Aging

One of the characteristic hallmarks of Alzheimer’s disease (AD) is the buildup of amyloid-beta plaques in the brain. Most therapies designed to treat AD target these plaques, but they’ve largely failed in clinical trials. New research by Professor Greg Lemke and Youtong Huang, a postdoctoral researcher and first author of the study, upends conventional views of the origin of one prevalent type of plaque, indicating a reason why treatments have been unsuccessful. The research suggests that dense-core plaques play a protective role, so treatments to destroy them may do more harm than good.

Despite the prevalence of Alzheimer’s, there are still no treatments, in part because it has been challenging to study how the disease develops. Now, Salk President and Professor Rusty Gage and Jerome Mertens, assistant adjunct professor and first author of a new paper, have uncovered new insights into what goes awry during Alzheimer’s by growing neurons that resemble—more accurately than ever before—brain cells in older patients. And like patients themselves, the afflicted neurons appear to lose their cellular identity. The findings showed that these brain cells are characterized by markers of stress as well as changes in which the cells become less specialized. Interestingly, many of the alterations seen in these cells are similar to what’s been observed in the cells of cancer—another disease linked to aging.