Accumulation of tau protein in the frontal cortex disrupts the synchronized firing of slow waves during deep sleep and interferes with the overnight consolidation of memories — long before clinical signs of dementia appear. Neuroscientists at the University of California, Berkeley, reached these conclusions, infohub.kz reports.
The study, published in the journal Nature Neuroscience, explains a fundamental cause of age-related decline in episodic memory. As ScienceDaily notes, the researchers found that pathological tau protein in the frontal cortex disrupts the coordinated spread of slow electrical impulses during the deep phase of sleep.
Normally, during deep slow-wave sleep, large groups of neurons switch off and on simultaneously, generating coordinated waves. These waves originate in the frontal cortex and sweep across the entire cerebral cortex. An analysis of electroencephalograms from young people around age 20 showed consistent group movement of these signals. In older participants aged 65 to 75, the waves lost coherence, traveled significantly shorter distances and arose in isolation. The authors called these fragmented impulses "lonely waves."
Positron emission tomography confirmed that excess tau protein in the frontal lobes leads to the breakdown of a unified front of brain activity. Notably, none of the older participants had Alzheimer's disease, and their memory decline was within the normal range for their age. In tests to memorize word pairs, volunteers with frequent isolated impulses performed worse the following morning.
The findings of the California researchers, led by Omer Sharon, were confirmed by an analysis of cerebrospinal fluid from an independent group of patients conducted at Washington University in St. Louis. People with a high proportion of lonely waves showed an elevated ratio of tau protein to amyloid. According to the authors, the quality of nighttime brain rhythms could become a reliable marker for the early diagnosis of cognitive impairment.