Intraneuronal amyloid β (Aβ) oligomer accumulation precedes the appearance of amyloid
plaques or neurofibrillary tangles and is neurotoxic. In Alzheimer's disease (AD)-affected …

Amyloid β-peptides (Aβ) are a major hallmark of Alzheimer's disease (AD) and their
neurotoxicity develop with cytosolic calcium dysregulation. On the other hand, calmodulin …

Lipid rafts are a primary target in studies of amyloid β (Aβ) cytotoxicity in neurons.
Exogenous Aβ peptides bind to lipid rafts, which in turn play a key role in Aβ uptake, leading …

Calmodulin (CaM) and a diversity of CaM-binding proteins (CaMBPs) are involved in the
onset and progression of Alzheimer's disease (AD). In the amyloidogenic pathway, AβPP1 …

Amyloid β1–42 (Aβ (1–42)) oligomers have been linked to the pathogenesis of Alzheimer's
disease (AD). Intracellular calcium (Ca2+) homeostasis dysregulation with subsequent …

A multifactorial syndrome, Alzheimer's disease is the main cause of dementia, but there is no
existing therapy to prevent it or stop its progression. One of the earliest events of Alzheimer's …

J. Neurochem.(2011) 119, 791–804. Abstract Alzheimer's disease (AD) is a progressive,
neurodegenerative disorder and the most prevalent senile dementia. The early symptom of …

The calcium hypothesis of Alzheimer's disease (AD) invokes the disruption of calcium
signaling as the underlying cause of neuronal dysfunction and ultimately apoptosis. As a …

Neurotoxicity of Alzheimer's β-amyloid protein (AβP) is central to the pathogenesis of
Alzheimer's disease (AD). Recent approaches have emphasized the importance of AβP …

Key neuropathological hallmarks of Alzheimer's disease include the accumulation of
amyloid-β (Aβ), disruption of Ca2+ homeostasis and neurodegeneration. However, the …