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Background This study assesses the relationships between dynamic functional network connectivity (DFNC) and dementia risk. Methods DFNC of the default mode (DMN), salience (SN), and executive control networks was assessed in 127 cognitively unimpaired older adults. Stepwise regressions were performed with dementia risk and protective factors and biomarkers as predictors of DFNC. Results Associations were found between times spent in (i) a "weakly connected" state and lower self-reported engagement in early- and mid-life cognitive activity and higher LDL cholesterol; (ii) a "SN-negatively connected" state and higher blood pressure, higher depression score, and lower body mass index (BMI); (iii) a "strongly connected" state and higher self-reported engagement in early-life cognitive activity, Preclinical Alzheimer's cognitive composite-5 score, and BMI; and (iv) a "DMN-negatively connected" state and higher self-reported engagement in early- and mid-life stimulating activities and lower LDL cholesterol and blood pressure. The lower number of state transitions was associated with lower brain perfusion. Conclusion DFNC states are differentially associated with dementia risk and could underlie reserve.

The mechanism by which information is bound together in working memory is a central question for cognitive neuroscience. This binding is transiently disrupted during periods of post-traumatic amnesia following significant head injuries. The reason for this impairment is unclear but may be due to electrophysiological changes produced by head impacts. These are common and include pathological low frequency activity, which is associated with poorer neurological outcomes and may disrupt cortical communication. Here, we investigate associative memory binding during post-traumatic amnesia and test the hypothesis that misbinding is caused by a disruption in cortical communication produced by the pathological slowing of brain activity. Thirty acute moderate-severe traumatic brain injury patients (mean time since injury = 10 days) and 26 healthy controls were tested with a precision working memory paradigm that required the association of object and location information. A novel entropy ratio measure was calculated from behavioural performance. This provided a continuous measure of the degree of misbinding and the influence of distracting information. Resting state EEG was used to assess the electrophysiological effects of traumatic brain injury. Patients in post-traumatic amnesia showed abnormalities in working memory function and made significantly more misbinding errors than patients who were not in post-traumatic amnesia and controls. Patients showed a higher entropy ratio in the distribution of spatial responses, indicating that working memory recall was abnormally biased by the locations of non-target items suggesting a specific impairment of object and location binding. Slow wave activity was increased following traumatic brain injury. Increases in the delta-alpha ratio indicative of an increase in low frequency power specifically correlated with binding impairment in working memory. In contrast, although connectivity was increased in the theta band and decreased in the alpha band after traumatic brain injury, this did not correlate with working memory impairment. Working memory and electrophysiological abnormalities both normalised at six-month follow-up, in keeping with a transient increase in slow-wave activity causing post-traumatic amnesia that impaired working memory function. These results show that patients in post-traumatic amnesia show high rates of working memory misbinding that are associated with a pathological shift towards lower frequency oscillations.