Mitochondrial hypermetabolism precedes impaired autophagy and synaptic disorganization in App knock-in Alzheimer mouse models.

Accumulation of amyloid β-peptide (Aβ) is a driver of Alzheimer's disease (AD). Amyloid precursor protein (App) knock-in mouse models recapitulate AD-associated Aβ pathology, allowing elucidation of downstream effects of Aβ accumulation and their temporal appearance upon disease progression. Here we have investigated the sequential onset of AD-like pathologies in App and App knock-in mice by time-course transcriptome analysis of hippocampus, a region severely affected in AD.

C-PiB and I-Antibody PET Provide Differing Estimates of Brain Amyloid-β After Therapeutic Intervention.

PET imaging of amyloid-β (Aβ) has become an important component of Alzheimer disease diagnosis. C-Pittsburgh compound B (C-PiB) and analogs bind to fibrillar Aβ. However, levels of nonfibrillar, soluble, aggregates of Aβ appear more dynamic during disease progression and more affected by Aβ-reducing treatments.