Electrophysiology pinpoints brain function abnormalities in young people genetically at risk of developing Alzheimer's disease much later in life, supporting theories of initial hyperconnectivity driving eventual profound disconnection.

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.

Sex differences in the age-related decline of blood-brain barrier function vary across brain regions, with a more pronounced decrease observed in males beginning in the early 60s.