A brain at rest offers clues to Parkinson’s, Alzheimer’s

Networks of brain regions that are active when the brain is at rest — not thinking about anything in particular — differ between healthy people and those with Parkinson’s or Alzheimer’s diseases, a new study finds.

Measurements of how much glucose brain cells consume reveal that one important resting network, called the default mode network, rapidly and continually loses activity in people with Alzheimer’s disease, researchers report February 9 in the Proceedings of the National Academy of Sciences. In contrast, the network remains largely intact during the early stages of Parkinson’s disease.

The default mode network is series of brain regions that are active when people are sitting quietly thinking of nothing in particular. Scientists debate the network’s role, but some evidence has indicated that it breaks down in a wide variety of brain disorders and diseases (SN: 7/18/09, p. 16).

Researchers discovered the default mode network using brain scans known as functional magnetic resonance imaging, or fMRI. That technique measures blood flow, which is an indirect gauge of brain cell activity. David Eidelberg, a neuroscientist at the Feinstein Institute for Medical Research in Manhasset, N.Y., and colleagues decided to use a more direct brain imaging technique, known as a PET scan, to measure how much glucose brain cells use. More active brain cells burn more glucose.

The researchers first scanned the brains of 63 healthy people. The default mode network found in fMRI scans was also detectable in the PET scans, the team discovered. In fact, the network signals were stronger in PET scans than in fMRIs, Eidelberg says.

The scientists then analyzed PET scans of the brains of Parkinson’s and Alzheimer’s patients. The scans of Parkinson’s patients showed that the default mode network was no longer the dominant resting network. “There was a new sheriff in town,” in the form of a new abnormal network not seen in healthy people, Eidelberg says. In the early stages of Parkinson’s disease, this new network dominated resting brain activity, but otherwise didn’t interfere with the default mode network. As the disease progressed and the patients began to develop dementia, the default mode network started to break down, the researchers found. But its activity could be partially restored by treating patients with levodopa, a drug that converts to dopamine in the body.

To find out what happens in Alzheimer’s disease, the researchers examined PET scans from a database compiled by the Alzheimer’s Disease Neuroimaging Initiative.

Alzheimer’s disease patients also had a new abnormal dominant resting network in their brains, but it was different from the abnormal network seen in Parkinson’s disease patients.  Also, unlike in Parkinson’s patients, the default mode network of Alzheimer’s patients had already started to decay even in people with mild symptoms that couldn’t yet be reliably diagnosed as Alzheimer’s disease. PET scans taken six months, a year and two years after the initial one showed ever lower activity in default mode networks of the Alzheimer’s patients.

The differences may stem from the nature of the diseases, says Douglas Rothman, an imaging scientist at Yale University who wasn’t involved in the work. In Parkinson’s disease, people lose brain cells that make dopamine, which helps coordinate communication. Restoring dopamine facilitates smoother talk in the brain networks. But in Alzheimer’s disease, brain cells in critical regions of the default mode network die. “You really have a massive disruption in neuroanatomy,” Rothman says. That damage probably cannot be reversed.

PET scans may one day be helpful in diagnosing brain diseases at earlier stages, and in monitoring how well drugs and treatments work to slow disease progression, Rothman says.