Significant progress is being made in the fight against the “silver tsunami,” said Scott Turner, M.D., Ph.D., director of the memory disorders program at Georgetown University, during a panel at Health Journalism 2013.
The FDA has changed regulations so that new drugs to fight Alzheimer’s can go to clinical trial and potentially go on the market more quickly and researchers are creating new “biomarkers” to diagnose Alzheimer’s earlier.
“We’re moving to earlier and earlier disease, trying to target people at risk,” Turner said. “It’s a huge development in our thinking about Alzheimer’s disease.” Two significant biomarkers begin to show up 20 years before someone might show clinical symptoms of disease: Both cerebrospinal fluid and PET scans show abnormal build-up of A-beta amyloid.
Abnormal amyloid plaques and tangles of Tau proteins are hallmarks of Alzheimer’s. The first shows up in imaging as colorless clumping; the second as black spots.
Of note, Turner mentioned a provocative study that came out last year in Nature (2012) by Jonsson et al. in which they discovered a genetic variant in Norwegian participants that seemed to protect elderly not only from Alzheimer’s but even “normal” cognitive decline with aging.
Gad Marshall, M.D., the associate medical director of clinical trials at Brigham and Women’s Hospital’s Center for Alzheimer Research and Treatment, discussed what progress has been made in developing these biomarkers that will enable doctors to see who’s developing Alzheimer’s before dementia strikes. So far, cerebrospinal fluid can be tested for A-beta amyloid and Tau protein tangles. “Testing blood and urine isn’t well established yet, but would be much nicer” than a lumbar puncture, Marshall said. MRI brain imaging is effective, and the “new kid on the block” is molecular imaging of pathology – amyloid PET imaging.
The presentation took a new turn with a slideshow from Robert Stern, Ph.D., professor of neurology and neurosurgery and director of the Alzheimer’s Disease Clinical and Research Program at the Boston University School of Medicine. As an Alzheimer’s researcher, Stern’s interest in chronic traumatic encephalopathy came about in seeing ways in which this form of dementia may mirror or may diverge from Alzheimer’s.
CTE is caused not only by concussion but also by repeated brain trauma that does NOT cause concussion. (Concussion was defined, by the way, not by loss of consciousness or even “bruising” of the brain, but by temporary disruption of brain function – so a concussion can occur without somebody knowing it.)
Concussion is the “tip of the iceburg” for CTE, according to Stern. More important are repeated, subconcussive traumas to the brain. An admitted football devotee, Stern showed that not only football players are subject to CTE, but also those who have milder but regular head trauma, like soccer players. The disease is not a cumulative result of head traumas; rather, the trauma starts the problem and then there is a cascade of spreading damage. In contrast to Alzheimer’s, CTE does not show a build-up of amyloid plaque, but it does show Tau neurofibrillary tangles. Stern’s work can be found at the BU Center for the Study of Traumatic Encephalopathy.
