Cynthia Bleiwas

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: It is shown that partial BACE1 genetic reduction prevents these AD-related pathological features in the Ts2 mouse model of Down syndrome and highlights the additional potential value of Bace1 modulation in therapeutic targeting of endocytic dysfunction and cholinergic neurodegeneration in Down Syndrome and AD.

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: It is indicated that the cortex has substantial capacity to develop normal cytoarchitectonic organization after early postnatal ethanol toxicity, but there is a selective and persistent reduction of GABA cells that may contribute to the lasting cognitive and behavioral deficits in FASD.

TL;DR: Partially lowering NFL in NFL+/− mice to levels seen regionally in schizophrenia, induced similar but milder NMDAR-related synaptic and behavioral deficits, which support an emerging view that central nervous system neurofilament subunits including NFL serve distinctive, critical roles in synapses relevant to neuropsychiatric diseases.