Resting-State fMRI Reveals Decay in Brain Network associated in Early Alzheimer’s

In patients with early Alzheimer’s disease (AD), brain network disruptions are present about the same time as chemical markers of the disease appear in the spinal fluid, according to new research.

While two chemical markers in the spinal fluid are regarded as effective indicators of early disease, the new study, researchers from Washington University School of Medicine in St. Louis (MO, USA) published their findings August 19, 2013, in JAMA Neurology, is among the first to show that scans of brain networks may be an equally effective and less invasive approach to identify early disease.

“Tracking damage to these brain networks may also help us formulate a more detailed understanding of what happens to the brain before the onset of dementia,” said senior author Beau Ances, MD, PhD, associate professor of neurology and of biomedical engineering.

Diagnosing Alzheimer’s early is of vital urgency for physicians, many of whom believe that treating patients long before dementia begins greatly improves the chances of success. Dr. Ances and his colleagues assessed 207 older but cognitively normal research volunteers at the Charles F. and Joanne Knight Alzheimer’s Disease Research Center at Washington University. Over several years, spinal fluids from the volunteers were sampled multiple times and analyzed for two markers of early ADs: alterations in amyloid beta, the principal ingredient of Alzheimer’s brain plaques, and in tau protein, a structural component of nerve cells.

The volunteers were also scanned repeatedly using a technique called resting-state functional magnetic resonance imaging (fMRI). This scan tracks the rise and fall of blood flow in different brain regions as patients rest in the scanner. Scientists use the resulting data to assess the integrity of the default mode network, a set of connections between different brain regions that becomes active when the mind is at rest.

Earlier studies by Dr. Ances and other researchers have shown that AD damages connections in the default mode network and other brain networks. The new study revealed that this damage became detectable at about the same time that amyloid beta levels began to rise and tau levels started to fall in spinal fluid. The part of the default mode network most injured by the onset of AD was the connection between two brain regions associated with memory, the posterior cingulate and medial temporal regions.

The researchers have continuing strategy to study the connections between brain network damage and the progress of early AD in healthy volunteers and in patients in the early stages of Alzheimer’s-associated dementia.

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Washington University School of Medicine in St. Louis