Summary: Researchers examined resting-state functional MRI scans from more than 1,300 adults and found that poor sleep alters brain connectivity differently across the lifespan. In college-age adults, poor sleep produced overconnectivity in motor networks consistent with physical hyperarousal. In older adults (65+), poor sleep was associated with abnormal hyperconnectivity among higher-order cognitive networks—especially between the Default Mode Network (DMN) and the Frontal Parietal Network (FPN)—a pattern that resembles early, preclinical changes seen in Alzheimer’s disease.
Key Facts
- Lifespan differences: Poor sleep produces opposite brain-connection patterns in young versus older adults:
- College-age adults (18–25): Showed hyperconnectivity in motor-control regions, suggesting the body remains physiologically aroused and struggles to relax for sleep.
- Older adults (65+): Showed reduced connectivity in motor networks but abnormally increased connectivity in higher-level cognitive networks.
- DMN–FPN hyperconnectivity in older women: Older women with poor sleep displayed pronounced hyperconnectivity between the Default Mode Network (DMN) and the Frontal Parietal Network (FPN). This pattern—excessive cross-talk between networks involved in internal thought and active attention—parallels connectivity changes observed in the earliest, asymptomatic stages of Alzheimer’s disease.
- Negative cognitive impact: The DMN–FPN overconnectivity in older adults correlated with poorer memory performance and predicted faster cognitive decline, indicating the effect is harmful rather than compensatory.
- Different drivers of sleeplessness: Young adults’ sleep problems appear more driven by physical hyperarousal, while older adults’ sleep disturbances are more closely tied to cognitive hyperarousal—rumination or persistent thinking that keeps the brain active at night.
- Directionality remains unresolved: It is still unclear whether network degradation causes sleep problems or chronic poor sleep drives those network changes. However, the link between DMN–FPN hyperconnectivity and later cognitive decline suggests that chronic sleep disturbance may contribute to progressive cognitive impairment.
- Implications for treatment: Interventions should be age-tailored. Young adults may benefit most from physical wind-down routines before bed (exercise timing, relaxation, journaling to reduce racing thoughts), while older adults may require approaches that address network integrity and cognitive hyperarousal.
Source: Binghamton University
Difficulty sleeping? Your age may help explain why.
A recent study led by researchers at Binghamton University, State University of New York, explored how subjective sleep quality relates to resting-state brain connectivity across adulthood and how these relationships differ by age and biological sex. The article, titled “Sleep quality is associated with default mode and salience network connectivity differently across age and sex,” was published in the journal Neurobiology of Aging. Co-authors include Sepehr Gourabi and Associate Professor Ian McDonough (Binghamton), along with Selene Tan, Matthew Cribbet, and Jeanne Cundiff (University of Alabama).
The team combined two datasets totaling over 1,300 participants to examine how subjective sleep quality relates to resting-state functional connectivity (rsFC) among core brain networks: the Default Mode Network (DMN), the Salience Network (SN), and the amygdala’s connectivity to the rest of the brain. Using an exploratory-confirmatory design, the study compared younger and older adults and examined sex-specific patterns.
Results showed clear age- and sex-dependent differences. In younger adults, poor sleep was linked to heightened SN–sensorimotor connectivity, supporting a hyperarousal model in which motor and sensorimotor systems remain overly engaged at night. In older adults—particularly older women—poor sleep correlated with DMN hyperconnectivity to regions such as the superior parietal lobule and increased cross-talk between the DMN and FPN. That DMN–FPN hyperconnectivity was associated with worse episodic memory and tracked with longitudinal cognitive decline, echoing connectivity patterns seen in preclinical Alzheimer’s disease.
Why the differences arise remains an open question. Older adults may adapt differently to sleep loss, develop coping behaviors (including medication use), or experience more cognitive-driven sleep disruption such as rumination. Rumination—persistent, repetitive thinking before bedtime—can keep the mind active and interfere with the calm mental state needed for sleep.
The study did not find significant associations between sleep quality and amygdala connectivity, nor with blood-based biomarkers for Alzheimer’s pathology, inflammation, or sex hormones in these samples. Instead, the findings highlight a selective vulnerability of the DMN in older women and a shift from motor hyperarousal in youth to cognitive-network disruption in later life.
Dr. Ian McDonough summarizes the clinical takeaway: efforts to improve sleep should be matched to the likely cause. Younger adults may benefit from physical and behavioral strategies that reduce bodily arousal before bedtime—such as structured wind-down routines or journaling to clear intrusive thoughts—while older adults may need interventions that target cognitive hyperarousal and preserve network integrity. If sleep problems persist, consulting a physician is recommended.
Key Questions Answered:
A: The DMN supports internal thought, memory, and self-reflection and is usually active at rest. The FPN supports attention, working memory, and task control. Normally these networks balance activity. When they become abnormally synchronized—especially in older adults with poor sleep—that excessive cross-talk disrupts cognitive processing and impairs memory function.
A: In young adults, poor sleep is linked to motor and sensorimotor hyperconnectivity, consistent with physical restlessness or difficulty winding down. In older adults, motor systems tend to be less connected, while cognitive networks show abnormal increases in connectivity. This suggests a shift from bodily arousal in youth to cognitive-driven arousal or network breakdown in older age.
A: The relationships are interwoven. Chronic sleep disturbance, depression, and cognitive decline often interact and can amplify one another. The DMN–FPN hyperconnectivity pattern seen with poor sleep in older adults mirrors early connectivity changes linked to Alzheimer’s disease. Importantly, some cognitive deficits associated with mood disorders can improve with proper treatment, underscoring that protecting sleep and brain networks is a key preventive strategy for preserving cognition with age.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- The journal paper was reviewed in full by editorial staff.
- Additional context was added by the editorial team.
About this neuroscience and sleep research news
Author: John Brhel
Source: Binghamton University
Contact: John Brhel – Binghamton University
Image credit: Neuroscience News
Original Research: Open access. “Sleep quality is associated with default mode and salience network connectivity differently across age and sex” by Ian M. McDonough, Jeanne M. Cundiff, Matthew R. Cribbet, Selene Tan, Sepehr Gourabi. Neurobiology of Aging. DOI: 10.1016/j.neurobiolaging.2026.05.002
Abstract
Sleep quality is associated with default mode and salience network connectivity differently across age and sex
Aging and biological sex moderate how sleep quality relates to brain connectivity, influencing age-related cognitive decline and Alzheimer’s disease risk. This study tested whether subjective sleep quality differentially predicted resting-state functional connectivity (rsFC) among networks linked to hyperarousal and cognitive processing across younger and older adults. Using two datasets (N = 95 and N = 1,244), investigators examined connectivity of the Default Mode Network (DMN), Salience Network (SN), and amygdala with the rest of the brain. Findings revealed age- and sex-specific patterns: poorer sleep was linked to reduced DMN–superior parietal lobule connectivity in younger women but to DMN hyperconnectivity in older women, and DMN hyperconnectivity correlated with poorer episodic memory. For the SN, poorer sleep related to SN–sensorimotor hyperconnectivity in younger adults but to lower connectivity in older adults, indicating a shift from hyperarousal mechanisms to other age-related processes. No significant associations were observed for the amygdala or blood-based biomarkers. These results suggest a selective vulnerability of the DMN to sleep impairment in older women and a developmental shift from motor hyperarousal in youth to neurodegenerative-like network changes in later life.