Ten days ago I wrote about a new class of Alzheimer's drugs aimed at cutting long strands of what are called amyloid-beta proteins.
(Shown are models of amyloid beta proteins produced by a Madison, Wisconsin high school.)
Now new research pinpoints the specific types of amyloid-betas which may be causing the disease. They're called soluble two-molecule, or dimer, amyloid-betas.
In the new Harvard study (with Irish and Scottish help), to be published in Nature Medicine, researchers worked with brains donated for autopsy of patients who both had and did not have Alzheimer's or other dementia.
They extracted the dimer amyloid-betas, along with mono (single cell) and trimer (three-cell or larger) extracts, then injected them into rats and mice brains.
Only the dimers produced the key characteristics of Alzheimer's, by acting directly on the synapses of the brain.
To confirm the finding antibodies against amyloid-beta were injected, and these inactivated the dimers.
The studies help explain why some people found after death to have lots of insoluble Alzheimer's plaques never develop the disease.
Bapineuzumab is aimed directly at amyloid plaques, but a study with 240 patients showed it actually hurt patients with a genetic variant which makes them especially susceptible to the disease.
Because those with and without the genetic variant weren't pre-screened before the trial, it's hard to tell whether the drug is really useful.
Perhaps new findings, showing that only certain amyloid-beta plaques are dangerous, will lead to new drugs.
Or drug companies might look at another study, also from Nature Medicine, showing there may be yet another route to success.
All this proves that science remains a dance. Two steps forward and one step back.