• Users Online: 196
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 
REVIEW ARTICLE
Year : 2018  |  Volume : 3  |  Issue : 2  |  Page : 42-47

Modeling neurodegenerative diseases by human pluripotent stem cell-induced brain organoid


1 Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA
2 Program in Biological Sciences in Dental Medicine, Harvard School of Dental Medicine, Boston, MA, USA
3 Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore
4 Department of Wounds and Burns Center, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China
5 ApreX, Inc., 120 Wyllis Ave, U216, Everett, MA, USA

Correspondence Address:
Rui Sun
ApreX, Inc., 120 Wyllis Ave, U216, Everett, MA
USA
Xu Luo
Department of Wounds and Burns Center, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang
China
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ts.ts_4_18

Rights and Permissions

Neurodegenerative disease (ND) contains a range of conditions which are primarily characterized by progressive neuronal dysfunction and loss. ND is particularly difficult to cure, due to the vulnerability of the nervous system. Currently, few genes and pathways are found to be related to ND. However, no solitary mechanism appears to be primary in neurodegeneration, and these pathogenic mechanisms likely act synergistically through complex interactions to promote neurodegeneration. Moreover, the existing treatment is mainly focusing on alleviating the symptoms of the disease. Furthermore, recent studies reveal considerable overlaps of symptomatology and genetic risks across the disease subtypes by detailed studies at cellular, molecular and genetic level. To better understand the etiology and pathogenesis of ND, study of the abnormalities at patient level is most ideal. However, direct access to the brain tissues from healthy individuals and patients is very limited. Therefore, an alternative experimental model is required to study the mechanism of ND. The most commonly used models are animal models, including Caenorhabditis elegans, Drosophila, zebrafish, and genetically modified mice. However, animal models also have their limitations including partial recapitulation of the disease features and difficulties in modifying disease genes. The recent development in three-dimensional (3D) brain organoids might provide a better experimental model to study ND, because 3D brain organoid system carries great potential to expand the range of both physiological and pathological features that can be found during the development of disease, enabling higher order investigation of mechanism and functionality.


[FULL TEXT] [PDF]*
Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)
 

 Article Access Statistics
    Viewed368    
    Printed29    
    Emailed0    
    PDF Downloaded96    
    Comments [Add]    

Recommend this journal