0429 Chronic Sleep Disturbance Causes Cognitive Impairment and Alzheimer’S Disease-Like Neuropathology

Abstract Introduction Sleep disturbance is among the most common clinical problem and possesses a significant concern for the geriatric population. Recently, increasing evidence has indicated that disturbed sleep may not only affect neuropsychological functions, but also contribute to the cognitive impairment and, therefore, significantly increase dementia risk. Methods In the present study, we examined the potential impacts of chronic sleep deprivation (SD) on learning-memory and AD-related pathologies in AβPPswe/PS1ΔE9 transgenic (TG) mice and their wild-type (WT) littermates. Results Our results indicated that mice (both TG and WT) exposed to 2-month SD showed an altered amyloid-βprotein precursor processing, elevated level of phosphorylated tau protein, and impaired cognitive performance as compared to non-sleep deprivation (NSD) controls. Moreover, the SD-treated TG mice exhibited more amyloid-β1-42 production and developed more senile plaques in the cortex and hippocampus than NSD-treated TG mice. In addition, SD caused a striking neuronal mitochondrial damage, caspase cascade activation, and neuronal apoptosis in the hippocampus of both TG and WT mice. More importantly, all these behavioral, neuropathological, and biochemical changes induced by chronic SD were long lasting and were irreversible during a 3-month normal housing condition. Conclusion Collectively, these results indicate that chronic SD impairs learning and memory, exacerbates AD pathologies, and aggravates the mitochondria-mediated neuronal apoptosis in a long-lasting manner. Support Our findings provide important experimental evidence to prove that chronic sleep disturbance is a risk factor for AD.

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510 - EFFECT OF SLEEP DEPRIVATION ON SOCIAL RESILIENCE THROUGH ΔFOSB ACTIVATION

International Psychogeriatrics ◽

10.1017/s1041610221002052 ◽

2021 ◽

Vol 33 (S1) ◽

pp. 61-62

Author(s):

Neha Gregory ◽

Eva Andrews ◽

Caroline Donnay ◽

Darielle Lewis-Sanders ◽

Tayler Arnold ◽

...

Keyword(s):

Sleep Deprivation ◽

Social Stress ◽

Social Defeat ◽

Depression And Anxiety ◽

Social Resilience ◽

Geriatric Population ◽

Senior Population ◽

Neurochemical Changes ◽

The Brain ◽

Chronic Sleep

Introduction:Stress can have a variety of detrimental effects on humans. From depression and anxiety to schizophrenia, stress plays a factor in the development of these diseases through neurochemical changes in the brain and elevated levels of hormones. Among the geriatric population, decreased sleep levels are known to be a frequent issue; insomnia rates among the senior population are much higher in frequency compared to any other age group. Sleep deprivation also leads to major consequences in the brain and sleep disruption is linked to neuropsychological illness; however, the specific mechanisms involved in these effects are not understood. This study focuses on the resilient effects of ΔFosB, a protein known to mediate resilience to stress and the direct effect of sleep deprivation on ΔFosB expression in areas known to mediate resilience to social stress. We hypothesize that ΔFosB may be part of the mechanism through which sleep alters resilience to social stress.Methods:Mice were sleep-deprived for an eight-hour period for five days. After sleep deprivation they were subject to social defeat and underwent avoidance testing. The brains of these mice were removed, and immunohistochemistry analysis was conducted to determine ∆FosB expression in various sections of the brain.Results:The preliminary findings of this study indicates that sleep is altered in resilient animals and that sleep deprivation may lead to increased resilience to social defeat. The most significant decrease in ∆FosB expression was found in the prelimbic cortex, a change associated with resilience, and which was observed after chronic sleep deprivation. Contrarily, there was also an increase of ∆FosB expression in the nucleus accumbens.Conclusion:These findings indicate that changes in ∆FosB activation in the brain is a significant factor for promoting resilient behavior in situations of social stress. In particular, a decrease in ∆FosB activation in the PLC plays a role in explaining how sleep deprivation contributes to decreased social resilience in situations of social stress.

