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[P4–431]: MITOCHONDRION HYPERFUSION AND HYPERMOTILITY IN APOE4 ASTROCYTES
Author(s) -
Larramona Raquel,
Cobos Cristina,
ErasoPichot Abel,
Golbano Arantxa,
Menacho Carmen,
Masgrau Roser,
Galea Elena
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.2017.07.591
Subject(s) - mitochondrion , astrocyte , mitophagy , biology , dnm1l , mitochondrial fission , microbiology and biotechnology , neurodegeneration , oligomycin , motility , neuroscience , medicine , apoptosis , biochemistry , central nervous system , autophagy , disease , atpase , enzyme
neflamapimod for inhibition of cytokine production (Duffy, 2011), and correlates well with dose/concentration-response seen for episodic memory in the human clinical studies. Conclusions: The findings provide the first evidence that p38a antagonism could be a means to therapeutically target Alzheimer-related endosomal dysfunction. Further, the correlation between in vitro potency of neflamapomid on reversing endolysosomal dysfunction with clinical dose-response suggests that this pharmacological effect, rather than anti-inflammatory activity, may underlie the clinical activity of neflamapimod on episodic memory.