Developmental traumatic brain injury decreased brain derived neurotrophic factor expression late after injury

Schober, Michelle E.; Block, Benjamin; Requena, Daniela F.; Hale, M.; Lane, Robert H.

doi:10.1007/s11011-012-9309-7

Cited by 33 publications

(25 citation statements)

References 40 publications

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“…Comparably, BDNF protein levels, measured by reverse phase protein microarray, increased in rat injured brains, and no significant level variations were reported over 2 weeks following the injury (Rostami et al, ). In contrast, mild severity level of TBI obtained by lateral percussion displayed unchanged BDNF mRNA levels in hippocampal homogenates of 17 days old rat pups (Schober, Block, Requena, Hale, & Lane, ).…”

Section: Discussionmentioning

confidence: 99%

Neuronal expression of brain derived neurotrophic factor in the injured telencephalon of adult zebrafish

Cacialli

D’Angelo

Kah

et al. 2017

J of Comparative Neurology

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The reparative ability of the central nervous system varies widely in the animal kingdom. In the mammalian brain, the regenerative mechanisms are very limited and newly formed neurons do not survive longer, probably due to a non-suitable local environment. On the opposite, fish can repair the brain after injury, with fast and complete recovery of damaged area. The brain of zebrafish, a teleost fish widely used as vertebrate model, also possesses high regenerative properties after injury. Taking advantage of this relevant model, the aim of the present study was to investigate the role of brain-derived neurotrophic factor (BDNF) in the regenerative ability of adult brain, after stab wound telencephalic injury. BDNF is involved in many brain functions and plays key roles in the repair process after traumatic brain lesions. It has been reported that BDNF strengthens the proliferative activity of neuronal precursor cells, facilitates the neuronal migration toward injured areas, and shows survival properties due to its anti-apoptotic effects. BDNF mRNA levels, assessed by quantitative PCR and in situ hybridization at 1, 4, 7, and 15 days after the lesion, were increased in the damaged telencephalon, mostly suddenly after the lesion. Double staining using in situ hybridization and immunocytochemistry revealed that BDNF mRNA was restricted to cells identified as mature neurons. BDNF mRNA expressing neurons mostly increased in the area around the lesion, showing a peak 1 day after the lesion. Taken together, these results highlight the role of BDNF in brain repair processes and reinforce the value of zebrafish for the study of regenerative neurogenesis.

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Section: Discussionmentioning

confidence: 99%

Neuronal expression of brain derived neurotrophic factor in the injured telencephalon of adult zebrafish

Cacialli

D’Angelo

Kah

et al. 2017

J of Comparative Neurology

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“…Double labeling studies showed that a subpopulation of CD68-immunoreactive microglia/macrophage co-expressed BDNF in the cortex and spinal cord, and also TrkB[gp145] or TrkB[TK-] in the spinal cord; whereas cytokine expression of TNF-α, IL-6, and IL-1-β was less prominent at the 1, 6, and 12-month intervals, suggesting that immediate inflammatory responses had subsided (Nagamoto-Combs et al, 2007). Yet, in a CCI rat model there is a decline in BDNF-mRNA and protein levels measured at 1–14 days post injury (Schober et al, 2012). Moreover, specific BDNF polymorphisms may not be involved in TBI pathology (Bagnato et al, 2012).…”

Section: Harnessing Microglial Pro-survival Functionsmentioning

confidence: 99%

Microglia Activation as a Biomarker for Traumatic Brain Injury

Hernandez-Ontiveros¹,

Tajiri²,

Acosta³

et al. 2013

Front. Neurol.

248

236

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Traumatic brain injury (TBI) has become the signature wound of wars in Afghanistan and Iraq. Injury may result from a mechanical force, a rapid acceleration-deceleration movement, or a blast wave. A cascade of secondary cell death events ensues after the initial injury. In particular, multiple inflammatory responses accompany TBI. A series of inflammatory cytokines and chemokines spreads to normal brain areas juxtaposed to the core impacted tissue. Among the repertoire of immune cells involved, microglia is a key player in propagating inflammation to tissues neighboring the core site of injury. Neuroprotective drug trials in TBI have failed, likely due to their sole focus on abrogating neuronal cell death and ignoring the microglia response despite these inflammatory cells’ detrimental effects on the brain. Another relevant point to consider is the veracity of results of animal experiments due to deficiencies in experimental design, such as incomplete or inadequate method description, data misinterpretation, and reporting may introduce bias and give false-positive results. Thus, scientific publications should follow strict guidelines that include randomization, blinding, sample-size estimation, and accurate handling of all data (Landis et al., 2012). A prolonged state of inflammation after brain injury may linger for years and predispose patients to develop other neurological disorders, such as Alzheimer’s disease. TBI patients display progressive and long-lasting impairments in their physical, cognitive, behavioral, and social performance. Here, we discuss inflammatory mechanisms that accompany TBI in an effort to increase our understanding of the dynamic pathological condition as the disease evolves over time and begin to translate these findings for defining new and existing inflammation-based biomarkers and treatments for TBI.

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“…There is evidence that upregulation of BDNF reduces the impact of secondary injury following TBI (Kaplan et al, 2010). However, there might be decreases in BDNF with increased time since injury, resulting from tissue loss over the first year post-injury (Schober, Block, Requena, Hale, & Lane, 2012). Previous work suggests a causal link between BDNF expression during wakefulness and subsequent slow-wave activity (SWA) during sleep (Faraguna et al, 2008).…”

Section: Sleep Disturbances Following Traumatic Brain Injurymentioning

confidence: 99%

Sleep disturbances, TBI and PTSD: Implications for treatment and recovery

Gilbert

Kark

Gehrman

et al. 2015

Clinical Psychology Review

117

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Post-Traumatic Stress Disorder (PTSD), traumatic brain injury (TBI), and sleep problems significantly affect recovery and functional status in military personnel and Veterans returning from combat. Despite recent attention, sleep is understudied in the Veteran population. Few treatments and rehabilitation protocols target sleep, although poor sleep remains at clinical levels and continues to adversely impact functioning even after the resolution of PTSD or mild TBI symptoms. Recent developments in non-pharmacologic sleep treatments have proven efficacious as stand-alone interventions and have potential to improve treatment outcomes by augmenting traditional behavioral and cognitive therapies. This review discusses the extensive scope of work in the area of sleep as it relates to TBI and PTSD, including pathophysiology and neurobiology of sleep; existing and emerging treatment options; as well as methodological issues in sleep measurements for TBI and PTSD. Understanding sleep problems and their role in the development and maintenance of PTSD and TBI symptoms may lead to improvement in overall treatment outcomes while offering a non-stigmatizing entry in mental health services and make current treatments more comprehensive by helping to address a broader spectrum of difficulties.

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Developmental traumatic brain injury decreased brain derived neurotrophic factor expression late after injury

Cited by 33 publications

References 40 publications

Neuronal expression of brain derived neurotrophic factor in the injured telencephalon of adult zebrafish

Neuronal expression of brain derived neurotrophic factor in the injured telencephalon of adult zebrafish

Microglia Activation as a Biomarker for Traumatic Brain Injury

Sleep disturbances, TBI and PTSD: Implications for treatment and recovery

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