Sleep Modulation Alleviates Axonal Damage and Cognitive Decline after Rodent Traumatic Brain Injury

Morawska, Marta M; Büchele, Fabian; Moreira, Carlos G.; Imbach, Lukas L.; Noaín, Daniela; Baumann, Christian R.

doi:10.1523/jneurosci.3274-15.2016

Cited by 38 publications

(48 citation statements)

References 42 publications

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“…It has also been reported that TBI can contribute to nigrostriatal damage (33). Cognitive deficits have also been observed in a model of diffuse axonal injury (34), and blast injury (11). Herein, we utilized the EPM to evaluate aberrant behaviors associated with blast injury.…”

Section: Discussionmentioning

confidence: 99%

A mouse Model of Focal Vascular Injury Induces Astrocyte Reactivity, Tau Oligomers, and Aberrant Behavior

et al. 2017

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Neuropsychiatric symptom development has become more prevalent with 270,000 blast exposures occurring in the past 10 years in the United States. How blast injury leads to neuropsychiatric symptomology is currently unknown. Preclinical models of blast-induced traumatic brain injury have been used to demonstrate blood-brain barrier disruption, degenerative pathophysiology, and behavioral deficits. Vascular injury is a primary effect of neurotrauma that can trigger secondary injury cascades and neurodegeneration. Here we present data from a novel scaled and clinically relevant mouse blast model that was specifically developed to assess the outcome of vascular injury. We look at the biochemical effects and behavioral changes associated with blast injury in young-adult male BALB/c mice. We report that blast exposure causes focal vascular injury in the Somatosensory Barrel Field cortex, which leads to perivascular astrocyte reactivity, as well as acute aberrant behavior. Biochemical analysis revealed that mild blast exposure also invokes tauopathy, neuroinflammation, and oxidative stress. Overall, we propose our model to be used to evaluate focal blood-brain barrier disruption and to discover novel therapies for human neuropsychiatric symptoms.This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/) which permits copy and redistribute the material just in noncommercial usages, provided the original work is properly cited.

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Section: Discussionmentioning

confidence: 99%

A mouse Model of Focal Vascular Injury Induces Astrocyte Reactivity, Tau Oligomers, and Aberrant Behavior

et al. 2017

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“…Nevertheless, recent evidence suggests that sleep deprivation for shorter periods may be neuroprotective. Indeed, several studies in focal and global cerebral ischemia [59,61,[65][66][67], cardiac arrest [60] or TBI [64,68,69] murine models have documented that both TSD [59,61,[64][65][66]69] and REMSD [60,64,67] have neuroprotective effects, whether they are applied before the insult [59-61, 65, 66] or after it [64,67,69] as summarized in Table 1. However, some studies indicate that sleep deprivation for short periods had no effect [68] or, its effect was deleterious [62,63] (see Table 1).…”

Section: Neuroprotection and Sleepmentioning

confidence: 99%

Neuroprotection, Photoperiod, and Sleep

Martínez-Vargas¹,

Porras-Villalobos²,

Estrada-Rojo³

et al. 2019

Traumatic Brain Injury - Neurobiology, Diagnosis and Treatment

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After an acquired brain injury, responses that induce cell death are activated; however, neuroprotective mechanisms are also activated. The relation between these responses determines the destination of the damaged tissue. This relation presents variations throughout the day; numerous studies have shown that the onset of a stroke occurs preferably in the morning. In the rat, ischemia causes more damage when it is induced during the night. The damage caused by a traumatic brain injury (TBI), in the rat, varies depending on the time of day it is induced. Minor behavioral damage has been reported when the TBI occurs during the night, a period that coincides with the wakefulness of the rat. It also has been observed that sleep deprivation accelerates the recovery. Our group has documented that this is due, in part, to a difference in the degree of activation of cannabinergic, GABAergyc, and glutamatergic systems.

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“…Holtzman’s group is generating further data which suggests a positive feedback cycle of sleep disruption that could accelerate neurodegeneration during AD [46,53]. On the positive side, sleep induction decreased axonal injury in a rat model of traumatic brain injury [54], and sleep may more generally reduce AD-related neuropathology [55]. …”

Section: Links Between Short Sleep Evolution and Admentioning

confidence: 99%

Does selection for short sleep duration explain human vulnerability to Alzheimer’s disease?

Nesse

Finch

Nunn

2017

Evolution, Medicine, and Public Health

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Compared with other primates, humans sleep less and have a much higher prevalence of Alzheimer ’s disease (AD) pathology. This article reviews evidence relevant to the hypothesis that natural selection for shorter sleep time in humans has compromised the efficacy of physiological mechanisms that protect against AD during sleep. In particular, the glymphatic system drains interstitial fluid from the brain, removing extra-cellular amyloid beta (eAβ) twice as fast during sleep. In addition, melatonin—a peptide hormone that increases markedly during sleep—is an effective antioxidant that inhibits the polymerization of soluble eAβ into insoluble amyloid fibrils that are associated with AD. Sleep deprivation increases plaque formation and AD, which itself disrupts sleep, potentially creating a positive feedback cycle. These and other physiological benefits of sleep may be compromised by short sleep durations. Our hypothesis highlights possible long-term side effects of medications that reduce sleep, and may lead to potential new strategies for preventing and treating AD.

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Sleep Modulation Alleviates Axonal Damage and Cognitive Decline after Rodent Traumatic Brain Injury

Cited by 38 publications

References 42 publications

A mouse Model of Focal Vascular Injury Induces Astrocyte Reactivity, Tau Oligomers, and Aberrant Behavior

A mouse Model of Focal Vascular Injury Induces Astrocyte Reactivity, Tau Oligomers, and Aberrant Behavior

Neuroprotection, Photoperiod, and Sleep

Does selection for short sleep duration explain human vulnerability to Alzheimer’s disease?

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