Double trouble for neurons

摘要

Working in Frankfurt, Germany, in 1901, Alois Alzheimer encountered a middle-aged patient named Auguste D. suffering from confusion and memory loss. Alzheimer's curiosity about her symptoms would lead to the recognition of the neurological syndrome that now bears his name. More than a century later, Alzheimer's disease is fixed in the public's consciousness as a devastating senile dementia that stubbornly resists effective medical treatment. But stunning advances are now being made in unravelling the molecular causes of this disease. Writing in Cell, Marambaud et al. present evidence for a new molecular mechanism that is connected with Alzheimer's disease. They suggest that N-cadherin ― a cell-surface protein that helps neurons adhere to one another ― might relay signals associated with neuronal survival and 'plasticity', processes that underlie learning and memory. This signalling depends on the protein pre-senilin, mutations in which account for some cases of Alzheimer's disease.