A study by UC Berkeley researchers has found a correlation between changes in brain wave patterns during non-REM sleep, poor episodic memory formation, and the accumulation of tau protein, a known marker for Alzheimer's disease. This research, led by neuroscientist Omer Sharon and former sleep researcher Matthew Walker, was published in *Nature Neuroscience* on September 11.
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Episodic memory involves recalling personal experiences, which can diminish over time, especially in aging individuals and those developing Alzheimer's. The researchers discovered that as tau proteins accumulate in the brain's frontal cortex, the slow brain waves crucial for memory consolidation become erratic.
“Each slow wave reflects an enormous population of neurons switching off and back on together,” Sharon explained. This coordinated neuronal activity is observed during deep non-REM sleep, which is essential for mental health. In previous, younger cohorts, slow waves would travel considerable distances across the brain, but in older adults, these waves were shorter and less synchronized, indicating potential cognitive decline.
To investigate this, the study employed electroencephalograms (EEGs) to measure brain waves during sleep in participants ranging from their early 20s to their mid-60s and 70s. Positive emission tomography (PET) scans conducted alongside these measurements confirmed a direct link between tau buildup in the frontal cortex and the irregular slow waves observed in older participants.
This breakdown of slow waves was found even in cognitively healthy older participants who showed early signs of tau buildup without any Alzheimer’s diagnosis. Furthermore, those with fewer synchronized slow waves performed worse on memory retention tests that involved word associations.
The researchers also collaborated with neurologist Yo-El Ju at Washington University in St. Louis to analyze tau levels in the spinal fluid of a different elderly cohort. Though the spinal fluid did not specifically indicate tau accumulation in the frontal cortex, a related pattern emerged with higher ratios of tau relative to amyloid protein in participants exhibiting solitary slow waves.
Sharon noted that the convergence of findings from various methodologies enhances the validity of the results. “This longitudinal correlation suggests that Alzheimer’s disease pathology is associated with a disruption of this main sleep feature,” he stated, emphasizing the complexity of memory loss and its connection to both aging and protein pathology.
The study was supported by the National Institute on Aging and included contributions from several authors at UC Berkeley and Washington University in St. Louis.