The amyloid-β oligomer (AβO) hypothesis was introduced in 1998. It proposed that the brain
damage leading to Alzheimer's disease (AD) was instigated by soluble, ligand-like AβOs …

The function of neural circuits and networks can be controlled, in part, by modulating the
synchrony of their components' activities. Network hypersynchrony and altered oscillatory …

Animal models are indispensable tools for Alzheimer disease (AD) research. Over the
course of more than two decades, an increasing number of complementary rodent models …

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 …

Most neurodegenerative diseases are proteinopathies, which are characterized by the
aggregation of misfolded proteins. Although many proteins have an intrinsic propensity to …

The first description of Alzheimer's disease (AD) was made in 1907 by Alois Alzheimer
(Allgemeine Zeitschrift fur Psyciatrie und Psychisch‐Gerichtliche Medizin 64, 3, 1907) …

Amyloid-β peptide (Aβ) forms metastable oligomers> 50 kDa, termed AβOs, that are more
effective than Aβ amyloid fibrils at triggering Alzheimer's disease-related processes such as …

The cascade of amyloid formation relates to multiple complex events at the molecular level.
Previous research has established amyloid plaque deposition as the leading cause of …

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 …

Cellular deposition of protein aggregates, one of the hallmarks of neurodegeneration,
disrupts cellular functions and leads to neuronal death. Mutations, posttranslational …