Doorways to Discovery
November 11, 2014

Alzheimer’s disease doesn’t arise suddenly. It begins years earlier as the brain starts accumulating two proteins: amyloid protein that forms plaques and tau protein that forms tangles. Ultimately, related to damage from these proteins, brain cells die, brain regions responsible for memory and cognition shrink, and symptoms of dementia emerge.

Cognitive neuroscientist Marilyn Albert and her collaborators measure these proteins in cerebrospinal fluid (CSF), use sophisticated MRI brain imaging techniques to study affected brain regions, and draw parallels between their findings and the progression of cognitive decline.

Most recently, she and colleagues at Johns Hopkins studied several hundred people, most of whom were first evaluated when they were middle-aged and symptom-free. About one-fifth have progressed to mild cognitive impairment or dementia. The researchers are looking for markers in normal individuals that predict who will develop symptoms many years later. Why? So treatment regimens can be started at the optimal time—not too late and not too soon for the best effect. Baseline ratios of amyloid and tau in CSF, as well as measures on MRI scans, appear to be good predictors. 

“We think that current drugs for Alzheimer’s disease might be failing because the timing is off. And we think that the markers from CSF or from brain imaging will tell us when to start treating,” says Albert.

She is director of the Alzheimer’s Disease Research Center at Johns Hopkins and of this project, known as BIOCARD. Recently re-funded by the National Institute on Aging, she and her colleagues are expanding their evaluations to include several innovative new procedures.

“When better treatments become available, combined with early diagnosis, we could help change the course of Alzheimer’s and the future of aging.”