Alzheimer's disease (AD) is characterized by a progressive dysfunction of central neurons.
Recent experimental evidence indicates that in the cortex, in addition to the silencing of a …

Neuronal activity directly promotes the production and secretion of amyloid β (Aβ).
Interestingly, neuronal hyperactivity can be observed in presymptomatic stages of both …

β-amyloid (Aβ)–dependent neuronal hyperactivity is believed to contribute to the circuit
dysfunction that characterizes the early stages of Alzheimer's disease (AD). Although …

The accumulation of amyloid-β in the brain is an essential feature of Alzheimer's disease.
However, the impact of amyloid-β-accumulation on neuronal dysfunction on the single cell …

An unresolved debate in Alzheimer's disease (AD) is whether amyloid plaques are
pathogenic, causing overt physical disruption of neural circuits, or protective, sequestering …

Neuronal hyperactivity is the emerging functional hallmark of Alzheimer's disease (AD) in
both humans and different mouse models, mediating an impairment of memory and …

Amyloid-β (Aβ) peptides are constitutively produced in the brain throughout life via
mechanisms that can be regulated by synaptic activity. Although Aβ has been extensively …

Growing evidence supports the hypothesis that soluble, diffusible forms of the amyloid β-
peptide (Aβ) are pathogenically important in Alzheimer's disease (AD) and thus have both …

An essential feature of Alzheimer's disease (AD) is the accumulation of amyloid-β (Aβ)
peptides in the brain, many years to decades before the onset of overt cognitive symptoms …

Amyloid plaques are a neuropathological hallmark of Alzheimer's disease (AD), but their
relationship to neurodegeneration and dementia remains controversial. In contrast, there is …