Obstructive sleep apnea severity affects amyloid burden in cognitively normal elderly a longitudinal study

Recent evidence suggests that Obstructive Sleep Apnea (OSA) may be a risk factor for developing Mild Cognitive Impairment and Alzheimer’s disease. However, how sleep apnea affects longitudinal risk for Alzheimer’s disease is less well understood.Postprint (author's final draft

Injuries among Young Florida Athletes Playing Sports in Recreational Leagues

The purpose of this study was to identify the injury rates and mechanisms of sports injuries among 5-11-year-old athletes, and to provide preliminary guidance for decreasing injuries in this population. A total of 1511 athletes ages 5- 11 playing football, soccer, baseball and softball participated in our research. One certified athletic trainer (ATC) used Reporting Information Online (RIO) to collect the data on athletic exposure, injuries and injury mechanisms weekly during the 2016-2017 season in Hillsborough County, Florida. A total of 18 injuries occurred in practices or competitions. Football had the leading rate of injuries for both competitions and practices (1.18 and 0.68, per 1000 athlete-exposures respectively). Most injuries occurred during competition (66.7%) and the leading types of injuries were concussions (22.2%) and fractures (22.2%). The leading injury mechanisms were contact with another person (33.3%) and playing apparatus (33.3%). It is advantageous to have ATCs on site for initial injury evaluation and post injury management. Future studies should include additional study venues to provide more evidence on children’s sports injuries

Sleep oscillation-specific associations with Alzheimer’s disease CSF biomarkers : novel roles for sleep spindles and tau

Background: Based on associations between sleep spindles, cognition, and sleep-dependent memory processing, here we evaluated potential relationships between levels of CSF Aβ42, P-tau, and T-tau with sleep spindle density and other biophysical properties of sleep spindles in a sample of cognitively normal elderly individuals. Methods: One-night in-lab nocturnal polysomnography (NPSG) and morning to early afternoon CSF collection were performed to measure CSF Aβ42, P-tau and T-tau. Seven days of actigraphy were collected to assess habitual total sleep time. Results: Spindle density during NREM stage 2 (N2) sleep was negatively correlated with CSF Aβ42, P-tau and T-tau. From the three, CSF T-tau was the most significantly associated with spindle density, after adjusting for age, sex and ApoE4. Spindle duration, count and fast spindle density were also negatively correlated with T-tau levels. Sleep duration and other measures of sleep quality were not correlated with spindle characteristics and did not modify the associations between sleep spindle characteristics and the CSF biomarkers of AD. Conclusions: Reduced spindles during N2 sleep may represent an early dysfunction related to tau, possibly reflecting axonal damage or altered neuronal tau secretion, rendering it a potentially novel biomarker for early neuronal dysfunction. Given their putative role in memory consolidation and neuroplasticity, sleep spindles may represent a mechanism by which tau impairs memory consolidation, as well as a possible target for therapeutic interventions in cognitive decline

Obstructive Sleep Apnea Severity Affects Amyloid Burden in Cognitively Normal Elderly. A Longitudinal Study

Rationale: Recent evidence suggests that obstructive sleep apnea (OSA) may be a risk factor for developing mild cognitive impairment and Alzheimer’s disease. However, how sleep apnea affects longitudinal risk for Alzheimer’s disease is less well understood. Objectives: To test the hypothesis that there is an association between severity of OSA and longitudinal increase in amyloid burden in cognitively normal elderly. Methods: Data were derived from a 2-year prospective longitudinal study that sampled community-dwelling healthy cognitively normal elderly. Subjects were healthy volunteers between the ages of 55 and 90, were nondepressed, and had a consensus clinical diagnosis of cognitively normal. Cerebrospinal fluid amyloid β was measured using ELISA. Subjects received Pittsburgh compound B positron emission tomography scans following standardized procedures. Monitoring of OSA was completed using a home sleep recording device. Measurements and Main Results: We found that severity of OSA indices (AHIall [F1,88 = 4.26; P < 0.05] and AHI4% [F1,87 = 4.36; P < 0.05]) were associated with annual rate of change of cerebrospinal fluid amyloid β42 using linear regression after adjusting for age, sex, body mass index, and apolipoprotein E4 status. AHIall and AHI4% were not associated with increases in ADPiB-mask (Alzheimer’s disease vulnerable regions of interest Pittsburg compound B positron emission tomography mask) most likely because of the small sample size, although there was a trend for AHIall (F1,28 = 2.96, P = 0.09; and F1,28 = 2.32, not significant, respectively). Conclusions: In a sample of cognitively normal elderly, OSA was associated with markers of increased amyloid burden over the 2-year follow-up. Sleep fragmentation and/or intermittent hypoxia from OSA are likely candidate mechanisms. If confirmed, clinical interventions for OSA may be useful in preventing amyloid build-up in cognitively normal elderly

