Alzheimer's disease (AD) is caused by synaptic and neuronal loss in the brain. One of the
characteristic hallmarks of AD is senile plaques containing amyloid β-peptide (Aβ). Aβ is …

Animal models are indispensable tools for Alzheimer disease (AD) research. Over the
course of more than two decades, an increasing number of complementary rodent models …

Familial Alzheimer's disease (FAD), caused by mutations in Presenilin (PSEN1/2) and
Amyloid Precursor Protein (APP) genes, is associated with an early age at onset (AAO) of …

The zebrafish is increasingly recognized as a model organism for translational research into
human neuropathology. The zebrafish brain exhibits fundamental resemblance with human …

The amyloid cascade hypothesis, which posits that the deposition of the amyloid-β peptide
in the brain is a central event in Alzheimer's disease pathology, has dominated research for …

The past 15 years have witnessed tremendous progress in the molecular understanding of
osteoblasts, the main bone-forming cells in the vertebrate skeleton. In particular, all of the …

Reduction of amyloid beta (Aβ) has been shown to be effective in treating Alzheimer's
disease (AD), but the underlying assumption that neurons are the main source of pathogenic …

Significant insights into the function of genes associated with Alzheimer disease and related
dementias have occurred through studying genetically modified animals. Although none of …

Notch 1 to 4 receptors are important determinants of cell fate and function, and Notch
signaling plays an important role in skeletal development and bone remodeling. After direct …

The Alzheimer's disease (AD)-associated amyloid-β protein precursor (AβPP) is cleaved by
α-, β-, and presenilin (PS)/γ-secretases through sequential regulated proteolysis. These …