Dysfunction of pyramidal neuron-PV interneuron circuits contributes to cognitive failure in Alzheimer's disease.

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.

Increased levels of brain Hebp1 starting from the presymptomatic stage of Alzheimer’s disease contributes to progressive neuronal loss by triggering mitochondrial-dependent apoptosis in neurons exposed to elevated heme.

An internet-based cohort study of paired associate learning shows that a first-degree family history of dementia is associated with lowered performance, an effect modified by apolipoprotein E genotype and diabetes.

Amyloid-β oligomers associated with Alzheimer’s disease interact with dynein motors to impair retrograde transport of autophagic vesicles in neurons.

By binding to Fc gamma receptor IIb, amyloid beta induces a series of phosphorylation events that mediate the damaging effects of hyperphosphorylated tau proteins in Alzheimer's disease.

Somatically derived genomic mosaicism in the form of increased DNA content and APP copy number in single neurons plausibly has a function in sporadic Alzheimer’s disease and points to functions for single-neuron gene copy number changes.

A protein called NPTX2 may be a useful marker of neural circuit defects in patients with Alzheimer's disease.

Tau proteins can convert from an inert shape to a misfolded shape that seeds the growth of fibers that contribute to the pathology of Alzheimer's disease.

The APP intracellular domain (AICD) physiologically regulates synaptic GluN2B-containing NMDA receptor current, a process that could contribute to pathological Alzheimer's disease-related synaptic failure upon increase of AICD levels in adult neurons.