Increasing evidence has suggested that formation and propagation of misfolded aggregates of 42-residue human amyloid β (Aβ(1–42)), rather than of the more abundant Aβ(1–40), provokes the Alzheimer's ...

Amyloid-beta (Aβ) accumulation in the brain is proposed to be an early toxic event in the pathogenesis of Alzheimer’s disease (AD). Although there have been many studies done, there is great ...

Researchers from the National Institutes of Natural Sciences and Nagoya City University have achieved a significant breakthrough by elucidating the structure of amyloid β (Aβ) bound to glycolipids on ...

The LilrB2 receptor on the surface of neurons binds Aβ and is thought to mediate some of its toxicity. Researchers led by Lin Jiang and David Eisenberg at the University of California, Los Angeles, ...

The brains of millions of people suffering from Alzheimer´s disease (AD) are slowly and inescapably being depleted of neurons, which leads to the characteristic loss of memory and cognitive function ...

The brains of millions of people suffering from Alzheimer´s disease (AD) are slowly and inescapably being depleted of neurons, which leads to the characteristic loss of memory and cognitive function ...

The main component of Alzheimer’s plaques—fibrillar aggregates of amyloid-β(1-42) (Aβ42)—pose a sticky problem for structural biologists. In the past few years, groups have used various biophysical ...