Top of Kolata’s list is the finding that in people with late-onset AD, clearance of amyloid-β (Aβ) from the brain is more of a problem than overproduction. Alzforum reported this when Randall Bateman, Washington University, St. Louis, Missouri, presented it at the International Conference on Alzheimer’s Disease in Honolulu last July (see ARF related news story). Formally published in the December 9 Sciencexpress (see ARF related news story), the study found that Aβ exits the CSF more slowly as people age, and most slowly in those with AD. This is the latest study in bold research on human volunteers Bateman first published in 2006 (see ARF related news story).

Kolata also highlights work from David Holtzman’s lab, also at WashU, and Roberto Malinow’s lab at University of California, San Diego, revealing roles for Aβ in normal (see ARF related news story) and dysfunctional synaptic activity (see ARF related news story), and tying Aβ to synaptic activity in humans for the first time (see ARF related news story).

The place of tau in pathology, as described in recent studies from Lennart Mucke’s lab at University of California, San Francisco (see ARF related news story and ARF news story), also makes the list, as does the default-mode network, a matrix of interconnected brain regions that are particularly prone to accumulate amyloid plaques and succumb to neurodegeneration in AD (see, e.g., ARF related news story, ARF news story, and ARF news story). Taken together, these advances point to new ways to understand and attack the disease, writes Kolata. Recycling gone? Read the New York Times piece here. And while you are already taking in Alzheimer's coverage in one major newspaper, read also Sandra Day O'Connor and Maria Shriver's call in the Washington Post for visionary leadership so this nation can rally the will and resources to averting a national epidemic of this disease.—Tom Fagan and Gabrielle Strobel.