[P4–431]: MITOCHONDRION HYPERFUSION AND HYPERMOTILITY IN APOE4 ASTROCYTES | Zendy

Larramona Raquel | Zendy; Cobos Cristina | Zendy; ErasoPichot Abel | Zendy; Golbano Arantxa | Zendy; Menacho Carmen | Zendy; Masgrau Roser | Zendy; Galea Elena | Zendy

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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.

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