James Peddy

TL;DR: The authors revealed unique autophagy dysregulation within neurons in five AD mouse models in vivo and identified its basis using a neuron-specific transgenic mRFP-eGFP-LC3 probe of autophag and pH, multiplex confocal imaging and correlative light electron microscopy.

TL;DR: Aberrant neuronal Rab5-endosome signaling drives a pathogenic cascade distinct from β-amyloid-related neurotoxicity, which includes prodromal and neurodegenerative features of AD, and suggests Rab5 overactivation as a potential therapeutic target.

TL;DR: Neflamapimod (oral small molecule p38α inhibitor) reduces Rab5 activity, reverses endosomal pathology, and restores the numbers and morphology of BFCNs in a mouse model that develops BFCN degeneration as discussed by the authors .

TL;DR: Autophagy is identified as a previously unrecognized pathway for NF subunit protein degradation that modulates constitutive and inducible NF turnover in vivo and establishes a prominent role for autophagy in NF proteolysis.