Alzheimer disease (AD) is characterized by progressive cognitive decline in older
individuals accompanied by the presence of two pathological protein aggregates—amyloid …

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 …

Neuronal hyperactivity is a key feature of early stages of Alzheimer's disease (AD). Genetic
studies in AD support that microglia act as potential cellular drivers of disease risk, but the …

Self-assembled peptide and protein amyloid nanostructures have traditionally been
considered only as pathological aggregates implicated in human neurodegenerative …

A major feature of Alzheimer's disease (AD) pathology is the plaque composed of
aggregated amyloid-β (Aβ) peptide. Although these plaques may have harmful properties …

A variety of cognitive disorders are worsened by stress exposure and involve dysfunction of
the newly evolved prefrontal cortex (PFC). Exposure to acute, uncontrollable stress …

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 …

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

Microglia-mediated synaptic loss contributes to the development of cognitive impairments in
Alzheimer's disease (AD). However, the basis for this immune-mediated attack on synapses …

Protein aggregation is common to dozens of diseases including prionoses, diabetes,
Parkinson's and Alzheimer's. Over the past 15 years, there has been a paradigm shift in …