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Chronic sleep disturbance, not chronic sleep deprivation, is associated with self-rated health in adolescents

Preventive Medicine ◽

10.1016/j.ypmed.2019.04.014 ◽

2019 ◽

Vol 124 ◽

pp. 11-16 ◽

Cited By ~ 5

Author(s):

Annalijn I. Conklin ◽

Christopher A. Yao ◽

Christopher G. Richardson

Keyword(s):

Sleep Deprivation ◽

Sleep Disturbance ◽

Self Rated Health ◽

Chronic Sleep Deprivation ◽

Chronic Sleep

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Mild cognitive impairment: associations with sleep disturbance, apolipoprotein e4, and sleep medications

Sleep Medicine ◽

10.1016/j.sleep.2018.09.001 ◽

2018 ◽

Vol 52 ◽

pp. 168-176 ◽

Cited By ~ 7

Author(s):

Shanna L. Burke ◽

Tianyan Hu ◽

Christine E. Spadola ◽

Tan Li ◽

Mitra Naseh ◽

...

Keyword(s):

Cognitive Impairment ◽

Mild Cognitive Impairment ◽

Sleep Disturbance ◽

Apolipoprotein E4

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Residual, differential neurobehavioral deficits linger after multiple recovery nights following chronic sleep restriction or acute total sleep deprivation

SLEEP ◽

10.1093/sleep/zsaa224 ◽

2020 ◽

Author(s):

Erika M Yamazaki ◽

Caroline A Antler ◽

Charlotte R Lasek ◽

Namni Goel

Keyword(s):

Sleep Deprivation ◽

Response Speed ◽

Sleep Loss ◽

Sleep Restriction ◽

Total Sleep Deprivation ◽

Psychomotor Vigilance Test ◽

Recovery Sleep ◽

Time In Bed ◽

Neurobehavioral Deficits ◽

Chronic Sleep

Abstract Study Objectives The amount of recovery sleep needed to fully restore well-established neurobehavioral deficits from sleep loss remains unknown, as does whether the recovery pattern differs across measures after total sleep deprivation (TSD) and chronic sleep restriction (SR). Methods In total, 83 adults received two baseline nights (10–12-hour time in bed [TIB]) followed by five 4-hour TIB SR nights or 36-hour TSD and four recovery nights (R1–R4; 12-hour TIB). Neurobehavioral tests were completed every 2 hours during wakefulness and a Maintenance of Wakefulness Test measured physiological sleepiness. Polysomnography was collected on B2, R1, and R4 nights. Results TSD and SR produced significant deficits in cognitive performance, increases in self-reported sleepiness and fatigue, decreases in vigor, and increases in physiological sleepiness. Neurobehavioral recovery from SR occurred after R1 and was maintained for all measures except Psychomotor Vigilance Test (PVT) lapses and response speed, which failed to completely recover. Neurobehavioral recovery from TSD occurred after R1 and was maintained for all cognitive and self-reported measures, except for vigor. After TSD and SR, R1 recovery sleep was longer and of higher efficiency and better quality than R4 recovery sleep. Conclusions PVT impairments from SR failed to reverse completely; by contrast, vigor did not recover after TSD; all other deficits were reversed after sleep loss. These results suggest that TSD and SR induce sustained, differential biological, physiological, and/or neural changes, which remarkably are not reversed with chronic, long-duration recovery sleep. Our findings have critical implications for the population at large and for military and health professionals.

