Breakthroughs in molecular medicine have positioned the amyloid-β (Aβ) pathway at the
center of Alzheimer's disease (AD) pathophysiology. While the detailed molecular …

It is increasingly accepted that early cognitive impairment in Alzheimer's disease results in
considerable part from synaptic dysfunction caused by the accumulation of a range of …

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 amyloid cascade hypothesis, according to which the self-assembly of amyloid-β peptide
(Aβ) is a causative process in Alzheimer's disease, has driven many therapeutic efforts for …

Soluble oligomers of amyloid β-protein (Aβ) have been defined as aggregates in
supernatants following ultracentrifugation of aqueous extracts from Alzheimer's disease (AD) …

It is widely accepted that β-amyloid oligomers (Aβos) play a key role in the progression of
Alzheimer's disease (AD) by inducing neuron damage and cognitive impairment, but Aβos …

Highlights•Lack of success of most anti-amyloid trials in symptomatic AD is attributable in
part to the pathology being too advanced.•Progress in quantifying tau and Aβ in plasma …

Protein misfolding and aggregation are characteristic of a wide range of neurodegenerative
disorders, including Alzheimer and Parkinson diseases. A hallmark of these diseases is the …

Mounting evidence suggests that the neuronal cell membrane is the main site of oligomer-
mediated neuronal toxicity of amyloid-β peptides in Alzheimer's disease. To gain a detailed …

Neuronal endosomal dysfunction, the earliest known pathobiology specific to Alzheimer's
disease (AD), is mediated by the aberrant activation of Rab5 triggered by APP-β secretase …