Research Frontiers in Traumatic Brain Injury

Gardner, Andrew J.; Shih, Shirley L; Adamov, Elizabeth; Zafonte, Ross

doi:10.1016/j.pmr.2016.12.014

Cited by 16 publications

(9 citation statements)

References 103 publications

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“…A previous study reported many TBI patients with olfactory dysfunction remain undiagnosed for a long time, probably due to the lack of rehabilitative and diagnostic services for patients suffering from olfactory dysfunction (Schofield et al 2014 ). Moreover, TBI is associated with the initiation of complex pathophysiological mechanisms (Gardner et al 2017 ).…”

Section: Discussionmentioning

confidence: 99%

A systematic review of olfactory-related brain structural changes in patients with congenital or acquired anosmia

et al. 2021

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Brain structural features of healthy individuals are associated with olfactory functions. However, due to the pathophysiological differences, congenital and acquired anosmia may exhibit different structural characteristics. A systematic review was undertaken to compare brain structural features between patients with congenital and acquired anosmia. A systematic search was conducted using PubMed/MEDLINE and Scopus electronic databases to identify eligible reports on anosmia and structural changes and reported according to PRISMA guidelines. Reports were extracted for information on demographics, psychophysical evaluation, and structural changes. Then, the report was systematically reviewed based on various aetiologies of anosmia in relation to (1) olfactory bulb, (2) olfactory sulcus, (3) grey matter (GM), and white matter (WM) changes. Twenty-eight published studies were identified. All studies reported consistent findings with strong associations between olfactory bulb volume and olfactory function across etiologies. However, the association of olfactory function with olfactory sulcus depth was inconsistent. The present study observed morphological variations in GM and WM volume in congenital and acquired anosmia. In acquired anosmia, reduced olfactory function is associated with reduced volumes and thickness involving the gyrus rectus, medial orbitofrontal cortex, anterior cingulate cortex, and cerebellum. These findings contrast to those observed in congenital anosmia, where a reduced olfactory function is associated with a larger volume and higher thickness in parts of the olfactory network, including the piriform cortex, orbitofrontal cortex, and insula. The present review proposes that the structural characteristics in congenital and acquired anosmia are altered differently. The mechanisms behind these changes are likely to be multifactorial and involve the interaction with the environment. Supplementary Information The online version contains supplementary material available at 10.1007/s00429-021-02397-3.

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Section: Discussionmentioning

confidence: 99%

A systematic review of olfactory-related brain structural changes in patients with congenital or acquired anosmia

et al. 2021

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“…There are two stages involved in TBI, including immediate brain damage and secondary injury. The immediate brain damage results in direct neuronal loss and necrotic death, which is followed by a series of injury cascades such as oxidative stress, mitochondrial dysfunction and inflammation (18). Of these injury cascades, inflammatory response accounts for major reasons (19).…”

Section: Discussionmentioning

confidence: 99%

Resveratrol pretreatment attenuates traumatic brain injury in rats by suppressing NLRP3 inflammasome activation via SIRT1

Zou

Liu

Li³

et al. 2017

Mol Med Report

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The inflammatory response in the cerebral cortex serves an important role in the progression of secondary injury following traumatic brain injury (TBI). The NLR family pyrin domain containing 3 (NLRP3) inflammasome is necessary for initiating inflammation and is involved in various central nervous system disorders. The aim of the present study was to investigate the neuroprotective effect of resveratrol and elucidate the underlying mechanisms of resveratrol associated regulation of the NLRP3 inflammasome in TBI. The results demonstrated that the activation of NLRP3, caspase‑1 and sirtuin 1 (SIRT1), enhanced the production of inflammatory cytokines and reactive oxygen species (ROS) following TBI. Administration of resveratrol alleviated the degree of TBI, as evidenced by the reduced neuron‑specific enolase (NSE) and brain water content (WBC). Resveratrol pretreatment also inhibited the activation of NLRP3 and caspase‑1, and reduced the production of inflammatory cytokines and ROS. In addition, resveratrol further promoted SIRT1 activation. Furthermore, the suppressing effect of resveratrol on the NLRP3 inflammasome and ROS was blocked by the SIRT1 inhibitor, sirtinol. The results revealed that the activation of the NLRP3 inflammasome and the subsequent inflammatory responses in the cerebral cortex were involved in the process of TBI. Resveratrol may attenuate the inflammatory response and relieve TBI by reducing ROS production and inhibiting NLRP3 activation. The effect of resveratrol on NLRP3 inflammasome and ROS may also be SIRT1 dependent.

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“…TBI occurs when the brain is exposed to external forces that induce focal and/or diffuse injuries that include axonal shearing, edema, vascular damage, and neuronal death [ 7 – 9 ]. Injuries from TBI can range from mild to severe [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Ablation of caspase-1 protects against TBI-induced pyroptosis in vitro and in vivo

Liu

Chen

Meng

et al. 2018

J Neuroinflammation

135

111

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BackgroundTraumatic brain injury (TBI) is a critical public health and socioeconomic problem throughout the world. Inflammation-induced secondary injury is one of the vital pathogenic parameters of TBI. Molecular signaling cascades of pyroptosis, a specific type of cellular necrosis, are key drivers of TBI-induced inflammation.MethodsIn this study, mice with genetically ablated caspase-1 (caspase-1−/−) were subjected to controlled cortical impact injury in vivo, and primary neuron deficient in caspase-1 through siRNA knockdown and pharmacologic inhibition was stimulated by mechanical scratch, equiaxial stretch, and LPS/ATP in vitro. We evaluated the effects of caspase-1 deficiency on neurological deficits, inflammatory factors, histopathology, cell apoptosis, and pyroptosis.ResultsDuring the acute post-injury period (0–48 h) in vivo, motor deficits, anti-inflammatory cytokines (TGF-β and IL-10), pro-inflammatory cytokines (IFN-γ, IL-1β, and IL-18), and blood lactate dehydrogenase (LDH), as well as pyroptosis-related proteins (caspase-1, caspase-1 fragments, caspase-11 and GSDMD), were increased. Caspase-1 was activated in the cortex of TBI mice. Inflammatory activation was more profound in injured wild-type mice than in caspase-1−/− mice. In vitro, mechanical scratch, equiaxial stretch, and LPS/ATP-induced neuron pyroptosis, apoptosis, LDH release, and increased expression of inflammatory factors. The effects of mechanical and inflammatory stress were reduced through inhibition of caspase-1 activity through siRNA knockdown and pharmacologic inhibition.ConclusionCollectively, these data demonstrate that pyroptosis is involved in neuroinflammation and neuronal injury after TBI, and ablation of caspase-1 inhibits TBI-induced pyroptosis. Our findings suggest that caspase-1 may be a potential target for TBI therapy.Electronic supplementary materialThe online version of this article (10.1186/s12974-018-1083-y) contains supplementary material, which is available to authorized users.

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Research Frontiers in Traumatic Brain Injury

Cited by 16 publications

References 103 publications

A systematic review of olfactory-related brain structural changes in patients with congenital or acquired anosmia

A systematic review of olfactory-related brain structural changes in patients with congenital or acquired anosmia

Resveratrol pretreatment attenuates traumatic brain injury in rats by suppressing NLRP3 inflammasome activation via SIRT1

Ablation of caspase-1 protects against TBI-induced pyroptosis in vitro and in vivo

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