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Homeostatic sleep and body temperature responses to acute sleep deprivation are preserved following chronic sleep restriction in rats

Journal of Sleep Research ◽

10.1111/jsr.13348 ◽

2021 ◽

Author(s):

Samuel Deurveilher ◽

Stephanie M. Shewchuk ◽

Kazue Semba

Keyword(s):

Body Temperature ◽

Sleep Deprivation ◽

Sleep Restriction ◽

Acute Sleep Deprivation ◽

Temperature Responses ◽

Chronic Sleep

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Managing Older Adults With Cognitive Impairment: An Interprofessional, Standardized Patient Approach

Innovation in Aging ◽

10.1093/geroni/igaa057.033 ◽

2020 ◽

Vol 4 (Supplement_1) ◽

pp. 10-10

Author(s):

Shaun Varrecchia ◽

Carol Maritz ◽

Colleen Maher ◽

Megan Strauss

Keyword(s):

Older Adults ◽

Cognitive Impairment ◽

Occupational Therapy ◽

Interprofessional Education ◽

Professional Organizations ◽

Standardized Patient ◽

Geriatric Population ◽

Roles And Responsibilities ◽

Interprofessional Teams ◽

Occupational Therapy Students

Abstract Several professional organizations have called for increased preparation of health professionals capable of working with older adults, including those with cognitive impairment. Standardized patients (SP) are often used in interprofessional education (IPE) in the health professions, but limited data exists to support their use when teaching about the care and management of older adults with cognitive impairment. The purposes of this project were to: 1) develop, implement, and assess an interprofessional standardized patient exercise involving physical and occupational therapy students and 2) to evaluate students’ perceptions of a SP encounter on relevance and utility to patients with cognitive impairment. 88 students representing physical therapy (DPT) and occupational therapy (DrOT) were assigned to interprofessional teams to evaluate an SP portraying an older adult with cognitive impairment. At the conclusion of the session the SP provided the group formative feedback. Student teams then completed an assignment to develop a collaborative intervention plan and addressed questions about roles and responsibilities and communication/teamwork. Pre-/post- surveys focusing on the knowledge of roles and responsibilities, communication, and teamwork were completed by all students. Students also completed an evaluation about the SP experience. Results demonstrated student agreement to understanding the role of the other’s profession improved 28.67%; being comfortable communicating with the geriatric population improved 27.31%; and working in interprofessional teams can improve geriatric patient care improved 32.11%. These findings demonstrate that use of SPs has several advantages in teaching students how to work and communicate with individuals with cognitive impairments as an interprofessional team.

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Sleep Deprivation and Sleep-Onset Insomnia are Associated with Blunted Physiological Reactivity to Stressors

Military Medicine ◽

10.1093/milmed/usaa464 ◽

2021 ◽

Vol 186 (Supplement_1) ◽

pp. 246-252

Author(s):

Devon A Hansen ◽

Brieann C Satterfield ◽

Matthew E Layton ◽

Hans P A Van Dongen

Keyword(s):

