scholarly journals Adverse Neurological Effects of Short-Term Sleep Deprivation in Aging Mice Are Prevented by SS31 Peptide

2020 ◽  
Vol 2 (3) ◽  
pp. 325-333
Author(s):  
Jinzi Wu ◽  
Yan Dou ◽  
Warren C. Ladiges
Keyword(s):  
Sleep Deprivation ◽  
Learning Ability ◽  
Older Individuals ◽  
Short Term ◽  
Regulatory Pathways ◽  
Therapeutic Benefits ◽  
Increased Risk ◽  
Neurological Effects ◽  
Learning Impairment ◽  
The Brain

Sleep deprivation is a potent stress factor that disrupts regulatory pathways in the brain resulting in cognitive dysfunction and increased risk of neurodegenerative disease with increasing age. Prevention of the adverse effects of sleep deprivation could be beneficial in older individuals by restoring healthy brain function. We report here on the ability of SS31, a mitochondrial specific peptide, to attenuate the negative neurological effects of short-term sleep deprivation in aging mice. C57BL/6 female mice, 20 months old, were subcutaneously injected with SS31 (3 mg/kg) or saline daily for four days. Sleep deprivation was 4 h daily for the last two days of SS31 treatment. Mice were immediately tested for learning ability followed by collection of brain and other tissues. In sleep deprived mice treated with SS31, learning impairment was prevented, brain mitochondrial ATP levels and synaptic plasticity regulatory proteins were restored, and reactive oxygen species (ROS) and inflammatory cytokines levels were decreased in the hippocampus. This observation suggests possible therapeutic benefits of SS31 for alleviating adverse neurological effects of short-term sleep loss.

scholarly journals Adverse neurological effects of short-term sleep deprivation in aging mice are prevented by SS31 peptide

2020 ◽  
Author(s):  
Jinzi Wu ◽  
Yan Dou ◽  
Warren C. Ladiges
Keyword(s):  
Sleep Deprivation ◽  
Learning Ability ◽  
Older Individuals ◽  
Short Term ◽  
Regulatory Pathways ◽  
Therapeutic Benefits ◽  
Increased Risk ◽  
Neurological Effects ◽  
Learning Impairment ◽  
The Brain

AbstractSleep deprivation is a potent stress factor that disrupts regulatory pathways in the brain resulting in cognitive dysfunction and increased risk of neurodegenerative disease with increasing age. Prevention of the adverse effects of sleep deprivation could be beneficial in older individuals by restoring healthy brain function. We report here on the ability of SS31, a mitochondrial specific peptide, to attenuate the negative neurological effects of short-term sleep deprivation in aging mice. C57BL/6 female mice, 20 months old, were subcutaneously injected with SS31 (3mg/kg) or saline daily for 4 days. Sleep deprivation was 4 hours daily for the last 2 days of SS31 treatment. Mice were immediately tested for learning ability followed by collection of brain and other tissues. In sleep deprived mice treated with SS31, learning impairment was prevented, brain mitochondrial ATP levels and synaptic plasticity regulatory proteins were restored, and ROS and inflammatory cytokines levels were decreased in the hippocampus. The observations suggest possible therapeutic benefits of SS31 for alleviating adverse neurological effects of acute sleep loss.

Use of Cannabis for Agitation in Patients With Dementia

2020 ◽  
Vol 35 (7) ◽  
pp. 312-317
Author(s):  
Amanda Mueller ◽  
Danielle R. Fixen
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Side Effects ◽  
Older People ◽  
Endocannabinoid System ◽  
First Line ◽  
Short Term ◽  
Therapeutic Benefits ◽  
The Brain

Studies have reported changes in the endocannabinoid system in the brain of patients with Alzheimer's disease (AD), playing a role in the pathophysiology of AD. Cannabinoids have been shown to have neuroprotective properties, reduce neuroinflammation, and enhance neurogenesis. Evidence suggests that the utilization of marijuana products containing both tetrahydrocannabinol (THC) and cannabidiol (CBD) or CBD alone have been effective and safe for use in older people with agitation associated with dementia. A review in 2017 summarized positive findings for therapeutic benefits of cannabinoids in agitation of AD and dementia, but there was no definitive conclusion because of varying cannabinoid products. Cannabinoids were shown to be well tolerated, with few short-term side effects. This differs from first-line medications utilized for dementia behaviors, which can have unwanted side effects. Further research regarding the safety, efficacy, and variability of these products in older people is needed.

scholarly journals Effects of Sleep Deprivation on the Brain Electrical Activity in Mice

2021 ◽  
Vol 11 (3) ◽  
pp. 1182
Author(s):  
Alexey N. Pavlov ◽  
Alexander I. Dubrovskii ◽  
Olga N. Pavlova ◽  
Oxana V. Semyachkina-Glushkovskaya
Keyword(s):  
Sleep Deprivation ◽  
Electrical Activity ◽  
Fluctuation Analysis ◽  
Brain Health ◽  
Short Term ◽  
Scaling Exponents ◽  
Sleep Deficit ◽  
The Impact ◽  
Detrended Fluctuation ◽  
The Brain