Obstructive sleep apnea severity affects amyloid burden in cognitively normal elderly a longitudinal study

Recent evidence suggests that Obstructive Sleep Apnea (OSA) may be a risk factor for developing Mild Cognitive Impairment and Alzheimer’s disease. However, how sleep apnea affects longitudinal risk for Alzheimer’s disease is less well understood

The Relationship between Obstructive Sleep Apnea and Alzheimer’s Disease

Obstructive sleep apnea (OSA) and Alzheimer’s disease (AD) are highly prevalent conditions with growing impact on our aging society. While the causes of OSA are now better characterized, the mechanisms underlying AD are still largely unknown, challenging the development of effective treatments. Cognitive impairment, especially affecting attention and executive functions, is a recognized clinical consequence of OSA. A deeper contribution of OSA to AD pathogenesis is now gaining support from several lines of research. OSA is intrinsically associated with disruptions of sleep architecture, intermittent hypoxia and oxidative stress, intrathoracic and hemodynamic changes as well as cardiovascular comorbidities. All of these could increase the risk for AD, rendering OSA as a potential modifiable target for AD prevention. Evidence supporting the relevance of each of these mechanisms for AD risk, as well as a possible effect of AD in OSA expression, will be explored in this review

Ambient Stimuli Perpetuate Nighttime Sleep Disturbances in Hospital Patients With TBI

Background and Objectives: The effect of the ambient environment, sound, light, and movement, on the nighttime rest-activity of patients hospitalized with moderate-severe traumatic brain injury (TBI) is poorly understood. The purpose of this study was to examine how sound, light, and movement in these patients' hospital rooms may contribute to nighttime awakenings. Methods: An observational design was used with 18 adult participants on a neuroscience step-down unit diagnosed with moderate-severe TBI. For up to five consecutive nights, actigraphy was used to capture nighttime awakenings while a custom-made multisensory device captured sound, light, and movement exposures in the participant's room. Results: Participants were awake for 24% (or about 3 hr) of the time during the designated nighttime period of 8 pm to 8 am. Average nighttime exposures of sound was 52 dB, light was nine lumens, and movement, measured as a proportion, was 0.28% or 28%. With each stimuli exposure set at its average, there was a 20% probability of participant nighttime awakenings. Clinically meaningful reductions of movement in and out the participant's room and elevated sound significantly decreases the participant's probability of nighttime awakenings (p < .05), but reductions in light did not. Conclusion: The ambient environment seems to impede restful sleep in immediate post-injury phase of patients with moderate-severe TBI

Injuries and concussions among young children, ages 5-11, playing sports in recreational leagues in Florida.

BackgroundThe specific research aims of this study included: 1) Conduct an epidemiologic analysis of recreational sports injuries among 1500 children, ages 5-11 in Florida: and 2) Utilize the computerized pediatric concussion tool from ImPACT Applications, Inc. for baseline and follow-up testing to better understand these injuries. This research followed a prospective surveillance design utilizing a large cohort of children, ages, 5-11, who play recreational football, soccer, and baseball/softball in Florida. The study venue was a large athletic facility in Hillsborough County, Florida. The sports observed were soccer (girls' and boys'), baseball, softball, and football. Internal and external advisory boards were consulted throughout the study.MethodsCertified Athletic Trainers (ATCs) were hired to use High School Reporting Information Online (RIO) for injuries and the Ipad-administered pediatric concussion tool developed by ImPACT Applications, Inc for baseline/follow-up concussion data.ResultsOver the course of the project, 26 RIO-reported injuries were reported. Football and soccer produced the greatest rate of injuries. There were 12 concussions which comprised nearly half of all the RIO injuries (46%). We conducted 882 baseline concussion tests and 13 follow-up tests over the 2 years.ConclusionsTo the best of our knowledge, this is the first time data have been collected and reported on sports injuries in the study population. Future studies built on these findings will allow for the development of targeted guidelines and interventions for coaches, players, and parents so sports injury-related morbidity and mortality decrease in our youngest athletes

Interaction of obstructive sleep apnea severity and amyloid burden on novel plasma biomarkers of tau and neurofilament light protein in community‐dwelling cognitively normal older‐adults

