Sleep abnormalities are prevalent in autism spectrum disorders (ASD). Moreover, the severity of ASD symptoms are correlated with the degree of disturbed sleep. We asked if disturbed sleep during brain development itself could lead to ASD-like symptoms, particularly behavioral manifestations. We reasoned that sleep is known to be important for normal brain development and plasticity, so disrupted sleep during development might result in changes that contribute to behavioral impairments associated with ASD. We sleep-restricted C57BL/6J male mice [beginning at postnatal day 5 (P5) and continuing through P52] 3 h per day by means of gentle handling and compared the data with a stress group (handled every 15 min during the 3-h period) and a control group (no additional handling). From P42-P52, we assessed the behavioral effects of sleep-restriction in this pre-recovery phase. Then, we allowed the mice to recover for 4 weeks and tested behavior once again. Compared to the control group, we found that sleep restricted-mice had long-lasting hypoactivity, and impaired social behavior; repetitive behavior was unaffected. These behavior changes were accompanied by an increase in the downstream signaling products of the mammalian target of rapamycin pathway. These data affirm the importance of undisturbed sleep during development and show that, at least in this model, sleep-restriction can play a causative role in the development of behavioral abnormalities. Assessing and treating sleep abnormalities in ASD may be important in alleviating some of the symptoms.
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http://dx.doi.org/10.3389/fnbeh.2019.00090 | DOI Listing |
Alzheimers Dement
December 2024
School of Pharmacy, Chapman University, Irvine, CA, USA.
Background: Although novel treatments for Alzheimer's disease (AD) have begun to show modest therapeutic effects, agents that target hallmark AD pathology and offer neuroprotection are desired. Erythropoietin (EPO) is a glycoprotein hormone with neuroprotective effects but is faced with challenges including limited brain uptake and increased hematopoietic side effects with long-term dosing. Therefore, EPO has been modified and bound to a chimeric transferrin receptor monoclonal antibody (cTfRMAb); the latter shuttles EPO past the blood-brain barrier (BBB) into brain parenchyma and reduces its plasma exposure and potential for side effects.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab, India.
Background: Various studies have evidenced the neuroprotective role of SIRT1 activator. However, whether SIRT1 activator, Piceatannol pharmacological treatment is protective in chronic unpredictable stress induced memory dysfunction remains unknown. Therefore, this study design included testing the hypothesis that Piceatannol administered in chronic unpredictable stress induced memory dysfunction mice shows protective effects, explores & probes underlying the activation of SIRT1 pathway.
View Article and Find Full Text PDFBackground: Seizures in Alzheimer's Disease (AD) are increasingly recognized to occur and can increase cognitive decline and reduce survival compared to unaffected age-matched peers (Lyou et al. 2018). Administration of antiseizure medicines (ASMs) to AD patients with epileptiform activity may improve cognition (Vossel et al.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Afe-Babalola University, Ado-Ekiti, Ekiti State, Nigeria.
Background: Diabetic conditions are associated with alterations in brain functions like memory deficits through processes like synaptic dysfunction in the hippocampus. Administering a combination of silver nanonaringenin and vitamin E appears promising since they are known to prevent diabetes and memory deficits in previous studies, and nanoformulation of naringenin may be one way to improve delivery and bioavailability of naringenin in the brain. This study investigated the effects of co-administering silver nanonaringenin and vitamin E against memory deficits and synaptic dysfunction in the hippocampus of a mice model of high-fat diet and streptozotocin (HS).
View Article and Find Full Text PDFBackground: Alzheimer's disease (AD) is a progressive neurodegenerative disease associated with neuroinflammation and heightened production of reactive oxygen species (ROS) in the brain from overactive NADPH Oxidase 2 (NOX2). The current study examines whether administration of a novel, brain-penetrant NOX2 inhibitor (CPP11G & CPP11H) reduces amyloid plaque load and improves AD-associated vascular dysfunction in a male APP-PS1 mouse model of AD.
Method: Intraperitoneal injections of CPP11G (n = 1) or CPP11H (n = 2) three times per week began at 9-10 months of age in the treatment APP-PS1 group (15 mg/kg).
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