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

Autophagy, the major degradative pathway for organelles and long-lived proteins, is
essential for the survival of neurons. Mounting evidence has implicated defective autophagy …

The neuropathological correlates of Alzheimer's disease (AD) include amyloid-β (Aβ)
plaques and neurofibrillary tangles. To study the interaction between Aβ and tau and their …

Although extensive data support a central pathogenic role for amyloid β protein (Aβ) in
Alzheimer's disease, the amyloid hypothesis remains controversial, in part because a …

The primal role that the amyloid-β (Aβ) peptide has in the development of Alzheimer's
disease is now almost universally accepted. It is also well recognized that Aβ exists in …

Genetic evidence predicts a causative role for amyloid-β (Aβ) in Alzheimer's disease. Recent
debate has focused on whether fibrils (amyloid) or soluble oligomers of Aβ are the active …

Calcium modulates many neural processes, including synaptic plasticity and apoptosis.
Dysregulation of intracellular calcium signalling has been implicated in the pathogenesis of …

Alzheimer's disease (AD) is a neurodegenerative disorder that is characterized by amyloid
plaques in patients' brain tissue. The plaques are mainly made of β-amyloid peptides and …

Extensive research causally links amyloid-β peptide (Aβ) to Alzheimer's disease, although
the pathologically relevant Aβ conformation remains unclear. Aβ spontaneously aggregates …

Alzheimer's disease (AD) is characterized by the deposition of senile plaques (SPs) and
neurofibrillary tangles (NFTs) in vulnerable brain regions. SPs are composed of aggregated …