Background Recent evidence suggest that plasma Tau and neurofilament light (NfL) have high potential as markers of neurodegeneration in Alzheimer disease (AD). Obstructive sleep apnea (OSA) severity increases AD risk and is associated with well‐validated markers of AD pathology in cognitively normal older‐adults. We determined the independent and combined effects of OSA severity and amyloid burden on plasma levels of Tau, and NfL, in community‐dwelling cognitively normal older‐adults. Method Cross‐sectional analysis of baseline data from 70 community‐dwelling cognitively normal older‐adults, selected from ongoing NYU prospective longitudinal studies on memory, sleep and aging. CSF‐Aβ42 (measured using ELISA) quantified amyloid burden. OSA severity was defined using AHI4%. Levels of plasma Tau and NfL were determined using single molecule array (SIMOA) technology ultra‐sensitive assays. Associations of OSA severity and plasma Tau and NfL were assessed using Pearson correlation analysis. The interactive associations of OSA severity and CSF‐Aβ42 levels on plasma Tau and NfL was assessed using generalized linear models. Analyses were adjusted for age, sex, BMI, education and APOE4. Result Of the 70 participants, 42 (60%) were women. Mean (SD) age was 68.7 (7.1) years. Mean (SD) AHI was 11.4/hr. (13.7) {29 (40%) had AHI 30}. Independent of CSF‐Aβ42, OSA severity was not associated with plasma Tau (r=.11, p‐value=.38), or plasma NfL (r=.05, p‐value=.67). The interactive associations of OSA severity and CSF‐Aβ42 levels on plasma Tau (β =0.042; 95% CI, 0.013 to 0.070) and NfL (β = 0.055; 95% CI, 0.022 to 0.089) were significant, P < .05 for all. The analysis was not powered for generating dichotomized strata specific (i.e. OSA+/Aβ+, OSA+/Aβ‐, OSA‐/Aβ+ and OSA‐/Aβ‐) estimates. Conclusion In this sample of cognitively normal older‐adults, OSA severity was not associated with plasma levels of Tau and NfL. However, β estimates of the interactive associations of OSA severity and CSF‐Aβ42 levels suggest that their combined effect is associated with higher plasma levels of Tau or NfL. Larger cohorts are necessary to delineate mechanisms and examine for OSA/Aβ strata‐specific estimates

Interactive associations of nocturnal sleep disturbance and vascular risk with prospective cognitive decline in clinically normal elderly individuals: Findings from the National Alzheimer's Coordinating Center Uniform Data Set

Background We determined whether Nocturnal Sleep Disturbance (NSD) and vascular risk act together to promote prospective cognitive‐decline in clinically normal older adults; and, evaluated the unique influence of their combined risk on prospective cognitive decline beyond that of commonly used Alzheimer’s disease (AD) biomarkers. Method Longitudinal study utilizing data from the National Alzheimer's Coordinating Center (NACC) Uniform Data set (UDS). Participants (N=361) were cognitively normal at baseline and had baseline medical data to quantify vascular risk, using an adaptation of the Framingham Heart Study general cardiovascular disease (aFHS‐CVD) risk‐score and CSF‐Aβ, CSF P‐tau, CSF T‐tau and MRI‐imaging data with at least one UDS follow‐up visit. The Neuropsychiatric Inventory Questionnaire characterized NSD and incident mild cognitive impairment (MCI) diagnosis during UDS follow‐up characterized prospective cognitive decline. Logistic mixed‐effects models with random intercept and slope, controlling for age, sex, education, APOE‐ε4 and their interactions with time examined associations between the NSD/ FHS‐CVD risk score and longitudinal cognitive‐decline. Result Of the 361 participants, 223 (62%) were women and 35 (9.7%) had NSD. The proportion of males versus females with sleep problems was 10.9% vs. 9.3% respectively. For participants with NSD and no NSD, the mean (SD) age was 71 (7.3) and 70 (5.7) years and average follow‐up time was 5.2 (2.6) and 4.9 (2.7) years, respectively. Both NSD (OR: 1.42, P < .003) and higher aFHS‐CVD risk score (OR; 1.63, P < .001) were significantly associated with increased/faster likelihood to develop incident MCI. The interaction of NSD and the aFHS‐CVD risk‐score with time was significant (P < .001) suggesting an increase in the likelihood of conversion to MCI increased over time. Stratifying aFHS‐CVD risk score into tertiles, NSD participants in the highest (OR: 2.82, P < .003) and middle tertile (OR: 2.38, P < .001) were significantly more likely to develop incident MCI, compared with participants without NSD in the lowest aFHS‐CVD risk score tertile, suggesting a synergistic effect. This effect remained robustly associated with incident MCI even after adjustment for AD biomarkers. Conclusion In elderly cognitive‐normal individuals, NSD and vascular risk may be alternate and non‐invasive measures of assessing risk of prospective cognitive‐decline in preclinical AD