טוען...
TRPA1 channels promote astrocytic Ca(2+) hyperactivity and synaptic dysfunction mediated by oligomeric forms of amyloid-β peptide
BACKGROUND: Excessive synaptic loss is thought to be one of the earliest events in Alzheimer’s disease (AD). However, the key mechanisms that maintain plasticity of synapses during adulthood or initiate synapse dysfunction in AD remain unknown. Recent studies suggest that astrocytes contribute to fu...
שמור ב:
| הוצא לאור ב: | Mol Neurodegener |
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| Main Authors: | , , , , , |
| פורמט: | Artigo |
| שפה: | Inglês |
| יצא לאור: |
BioMed Central
2017
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| נושאים: | |
| גישה מקוונת: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5501536/ https://ncbi.nlm.nih.gov/pubmed/28683776 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1186/s13024-017-0194-8 |
| תגים: |
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