Animal models of human diseases that accurately recapitulate clinical pathology are
indispensable for understanding molecular mechanisms and advancing preclinical studies …

The function of neural circuits and networks can be controlled, in part, by modulating the
synchrony of their components' activities. Network hypersynchrony and altered oscillatory …

The β secretase, widely known as β-site amyloid precursor protein cleaving enzyme 1
(BACE1), initiates the production of the toxic amyloid β (Aβ) that plays a crucial early part in …

Accumulations of insoluble deposits of amyloid β-peptide are major pathological hallmarks
of Alzheimer disease. Amyloid β-peptide is derived by sequential proteolytic processing from …

Human Alzheimer's disease (AD) brains and transgenic AD mouse models manifest
hyperexcitability. This aberrant electrical activity is caused by synaptic dysfunction that …

Abstract β-site amyloid precursor protein cleaving enzyme 1 (BACE1) is the β-secretase
enzyme required for the production of the neurotoxic β-amyloid (Aβ) peptide that is widely …

Neurodegenerative diseases selectively target subpopulations of neurons, leading to the
progressive failure of defined brain systems, but the basis of such selective neuronal …

A growing number of diseases seem to be associated with inappropriate deposition of
protein aggregates. Some of these diseases—such as Alzheimer's disease and systemic …

The amyloid hypothesis has yielded a series of well-validated candidate drug targets with
potential for the treatment of Alzheimer disease (AD). Three proteases that are involved in …

Inhibitory interneurons regulate the oscillatory rhythms and network synchrony that are
required for cognitive functions and disrupted in Alzheimer's disease (AD). Network …