Alzheimer's disease is caused by increased production or reduced clearance of amyloid-β,
which results in the formation amyloid-β plaques and triggers a cascade of downstream …

The amyloid precursor protein (APP), whose mutations cause familial Alzheimer's disease,
interacts with the synaptic release machinery, suggesting a role in neurotransmission. Here …

Chronic inflammation during Alzheimer's disease (AD) is most often attributed to sustained
microglial activation in response to amyloid-β (Aβ) plaque deposits and cell death. However …

Amyloid beta (Aβ) peptides impair multiple cellular pathways and play a causative role in
Alzheimer's disease (AD) pathology, but how the brain proteome is remodeled by this …

Background Recent studies suggest that microglia contribute to tau pathology progression in
Alzheimer's disease. Amyloid plaque accumulation transforms microglia, the primary innate …

Neuronal aging increases the risk of late-onset Alzheimer's disease. During normal aging,
synapses decline, and β-amyloid (Aβ) accumulates intraneuronally. However, little is known …

The key role of APP for Alzheimer pathogenesis is well established. However, perinatal
lethality of germline knockout mice lacking the entire APP family has so far precluded the …

Synaptic degeneration, including impairment of synaptic plasticity and loss of synapses, is
an important feature of Alzheimer disease pathogenesis. Increasing evidence suggests that …

Background Knock-in (KI) mouse models of Alzheimer's disease (AD) that endogenously
overproduce Aβ without non-physiological overexpression of amyloid precursor protein …

Transgenic mice made by crossing animals expressing mutant amyloid precursor protein
(APPswe) to mutant presenilin 1 (PS1dE9) allow for incremental increases in Aβ42 …