In recent news stories about Alzheimer’s disease research, we noticed a word popping up: unbiased. Allan Levey, chair of Emory’s neurology department and head of Emory’s Alzheimer’s Disease Research Center, likes to use that word too. It’s key to a “back to the drawing board” shift taking place in the Alzheimer’s field.
Last week’s announcement of a link between herpes viruses and Alzheimer’s, which Emory researchers contributed to, was part of this shift. Keep in mind: the idea that viral infection contributes to Alzheimer’s has been around a long time, and the Neuron paper doesn’t nail down causality.
Still, here’s an example quote from National Institute on Aging director Richard Hodes: “This is the first study to provide strong evidence based on unbiased approaches and large data sets that lends support to this line of inquiry.”
What is the bias that needs to be wrung out of the science? The “amyloid hypothesis” has dominated drug development for the last several years. Amyloid is a main constituent of the plaques that appear in the brains of people with Alzheimer’s, so treatments that counteract amyloid’s accumulation should help, right? Unfortunately, antibodies against amyloid or inhibitors of enzymes that process it generally haven’t worked out in big clinical trials, although the possibility remains that they weren’t introduced early enough to have a decent effect.
So Alzheimer’s researchers have been saying: let’s take another look at the data, trying to steer clear of the amyloid hypothesis. Centers like Emory, which maintain large databases of patient-derived samples, are critical for this effort. And coming from Emory researchers, we can find several examples of this broad-based, agnostic approach:
*The discovery of splicing alterations in Alzheimer’s brain samples
*Nick Seyfried’s use of proteomics to comprehensively track changes in Alzheimer’s brain
*The finding by David Katz that loss of the LSD1 histone demethylase induces patterns of gene activity resembling Alzheimer’s