Sleep plays a crucial role in maintaining brain health. Insufficient sleep leads to an enhanced permeability of the blood–brain barrier and the development of diseases of small cerebral vessels. In this study, we discuss the possibility of detecting changes in the electrical activity of the brain associated with sleep deficit, using an extended detrended fluctuation analysis (EDFA). We apply this approach to electroencephalograms (EEG) in mice to identify signs of changes that can be caused by short-term sleep deprivation (SD). Although the SD effect is usually subject-dependent, analysis of a group of animals shows the appearance of a pronounced decrease in EDFA scaling exponents, describing power-law correlations and the impact of nonstationarity as a fairly typical response. Using EDFA, we revealed an SD effect in 9 out of 10 mice (Mann–Whitney test, p<0.05) that outperforms the DFA results (7 out of 10 mice). This tool may be a promising method for quantifying SD-induced pathological changes in the brain.

Use of Cannabis for Agitation in Patients With Dementia

2020 ◽  
Vol 35 (7) ◽  
pp. 312-317
Author(s):  
Amanda Mueller ◽  
Danielle R. Fixen
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Side Effects ◽  
Older People ◽  
Endocannabinoid System ◽  
First Line ◽  
Short Term ◽  
Therapeutic Benefits ◽  
The Brain

Studies have reported changes in the endocannabinoid system in the brain of patients with Alzheimer's disease (AD), playing a role in the pathophysiology of AD. Cannabinoids have been shown to have neuroprotective properties, reduce neuroinflammation, and enhance neurogenesis. Evidence suggests that the utilization of marijuana products containing both tetrahydrocannabinol (THC) and cannabidiol (CBD) or CBD alone have been effective and safe for use in older people with agitation associated with dementia. A review in 2017 summarized positive findings for therapeutic benefits of cannabinoids in agitation of AD and dementia, but there was no definitive conclusion because of varying cannabinoid products. Cannabinoids were shown to be well tolerated, with few short-term side effects. This differs from first-line medications utilized for dementia behaviors, which can have unwanted side effects. Further research regarding the safety, efficacy, and variability of these products in older people is needed.

scholarly journals Association between Sleep, Alzheimer’s, and Parkinson’s Disease

Biology ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1127
Author(s):  
Sumire Matsumoto ◽  
Tomomi Tsunematsu
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Protein Misfolding ◽  
Older Individuals ◽  
Cognitively Normal ◽  
Potential Biomarker ◽  
Increased Risk ◽  
Sleep Abnormalities ◽  
Protein Misfolding And Aggregation ◽  
The Brain

The majority of neurodegenerative diseases are pathologically associated with protein misfolding and aggregation. Alzheimer’s disease (AD) is a type of dementia that slowly affects memory and cognitive function, and is characterized by the aggregation of the β-amyloid protein and tau neurofibrillary tangles in the brain. Parkinson’s disease (PD) is a movement disorder typically resulting in rigidity and tremor, which is pathologically linked to the aggregation of α-synuclein, particularly in dopaminergic neurons in the midbrain. Sleep disorders commonly occur in AD and PD patients, and it can precede the onset of these diseases. For example, cognitively normal older individuals who have highly fragmented sleep had a 1.5-fold increased risk of subsequently developing AD. This suggests that sleep abnormalities may be a potential biomarker of these diseases. In this review, we describe the alterations of sleep in AD and PD, and discuss their potential in the early diagnosis of these diseases. We further discuss whether sleep disturbance could be a target for the treatment of these diseases.

scholarly journals Short-term sleep deprivation in mice induces B cell migration to the brain compartment

SLEEP ◽  
2019 ◽  
Author(s):  
Ben Korin ◽  
Shimrit Avraham ◽  
Hilla Azulay-Debby ◽  
Dorit Farfara ◽  
Fahed Hakim ◽  
...  
Keyword(s):  
B Cells ◽  
Sleep Deprivation ◽  
Immune Cells ◽  
Brain Function ◽  
Brain Activity ◽  
Short Term ◽  
Elevated Expression ◽  
Acute Sleep Deprivation ◽  
The Brain ◽  
Insight Into

Abstract Increasing evidence highlight the involvement of immune cells in brain activity and its dysfunction. The brain’s immune compartment is a dynamic ensemble of cells that can fluctuate even in naive animals. However, the dynamics and factors that can affect the composition of immune cells in the naive brain are largely unknown. Here, we examined whether acute sleep deprivation can affect the brain’s immune compartment (parenchyma, meninges, and choroid plexus). Using high-dimensional mass cytometry analysis, we broadly characterized the effects of short-term sleep deprivation on the immune composition in the mouse brain. We found that after 6 h of sleep deprivation, there was a significant increase in the abundance of B cells in the brain compartment. This effect can be accounted for, at least in part, by the elevated expression of the migration-related receptor, CXCR5, on B cells and its ligand, cxcl13, in the meninges following sleep deprivation. Thus, our study reveals that short-term sleep deprivation affects the brain’s immune compartment, offering a new insight into how sleep disorders can affect brain function and potentially contribute to neurodegeneration and neuroinflammation.

