dendritic spine dysgenesis in rett syndrome
Clicks: 194
ID: 258409
2014
Article Quality & Performance Metrics
Overall Quality
Improving Quality
0.0
/100
Combines engagement data with AI-assessed academic quality
Reader Engagement
Emerging Content
30.0
/100
193 views
15 readers
Trending
AI Quality Assessment
Not analyzed
Abstract
Spines are small cytoplasmic extensions of dendrites that form the postsynaptic compartment of the majority of excitatory synapses in the mammalian brain. Alterations in the numerical density, size, and shape of dendritic spines have been correlated with neuronal dysfunction in several neurological and neurodevelopmental disorders associated with intellectual disability, including Rett syndrome (RTT). RTT is a progressive neurodevelopmental disorder associated with intellectual disability that is caused by loss of function mutations in the transcriptional regulator methyl CpG-binding protein 2 (MECP2). Here, we review the evidence demonstrating that principal neurons in RTT individuals and Mecp2-based experimental models exhibit alterations in the number and morphology of dendritic spines. We also discuss the exciting possibility that signaling pathways downstream of brain-derived neurotrophic factor (BDNF), which is transcriptionally regulated by MeCP2, offer promising therapeutic options for modulating dendritic spine development and plasticity in RTT and other MECP2-associated neurodevelopmental disorders.
| Reference Key |
exu2014frontiersdendritic
Use this key to autocite in the manuscript while using
SciMatic Manuscript Manager or Thesis Manager
|
|---|---|
| Authors | ;Xin eXu;Eric C Miller;Lucas ePozzo-Miller |
| Journal | Journal of medical systems |
| Year | 2014 |
| DOI |
10.3389/fnana.2014.00097
|
| URL | |
| Keywords |
Citations
No citations found. To add a citation, contact the admin at info@scimatic.org
Comments
No comments yet. Be the first to comment on this article.