a detailed review of ubiquitin proteasome, mRNA splicing, mitochondrial dysfunction, and oxidative stress pathway interrelation on neurodegeneration can improve the understanding of the disease mechanism. The identified pathways common to AD and PD nominate promising new targets for further studies, and as well as biomarkers. These insights suggested would likely provide major stimuli for developing unified treatment approaches to combat neurodegeneration. More broadly, pathways can serve as vehicles for integrating findings from diverse studies of neurodegeneration. The evidence examined in this review provides a brief overview of the current literature on significant pathways in promoting in AD, PD. Additionally, these insights suggest that biomarkers and treatment strategies may require simultaneous targeting of multiple components.
Le texte complet de cet article est disponible en PDF.Abbreviations : OH, 4-HNE, AD, APOE- ε4, APP, ARJP, AS, ATP, ATP13A2, Aβ, BACE, Ca2+, CNS, DJ-1, Drp1, E1, E2, E3, ER-α, ETC, FBP1, FBXO7, Fis1, GABA B, GBA1, GFAP, GPCR51, GSH, H2O2, HT, KGDHC, LB, LRRK2, MAO-A, MAO-B, MAPT, MDA, Mfn1, Mfn2, mRNA, O2−, OMM, Opa1, Pael-R, PARK2, PARK6, PARK7, PD, PINK1, PKC, PLA2G6, PRKN, PS1, PS2, PSP, PTP, RAGE, ROS, SNCA, SNCAIP, SNPC, SOD, SRRM2, TFAM, TRX, TV12, TV3, UCH-L1, UPS, VDACs
Keywords : Alzheimer’s disease, Parkinson’s disease, Ubiquitin proteasome, mRNA splicing, Mitochondrial dysfunction, Oxidative stress, Biomarker
Plan
Vol 111
P. 765-777 - mars 2019 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
L’accès au texte intégral de cet article nécessite un abonnement.
Bienvenue sur EM-consulte, la référence des professionnels de santé.
L’achat d’article à l’unité est indisponible à l’heure actuelle.
Déjà abonné à cette revue ?