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Glial modulation by N-acylethanolamides in brain injury and neurodegeneration
dc.contributor.author | Herrera M.I. | |
dc.contributor.author | Kölliker-Frers R. | |
dc.contributor.author | Barreto G. | |
dc.contributor.author | Blanco E. | |
dc.contributor.author | Capani F. | |
dc.date.accessioned | 2020-09-02T22:20:26Z | |
dc.date.available | 2020-09-02T22:20:26Z | |
dc.date.issued | 2016 | |
dc.identifier | 10.3389/fnagi.2016.00081 | |
dc.identifier.citation | 8, APR, - | |
dc.identifier.issn | 16634365 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12728/4873 | |
dc.description | Neuroinflammation involves the activation of glial cells and represents a key element in normal aging and pathophysiology of brain damage. N-acylethanolamides (NAEs), naturally occurring amides, are known for their pro-homeostatic effects. An increase in NAEs has been reported in vivo and in vitro in the aging brain and in brain injury. Treatment with NAEs may promote neuroprotection and exert anti-inflammatory actions via PPARα activation and/or by counteracting gliosis. This review aims to provide an overview of endogenous and exogenous properties of NAEs in neuroinflammation and to discuss their interaction with glial cells. © 2016 Herrera, Kölliker-Frers, Barreto, Blanco and Capani. | |
dc.language.iso | en | |
dc.publisher | Frontiers Media S.A. | |
dc.subject | Gliosis | |
dc.subject | N-acylethanolamides | |
dc.subject | Neuroinflammation | |
dc.subject | Neuroprotection | |
dc.subject | PPARα | |
dc.subject | amide | |
dc.subject | anandamide | |
dc.subject | n acylethanolamide derivative | |
dc.subject | n oleoylethanolamine | |
dc.subject | palmidrol | |
dc.subject | peroxisome proliferator activated receptor | |
dc.subject | unclassified drug | |
dc.subject | aging | |
dc.subject | Alzheimer disease | |
dc.subject | antiinflammatory activity | |
dc.subject | astrocyte | |
dc.subject | astrocytosis | |
dc.subject | brain injury | |
dc.subject | brain ischemia | |
dc.subject | cell activation | |
dc.subject | cell interaction | |
dc.subject | cerebrovascular accident | |
dc.subject | degenerative disease | |
dc.subject | drug efficacy | |
dc.subject | drug structure | |
dc.subject | glia cell | |
dc.subject | gliosis | |
dc.subject | human | |
dc.subject | learning disorder | |
dc.subject | memory disorder | |
dc.subject | microglia | |
dc.subject | nerve degeneration | |
dc.subject | nervous system inflammation | |
dc.subject | neuromodulation | |
dc.subject | neuroprotection | |
dc.subject | nonhuman | |
dc.subject | Parkinson disease | |
dc.subject | pathophysiology | |
dc.subject | perinatal asphyxia | |
dc.subject | peripheral neuropathy | |
dc.subject | pleiotropy | |
dc.subject | receptor upregulation | |
dc.subject | Short Survey | |
dc.subject | signal transduction | |
dc.subject | spinal cord injury | |
dc.subject | traumatic brain injury | |
dc.title | Glial modulation by N-acylethanolamides in brain injury and neurodegeneration | |
dc.type | Short Survey |