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 …

Aggregation of the β-amyloid peptide (Aβ) in brain regions serving memory and cognition is
thought to initiate Alzheimer's disease (AD)(1). Despite myriad studies of the neurobiological …

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

Alzheimer's disease is the most frequent neurodegenerative disorder and the most common
cause of dementia in the elderly. Diverse lines of evidence suggest that amyloid-β (Aβ) …

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 …

Protein aggregation is an established pathogenic mechanism in Alzheimer's disease, but
little is known about the initiation of this process in vivo. Intracerebral injection of dilute …

In its earliest clinical phase, Alzheimer's disease characteristically produces a remarkably
pure impairment of memory. Mounting evidence suggests that this syndrome begins with …

Soluble amyloid-beta oligomers (Aβo) start to accumulate in the human brain one to two
decades before any clinical symptoms of Alzheimer's disease (AD) and are implicated in …

Alzheimer's disease is hypothesized to be caused by an imbalance between β-amyloid (Aβ)
production and clearance that leads to Aβ accumulation in the central nervous system …