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[P2–177]: NECROPTOSIS AS A NOVEL MECHANISM UNDERLYING NEURONAL LOSS IN ALZHEIMER'S DISEASE
Author(s) -
Oddo Salvatore,
Caccamo Antonella,
Branca Caterina
Publication year - 2017
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2017.06.828
Subject(s) - necroptosis , neurodegeneration , neuroscience , disease , biology , kinase , mechanism (biology) , pathogenesis , lineage (genetic) , alzheimer's disease , programmed cell death , medicine , microbiology and biotechnology , immunology , apoptosis , gene , genetics , pathology , philosophy , epistemology
glutamate) and elevation in neuroinflammatory cytokine (IL-1 b, IL6 and TNFa) levels. Embelin dose dependently attenuated STZinduced cognitive deficit and biochemical alterations and restored neurochemical levels. Conclusions: The observed protective effect might be attributed to the antioxidant and anti-inflammatory potential of embelin and its ability to restore the levels of hippocampal neurotransmitters. The outcomes of the current study suggest therapeutic potential of embelin in cognitive disorders such as SAD.