Introduction Sleep deprivation impairs hippocampal-dependent memory, and hippocampal-dependent memory impairments occur in some dementias, including Alzheimer’s disease. As our population continues to age, understanding the molecular basis for memory impairments is increasingly important. We hypothesized that early life sleep fragmentation would result in lasting increases in hippocampal calcium transient activity. Methods B6 mice were randomized to 12wk of sleep fragmentation or rested control conditions at age 8wk. Mice were microinjected with AAV9-CamKII-GCamp6F into the hippocampus and later implanted with a GRIN Lens into CA1 secured to a baseplate along with chronic EEG/EMG electrodes and recording connector. Calcium recordings were obtained two to three months after injection and recordings were obtained across sleep-wake cycles>4mins of wake and NREM sleep. Individual cells across animal were combined into sleep fragmented (n = 521 cells) or rested (n = 443 cells) groups during wake or sleep. Average FFx was analyzed by group and condition by T-tests, paired for within and unpaired across groups. A spatial object recognition assay was also performed on all mice (n=16 for both groups) and performance across group was analyzed by paired T-tests. Results Rested mice showed normal spatial object recognition (n = 16, p<0.05). In contrast, SF mice showed impaired spatial object recognition (n = 16, N.S.). There were no differences across sleep conditions in calcium transient FFx for waking (p>0.05). However, in sleep, cells in SF mice had significantly higher average FFx values than cells in rested mice (p<0.0001). Conclusion Early-life sleep fragmentation has long-lasting impacts on memory. Since spatial memory is dependent on hippocampal function, the calcium transient FFx data suggests that a driver of this hippocampal memory impairment may be higher firing rates in sleep and/or greater calcium exposure in hippocampal CamKII neurons in sleep, both of which may perturb microglial maintenance of synapses. Understanding the molecular drivers behind this calcium dysfunction will be essential in our understanding of neurodegeneration, dementia, and Alzheimer’s disease. Support (If Any) NIH AG054104; AG064231
Some have touted technology as a panacea for overcoming the isolation associated with COVID-19 mitigation policies; yet, these tools are not widely adopted by older adults. With data from the COVID-19 supplement to the National Health and Aging Trends Survey, we conduct adjusted Poisson regression modeling to examine digital communications use during COVID-19 and feelings of anxiety, depression, and loneliness during the COVID-19 pandemic among older adults (65+ years of age). Adjusted Poisson regression revealed that those who reported frequent use of video calls with friends and family (aPR = 1.22, 95% CI:1.06–1.41) and with healthcare providers (aPR = 1.22, 95% CI:1.03–1.45) were more likely to report feelings of anxiety than those not using these platforms; yet, reports of in-person visits with friends and family (aPR = 0.79, 95% CI: 0.66–0.93) and with healthcare providers (aPR = 0.88, 95% CI: 0.77–1.01) were associated with fewer feelings of depression and loneliness, respectively. Future research is needed to tailor digital technology to support older adults.
The aim of the current study was to collect qualitative data to understand the nature of sleep and sleep difficulties among Asian American older adults and identify daily routines that may lend insight into modifiable targets for future nursing interventions. We recruited Chinese and Bangladeshi older adults with low English proficiency from community-based settings in New York City. Eligible participants were aged ≥55 years and reported China or Bangladesh as their country of origin. Focus groups were conducted in their native language. Participants completed a questionnaire before joining the discussion. Participants ( N = 32) were 57% Chinese American and 43% Bangladeshi American. Average age was 73 years, 50% of the sample reported diabetes, and 22% reported sleep apnea. Our analysis revealed the daily routines among Chinese and Bangladeshi American older adults. Both groups reported general sleep difficulties and sleep difficulties related to health conditions as well as some subgroup differences. Future research may consider designing tailored nursing interventions to improve sleep among these groups. [ Journal of Gerontological Nursing, 47 (12), 35–41.]
Introduction Chronic sleep disruption (CSD) in young adult mice leads to phenotypes consistent with early (pre-plaque) Alzheimer’s Disease (AD), including increased Aβ and hippocampal neuron loss. Mechanisms underlying this injury are not known. Both acute sleep loss and AD activate cofilin, a regulator of actin dynamics. Activated cofilin (AC) in AD mouse models can impart neural injury, increase Aβ, and cofilin translocation to the mitochondria delays cytosolic Ca2+ clearance. We are critically testing the role of AC in chronic short sleep (CSS) and sleep fragmentation (SF) neural injury. Methods Synapse loss was studied using STED confocal microscopy and Imaris in CSS (n=9) and rested (n=10) mice. Synapses were identified as overlaps of pre- and postsynaptic densities. Percent area of cofilin was measured with FIJI. To further understand if and how wake-induced cofilin activation induces sleep-loss synapse and neural injury, we implanted AAV9CAMKII-GCaMP6f and then GRIN lenses, and later studied CAMKII calcium transients in CA1 of WT controls (n=4) and SF mice (n=4) by measuring GCaMP6f calcium transients. We developed a Shiny R application to analyze the frequency of Ca2+ spikes, ΔF/F0, and the rising and clearance patterns of spikes. To directly test cofilin’s role in delayed calcium clearance, we studied the calcium transients in hAPP mice (n=2) after injection of AAV-CAMKII-CofilinS3A to express AC and GCaMP6f. All data were analyzed with two-way ANOVA or unpaired t-tests. Results Results reveal significant synapse loss in CA1 of CSS mice (CSS=48.8±10.3; Rested=83.4±8.4), t(16)=2.63, p<0.02, and increased cofilin activation (AC=19.8±3.41; Rested=8.76±1.95), t(16)=8.43, p<0.0001. SF mice reveal an increase in NREM sleep firing rates, F(1,1)=22.0, p<0.001. In contrast, hAPP-AC mice show significantly increased ΔF/F0, F(1,1)=356, p<0.0001, prolonged calcium influx, F(1,1)=18.6, p<0.02, and prolonged calcium clearance duration, F(1,1)=23.9, p<0.01, but not increased firing frequencies. Conclusion CSS induces CA1 synapse loss and cofilin activation in WT mice. Increased CAMKII calcium ΔF/F0 occurs through different pathways in SF and AC, suggesting additional factors in CSD neural injury. Support (If Any) NIH AG054104; AG064231
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