Induced-pluripotent stem cells and neuroproteomics as tools for studying neurodegeneration

被引:0
作者
Brandao-Teles, Caroline [1 ]
Zuccoli, Giuliana S. [1 ]
Vrechi, Talita Aparecida de Moraes [1 ]
Ramos-da-Silva, Livia [1 ]
Santos, Aline Valeria Sousa [1 ]
Crunfli, Fernanda [1 ]
Martins-de-Souza, Daniel [1 ,2 ,3 ,4 ,5 ]
机构
[1] Univ Estadual Campinas, Inst Biol, Dept Biochem & Tissue Biol, Lab Neuroprote, Campinas, Brazil
[2] Univ Estadual Campinas, Expt Med Res Cluster EMRC, BR-13083862 Campinas, SP, Brazil
[3] Conselho Nacl Desenvolvimento Cientif & Tecnol, Inst Nacl Biomarcadores Neuropsiquiatria, Sao Paulo, Brazil
[4] INCT Modelling Human Complex Dis 3D Platforms Mod, Sao Paulo, Brazil
[5] DOr Inst Res & Educ IDOR, Sao Paulo, Brazil
基金
巴西圣保罗研究基金会;
关键词
PARKINSONS-DISEASE; ALZHEIMER-DISEASE; TARGET IDENTIFICATION; APOLIPOPROTEIN-E; GENE; MUTATIONS; NEURONS; PROTEOMICS; PATHOLOGY; IPSC;
D O I
10.1042/BST20230341
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The investigation of neurodegenerative diseases advanced significantly with the advent of cell-reprogramming technology, leading to the creation of new models of human illness. These models, derived from induced pluripotent stem cells (iPSCs), facilitate the study of sporadic as well as hereditary diseases and provide a comprehensive understanding of the molecular mechanisms involved with neurodegeneration. Through proteomics, a quantitative tool capable of identifying thousands of proteins from small sample volumes, researchers have attempted to identify disease mechanisms by detecting differentially expressed proteins and proteoforms in disease models, biofluids, and postmortem brain tissue. The integration of these two technologies allows for the identification of novel pathological targets within the realm of neurodegenerative diseases. Here, we highlight studies from the past 5 years on the contributions of iPSCs within neuroproteomic investigations, which uncover the molecular mechanisms behind these illnesses.
引用
收藏
页码:163 / 176
页数:14
相关论文
共 128 条
[31]   Mutations associated with familial Parkinson's disease alter the initiation and amplification steps of α-synuclein aggregation [J].
Flagmeier, Patrick ;
Meisl, Georg ;
Vendruscolo, Michele ;
Knowles, Tuomas P. J. ;
Dobson, Christopher M. ;
Buell, Alexander K. ;
Galvagnion, Celine .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2016, 113 (37) :10328-10333
[32]   Genetic Correction of Tauopathy Phenotypes in Neurons Derived from Human Induced Pluripotent Stem Cells [J].
Fong, Helen ;
Wang, Chengzhong ;
Knoferle, Johanna ;
Walker, David ;
Balestra, Maureen E. ;
Tong, Leslie M. ;
Leung, Laura ;
Ring, Karen L. ;
Seeley, William W. ;
Karydas, Anna ;
Kshirsagar, Mihir A. ;
Boxer, Adam L. ;
Kosik, Kenneth S. ;
Miller, Bruce L. ;
Huang, Yadong .
STEM CELL REPORTS, 2013, 1 (03) :226-234
[33]  
Freund C., 2020, CONCEPTS APPL STEM C, P57
[34]   Mechanisms of neural specification from embryonic stem cells [J].
Gaspard, Nicolas ;
Vanderhaeghen, Pierre .
CURRENT OPINION IN NEUROBIOLOGY, 2010, 20 (01) :37-43
[35]   Genetics of Parkinson's disease [J].
Gasser, T .
JOURNAL OF NEUROLOGY, 2001, 248 (10) :833-840
[36]  
Gu A, 2010, PLOS ONE, V5, DOI [10.1371/journal.pone.0010067, 10.1371/currents.RRN1193]
[37]  
Guest P C, 2019, Reviews on Biomarker Studies in Aging and Anti-Aging Research, DOI [10.1007/978-3-030-05542-4, DOI 10.1007/978-3-030-25650-0]
[38]   Bringing synapses into focus: Recent advances in synaptic imaging and mass-spectrometry for studying synaptopathy [J].
Hindley, Nicole ;
Avila, Anna Sanchez ;
Henstridge, Christopher .
FRONTIERS IN SYNAPTIC NEUROSCIENCE, 2023, 15
[39]   Modeling human neurological disorders with induced pluripotent stem cells [J].
Imaizumi, Yoichi ;
Okano, Hideyuki .
JOURNAL OF NEUROCHEMISTRY, 2014, 129 (03) :388-399
[40]   Tau pathology in Alzheimer disease and other tauopathies [J].
Iqbal, K ;
Alonso, ADC ;
Chen, S ;
Chohan, MO ;
El-Akkad, E ;
Gong, CX ;
Khatoon, S ;
Li, B ;
Liu, F ;
Rahman, A ;
Tanimukai, H ;
Grundke-Iqbal, I .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 2005, 1739 (2-3) :198-210