Effects of tapering neonatal dexamethasone on rat growth, neurodevelopment, and stress response

2002 ◽  
Vol 282 (1) ◽  
pp. R55-R63 ◽  
Author(s):  
Shelly B. Flagel ◽  
Delia M. Vázquez ◽  
Stanley J. Watson ◽  
Charles R. Neal
Keyword(s):  
Neonatal Intensive Care ◽  
Somatic Growth ◽  
Stress Axis ◽  
Increased Risk ◽  
Stress Responsiveness ◽  
Rat Growth ◽  
Nervous System Function ◽  
Corticosterone Response ◽  
Neurological Effects ◽  
Learning Impairment

Dexamethasone is commonly used to lessen the morbidity of chronic lung disease in premature infants, but little is known regarding neurological consequences of its prolonged use. To study neurological effects of dexamethasone, we have developed a rat model in which newborn pups are exposed to tapering doses of dexamethasone at a time corresponding neurodevelopmentally to human exposure in the neonatal intensive care unit. On postnatal day (PD) 2, litters were divided into three groups: 1) handled controls, 2) saline-injected animals, and 3) animals injected with tapering doses of intramuscular dexamethasone between PD 3 and 6. Somatic growth and brain weight were decreased in dexamethasone-treated animals. Dexamethasone-treated animals demonstrated delays in gross neurological development on PD 7 and 14 but not PD 20. In late adolescence ( PD 33), dexamethasone-treated animals were less active in light and dark environments, while demonstrating a blunted serum corticosterone response to a novel stress. The dissociation between behavioral and hormonal stress responsiveness suggests that neonatal dexamethasone exposure permanently alters central nervous system function, particularly within the neuroendocrine stress axis. This may lead to increased risk for learning impairment and maladaptive responses to the environment.

Polychlorinated biphenyl induced hepatocyte alterations

1987 ◽  
Vol 45 ◽  
pp. 716-717
Author(s):  
D.N. Collins ◽  
J.N. Turner ◽  
K.O. Brosch ◽  
R.F. Seegal
Keyword(s):  
Lipid Droplets ◽  
Wistar Rats ◽  
Homovanillic Acid ◽  
Polychlorinated Biphenyl ◽  
Corn Oil ◽  
Environmental Pollutants ◽  
Short Term ◽  
Pcb Congeners ◽  
Urinary Levels ◽  
The Brain

Polychlorinated biphenyls (PCBs) are a ubiquitous class of environmental pollutants with toxic and hepatocellular effects, including accumulation of fat, proliferated smooth endoplasmic recticulum (SER), and concentric membrane arrays (CMAs) (1-3). The CMAs appear to be a membrane storage and degeneration organelle composed of a large number of concentric membrane layers usually surrounding one or more lipid droplets often with internalized membrane fragments (3). The present study documents liver alteration after a short term single dose exposure to PCBs with high chlorine content, and correlates them with reported animal weights and central nervous system (CNS) measures. In the brain PCB congeners were concentrated in particular regions (4) while catecholamine concentrations were decreased (4-6). Urinary levels of homovanillic acid a dopamine metabolite were evaluated (7).Wistar rats were gavaged with corn oil (6 controls), or with a 1:1 mixture of Aroclor 1254 and 1260 in corn oil at 500 or 1000 mg total PCB/kg (6 at each level).

Morphological Changes in the Brain of Acutely Ill and Weight-Recovered Patients with Anorexia Nervosa

2014 ◽  
Vol 42 (1) ◽  
pp. 7-18 ◽  
Author(s):  
Jochen Seitz ◽  
Katharina Bühren ◽  
Georg G. von Polier ◽  
Nicole Heussen ◽  
Beate Herpertz-Dahlmann ◽  
...  
Keyword(s):  
Anorexia Nervosa ◽  
Cognitive Deficits ◽  
Time Course ◽  
Morphological Changes ◽  
Meta Analysis ◽  
Short Term ◽  
Clinical Prognosis ◽  
Qualitative Review ◽  
Brain Changes ◽  
The Brain

Objective: Acute anorexia nervosa (AN) leads to reduced gray (GM) and white matter (WM) volume in the brain, which however improves again upon restoration of weight. Yet little is known about the extent and clinical correlates of these brain changes, nor do we know much about the time-course and completeness of their recovery. Methods: We conducted a meta-analysis and a qualitative review of all magnetic resonance imaging studies involving volume analyses of the brain in both acute and recovered AN. Results: We identified structural neuroimaging studies with a total of 214 acute AN patients and 177 weight-recovered AN patients. In acute AN, GM was reduced by 5.6% and WM by 3.8% compared to healthy controls (HC). Short-term weight recovery 2–5 months after admission resulted in restitution of about half of the GM aberrations and almost full WM recovery. After 2–8 years of remission GM and WM were nearly normalized, and differences to HC (GM: –1.0%, WM: –0.7%) were no longer significant, although small residual changes could not be ruled out. In the qualitative review some studies found GM volume loss to be associated with cognitive deficits and clinical prognosis. Conclusions: GM and WM were strongly reduced in acute AN. The completeness of brain volume rehabilitation remained equivocal.

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