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 …

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 …

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 …

The accumulation of misfolded proteins in the human brain is one of the critical features of
many neurodegenerative diseases, including Alzheimer's disease (AD). Assembles of beta …

Synucleinopathies, such as Parkinson's disease and dementia with Lewy bodies, are
neurodegenerative disorders that are characterized by the accumulation of α-synuclein …

The causative role of amyloid β 1–42 (Aβ42) aggregation in the pathogenesis of Alzheimer's
disease (AD) has been under debate for over 25 years. Primarily, scientific efforts have …

Alzheimer9s disease (AD) is characterized by progressive cognitive decline, increasingly
attributed to neuronal dysfunction induced by amyloid-β oligomers (AβOs). Although the …

The prevalence, presentation, and progression of Alzheimer's disease (AD) differ between
men and women, although β-amyloid (Aβ) deposition is a pathological hallmark of AD in …

The prion glycoprotein (PrPC) is mostly located at the cell surface, tethered to the plasma
membrane through a glycosyl-phosphatydil inositol (GPI) anchor. Misfolding of PrPC is …

Synaptic vesicle glycoprotein 2A (SV2A) is expressed ubiquitously in neurons of the central
nervous system, and is the binding target of the anti-epileptic drug levetiracetam. Because of …