Using a mouse model, researchers from the TUM Institute of Neuroscience in Munich, Germany have uncovered how pathological changes in the brain that occur in Alzheimer’s disease disrupt information-storing processes that occur during sleep.
Dr. Dr. Marc Aurel Busche, a scientist in the department of psychiatry and psychotherapy at TUM University Hospital Klinikum rechts der Isar and TUM Institute of Neuroscience, and colleagues found that deposits of beta-amyloid impair the ability of slow-wave oscillations during non-REM sleep to spread to corresponding regions throughout the brain, in turn blocking the transition of information in to long-term memories.
“These waves are a kind of signal through which these areas of the brain send mutual confirmation to say ‘I am ready, the exchange of information can go ahead’. Therefore, there is a high degree of coherence between very distant nerve cell networks during sleep,” said Dr. Busche.
In order to study this process, the researchers mapped and compared neuronal activity in wild-type mice and transgenic mouse models of Alzheimer’s disease. They found that calcium transients associated with slow-wave oscillations were highly coherent across the cortex in wild mice, however coherence was severely disrupted in the transgenic mice. They further demonstrated the breakdown in coherence by subdividing the cortex into eight domains: occipital (1 right, 5 left), somatosensory (2 right, 6 left), motor (3 right, 7 left), and frontal (4 right, 8 left). Testing showed that 9 of 9 wild mice showed strong correlations across all cortical domains, with only a small decrease as a function of distance. All transgenic mice showed significantly lower correlations across all cortical domains, especially between those widely separated along the anterior-posterior cortical axis.
“The slow oscillations do still occur, but they are no longer able to spread properly — as a result, the signal for the information cross-check is absent in the corresponding regions of the brain,” Dr. Busche explained.