Artificial evolution discovers biophysically plausible plasticity rules for spiking networks that perform competitively with and even outperform labor-intensive human-designed models in various learning scenarios, while providing new views on experimental data.
Striatal cholinergic interneurons and astrocytes lose cilia and show dysregulation of Hedgehog signaling in mice with a Parkinson's disease-associated, G2019S LRRK2 mutation or upon loss of PPM1H phosphatase specific for LRRK2-phosphorylated Rab GTPases.
Signals recorded directly from human anterior temporal cortex reveal that the brain represents animacy information using a distributed code that changes radically as a stimulus is processed, as predicted by an artificial neural network model.
Genetic disruption of sodium-hydrogen exchanger 6 (NHE6) reduces amyloid plaques in humanized Alzheimer's disease mouse models and restores normal synaptic responses to neuromodulatory input in humanized ApoE4-expressing animals.
Central damage and sensory deprivation caused by noise-induced hearing loss in the pre-symptomatic Alzheimer's disease (AD) phase can compromise auditory cortex-hippocampal circuitry, targeting common pathogenetic pathways, thereby accelerating onset and progression of AD phenotype.
Acetylcholine, released from cholinergic fibers originating from the medial septum, shapes social memory, and controls the CA2 hippocampal circuit via nicotinic receptors localized on GABAergic interneurons.