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Amyloid β oligomers elicit mitochondrial transport defects and fragmentation in a time-dependent and pathway-specific manner
Small oligomeric forms of amyloid-β (Aβ) are believed to be the culprit for declined brain functions in AD in part through their impairment of neuronal trafficking and synaptic functions. However, the precise cellular actions of Aβ oligomers and underlying mechanisms in neurons remain to be fully de...
Tallennettuna:
| Julkaisussa: | Mol Brain |
|---|---|
| Päätekijät: | , |
| Aineistotyyppi: | Artigo |
| Kieli: | Inglês |
| Julkaistu: |
BioMed Central
2016
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| Aiheet: | |
| Linkit: | https://ncbi.nlm.nih.gov/pmc/articles/PMC4989350/ https://ncbi.nlm.nih.gov/pubmed/27535553 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1186/s13041-016-0261-z |
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