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Traumatic brain injury decreases AMP-activated protein kinase activity and pharmacological enhancement of its activity improves cognitive outcome
BACKGROUND: Prolonged metabolic suppression in the brain is a well-characterized secondary pathology of both experimental and clinical traumatic brain injury (TBI). AMP-activated kinase (AMPK) acts as a cellular energy sensor that, when activated, regulates various metabolic and catabolic pathways t...
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| Publicat a: | J Neurochem |
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| Autors principals: | , , , , , , |
| Format: | Artigo |
| Idioma: | Inglês |
| Publicat: |
2016
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| Matèries: | |
| Accés en línia: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5037010/ https://ncbi.nlm.nih.gov/pubmed/27379837 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1111/jnc.13726 |
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