Two articles in this month's issue of Nature Reviews Neuroscience focus on Alzheimer's disease, an important research topic given the rapidly ageing population in many countries.

The two main players in Alzheimer's disease pathology are amyloid-β and tau. In a Progress article (page 65), Ittner and Götz discuss recent data showing that hyperphosphorylated tau accumulates in soma and dendrites, where it seems to increase the toxic effects of amyloid-β. As amyloid-β toxicity in turn promotes tau phosphorylation, this establishes a vicious circle, as proposed by the authors in the 'tau axis hypothesis'.

On page 73, Thathiah and De Strooper focus on the role of G protein-coupled receptors (GPCRs) in Alzheimer's disease. Different GPCRs regulate the production and degradation of amyloid-β, and amyloid-β influences GPCR function, which might contribute to the dysfunction of several neurotransmitter systems in Alzheimer's disease. These findings point to GPCRs as potential therapeutic targets.

Neurodegenerative disorders such as Alzheimer's disease could benefit from regenerative medicine. The neurogenic potential of astrocytes in vitro suggests that these cells could provide a novel source of new neurons, but overcoming inhibitory signals in vivo has yet to be achieved. On page 88, Götz and colleagues review data on reactive gliosis that could provide insights to address this challenge.

One of the hallmark symptoms of Alzheimer's disease is memory loss, but much remains to be learned about the processes underlying normal memory function. On page 105, Fell and Axmacher describe recent findings that phase synchronization between oscillations in different brain regions supports working memory and long-term memory. They propose that synchronization might also underlie interactions between the two memory systems.