The incidence of Alzheimer's disease (AD) is growing every day and finding an effective
treatment is becoming more vital. Amyloid-β (Aβ) has been the focus of research for several …

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 collapse of neural networks important for memory and cognition, including death of
neurons and degeneration of synapses, causes the debilitating dementia associated with …

Alzheimer's disease (AD) challenges our society with an annual estimated cost of $1.08
trillion in the United States alone by 2050. 1 AD is a progressive irreversible neurological …

Soluble oligomers of amyloid β-protein (oAβ) isolated from the brains of Alzheimer's disease
(AD) patients have been shown experimentally (in the absence of amyloid plaques) to …

Soluble amyloid-β oligomers (Aβo) trigger Alzheimer's disease (AD) pathophysiology and
bind with high affinity to cellular prion protein (PrP C). At the postsynaptic density (PSD) …

Amyloid-beta (Aβ) oligomers are thought to trigger Alzheimer's disease pathophysiology.
Cellular prion protein (PrPC) selectively binds oligomeric Aβ and can mediate Alzheimer's …

Objective Currently no effective disease‐modifying agents exist for the treatment of
Alzheimer disease (AD). The Fyn tyrosine kinase is implicated in AD pathology triggered by …

Alzheimer's disease is the leading cause of dementia in the elderly and is defined by two
pathological hallmarks; the accumulation of aggregated amyloid beta and excessively …