Sleep Deprivation ◽

Laboratory Study ◽

Salivary Cortisol ◽

Sleep Onset ◽

Deprivation Condition ◽

Increased Risk ◽

Significant Difference ◽

Sleep Deficiency ◽

The Impact ◽

Chronic Sleep

ABSTRACT Introduction Military operations often involve intense exposure to stressors combined with acute sleep deprivation, while military personnel also experience high prevalence of chronic sleep deficiency from insomnia and other sleep disorders. However, the impact of acute and chronic sleep deficiency on physiologic stressor responses is poorly understood. In a controlled laboratory study with normal sleepers and individuals with chronic sleep-onset insomnia, we measured responses to an acute stressor administered in a sleep deprivation condition or a control condition. Methods Twenty-two adults (aged 22-40 years; 16 females)—11 healthy normal sleepers and 11 individuals with sleep-onset insomnia—completed a 5-day (4-night) in-laboratory study. After an adaptation day and a baseline day, subjects were assigned to a 38-hour total sleep deprivation (TSD) condition or a control condition; the study ended with a recovery day. At 8:00 PM after 36 hours awake in the sleep deprivation condition or 12 hours awake in the control condition, subjects underwent a Maastricht Acute Stress Test (MAST). Salivary cortisol was measured immediately before the MAST at 8:00 PM, every 15 minutes after the MAST from 8:15 PM until 9:15 PM, and 30 minutes later at 9:45 PM. Baseline salivary cortisol was collected in the evening of the baseline day. Additionally, before and immediately upon completion of the MAST, self-report ratings of affect and pain were collected. Results The MAST elicited a stressor response in both normal sleepers and individuals with sleep-onset insomnia, regardless of the condition, as evidenced by increases in negative affect and pain ratings. Relative to baseline, cortisol levels increased immediately following the MAST, peaked 30 minutes later, and then gradually returned to pre-MAST levels. At the cortisol peak, there was a significant difference across groups and conditions, reflecting a pronounced blunting of the cortisol response in the normal sleepers in the TSD condition and the sleep-onset insomnia group in both the TSD and control conditions. Conclusions Blunted stressor reactivity as a result of sleep deficiency, whether acute or chronic, may reflect reduced resiliency attributable to allostatic load and may put warfighters at increased risk in high-stakes, rapid response scenarios.

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Sevoflurane Exacerbates Cognitive Impairment Induced by Aβ1–40 in Rats through Initiating Neurotoxicity, Neuroinflammation, and Neuronal Apoptosis in Rat Hippocampus

Mediators of Inflammation ◽

10.1155/2018/3802324 ◽

2018 ◽

Vol 2018 ◽

pp. 1-10 ◽

Cited By ~ 7

Author(s):

Yue Tian ◽

Ke-yan Chen ◽

Li-dan Liu ◽

Yun-xia Dong ◽

Ping Zhao ◽

...

Keyword(s):

Cognitive Impairment ◽

Calcium Binding ◽

Neuronal Apoptosis ◽

Treated Group ◽

Rat Hippocampus ◽

Inos Mrna ◽

Caspase 9 ◽

Glycation End Products ◽

Oxide Synthase ◽

The Brain

Objective. This study was aimed at investigating whether sevoflurane inhalation induced cognitive impairment in rats with a possible mechanism involved in the event. Methods. Thirty-two rats were randomly divided into four groups of normal saline (NS) + O2, NS + sevoflurane (sevo), amyloid-β peptide (Aβ) + O2, and Aβ + sevo. The rats in the four groups received bilateral intrahippocampus injections of NS or Aβ. The treated hippocampus was harvested after inhaling 30% O2 or 2.5% sevoflurane. Evaluation of cognitive function was performed by Morris water maze (MWZ) and an Aβ1–42 level was determined by ELISA. Protein and mRNA expressions were executed by immunohistochemical (IHC) staining, Western blotting, and qRT-PCR. Results. Compared with the NS-treated group, sevoflurane only caused cognitive impairment and increased the level of Aβ1–42 of the brain in the Aβ-treated group. Sevoflurane inhalation but not O2 significantly increased glial fibrillary acidic protein (GFAP) and ionized calcium-binding adaptor molecule (IBA)1 expression in Aβ-treated hippocampus of rats. Expression levels for Bcl-xL, caspase-9, receptor for advanced glycation end products (RAGE) and brain-derived neurotrophic factor (BDNF) were significantly different in quantification of band intensity between the rats that inhaled O2 and sevoflurane in Aβ-treated groups (all P<0.05). Interleukin- (IL-) 1β, nuclear factor-κB (NF-κB), and inducible nitric oxide synthase (iNOS) mRNA expression increased after the rats inhaled sevoflurane in the Aβ-treated group (both P<0.01). There were no significant differences in the change of GFAP, IBA1, Bcl-xL, caspase-9, RAGE, BDNF, IL-1β, NF-κB, and iNOS in the NS + O2 and NS + sevo group (all P>0.05). Conclusion. Sevoflurane exacerbates cognitive impairment induced by Aβ1–40 in rats through initiating neurotoxicity, neuroinflammation, and neuronal apoptosis in rat hippocampus.

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