Caffeine attenuates brain injury but increases mortality induced by high-intensity blast wave exposure

Ning, Yuping; Yang, Nan; Chen, Xing; Tian, Hongyu; Zhao, Zi‐Ai; Zhang, Xiu-Zhu; Liu, Dong; Li, Ping; Zhao, Yan; Peng, Yan; Wang, Zhengguo; Chen, Jiang‐Fan; Zhou, Yuan‐Guo

doi:10.1016/j.toxlet.2018.11.004

Cited by 4 publications

(4 citation statements)

References 49 publications

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“… 161 It is needed to note that under severe TBI, caffeine consumption, either acutely or chronically, leads to increased mortality but attenuated brain edema and reduced proinflammatory factors in the hippocampus and cortex. 160 Inconsistent with above study, acute (10 min post-injury) administration of an A 2A R antagonist did not exert a protective effect, but administration of caffeine reduced the acute phase mortality in a TBI animal model. 162 The above studies suggest that the effects of caffeine are not only through A 2A R receptors, but may also be related to the A 1 R, the interaction between A 1 R and A 2A R and other signal pathways.…”

Section: Introductionsupporting

confidence: 47%

“…In controlled cortical impact-induced TBI and bTBI models, pre-consumption of caffeine at 0.25 g/L reduces TNF-α level, IL-1β level and brain water content, and suppresses gliosis and alleviates synaptic structure damage. 134 , 160 In mice exposed/subjected to bTBI, chronic caffeine consumption exerts equally protective effects, regardless of pre-consumption, withdrawal after injury or administration only after injury. This study shows the elevation of A 1 R rather than A 2A R mRNA levels following bTBI.…”

Section: Introductionmentioning

confidence: 99%

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Targeting the adenosine A2A receptor for neuroprotection and cognitive improvement in traumatic brain injury and Parkinson's disease

Zhao,

Zhou,

Chen

2024

Chinese Journal of Traumatology

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Section: Introductionsupporting

confidence: 47%

Section: Introductionmentioning

confidence: 99%

Targeting the adenosine A2A receptor for neuroprotection and cognitive improvement in traumatic brain injury and Parkinson's disease

Zhao,

Zhou,

Chen

2024

Chinese Journal of Traumatology

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“…Indeed, preclinical studies with A 2A R antagonist effect on cognition in normal and MPTP-treated non-human primates (NHP) provide the experimental evidence that A 2A R antagonists including caffeine can improve cognitive impairments in PD models (Chen et al, 2013;Chen, 2014). Recent preclinical studies in rodents and non-human primates demonstrated that A 2A R antagonists not only enhance working memory (Zhou et al, 2009), reversal learning (Wei et al, 2011), set-shifting (Mingote et al, 2008), goal-directed behavior (Li et al, 2016), and Pavlovian conditioning (Wei et al, 2014) in normal animals, but also reverse working memory impairments in animal models of PD (Ko et al, 2016) and Huntington's disease (Li et al, 2015), traumatic brain injury (Ning et al, 2013(Ning et al, , 2015(Ning et al, , 2019 as well as Alzheimer's disease (AD) (Dall'Igna et al, 2007;Cunha and Agostinho, 2010;Laurent et al, 2014;Faivre et al, 2018). Furthermore, we recently demonstrated a pro-cognitive effect in normal as well as MPTP-treated Cynomolgus monkeys (Li et al, 2018b).…”

Section: Caffeine and Cognitive Improvement In Pdmentioning

confidence: 98%

Caffeine and Parkinson’s Disease: Multiple Benefits and Emerging Mechanisms

2020

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Parkinson’s disease (PD) is the second most common neurodegenerative disorder, characterized by dopaminergic neurodegeneration, motor impairment and non-motor symptoms. Epidemiological and experimental investigations into potential risk factors have firmly established that dietary factor caffeine, the most-widely consumed psychoactive substance, may exerts not only neuroprotective but a motor and non-motor (cognitive) benefits in PD. These multi-benefits of caffeine in PD are supported by convergence of epidemiological and animal evidence. At least six large prospective epidemiological studies have firmly established a relationship between increased caffeine consumption and decreased risk of developing PD. In addition, animal studies have also demonstrated that caffeine confers neuroprotection against dopaminergic neurodegeneration using PD models of mitochondrial toxins (MPTP, 6-OHDA, and rotenone) and expression of α-synuclein (α-Syn). While caffeine has complex pharmacological profiles, studies with genetic knockout mice have clearly revealed that caffeine’s action is largely mediated by the brain adenosine A2A receptor (A2AR) and confer neuroprotection by modulating neuroinflammation and excitotoxicity and mitochondrial function. Interestingly, recent studies have highlighted emerging new mechanisms including caffeine modulation of α-Syn degradation with enhanced autophagy and caffeine modulation of gut microbiota and gut-brain axis in PD models. Importantly, since the first clinical trial in 2003, United States FDA has finally approved clinical use of the A2AR antagonist istradefylline for the treatment of PD with OFF-time in Sept. 2019. To realize therapeutic potential of caffeine in PD, genetic study of caffeine and risk genes in human population may identify useful pharmacogenetic markers for predicting individual responses to caffeine in PD clinical trials and thus offer a unique opportunity for “personalized medicine” in PD.

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“…The bio-shock tube (BST-I) apparatus ( Figures 1B,C) was used to produce blast injury as previously described (Ning et al, 2019). All rats were anesthetized in an induction chamber with 4-5% isoflurane in 100% oxygen for approximately 5 min.…”

Section: Blast-induced Mtbi Modelmentioning

confidence: 99%

18F-FDG PET Combined With MR Spectroscopy Elucidates the Progressive Metabolic Cerebral Alterations After Blast-Induced Mild Traumatic Brain Injury in Rats

Liu

et al. 2021

Front. Neurosci.

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A majority of blast-induced mild traumatic brain injury (mTBI) patients experience persistent neurological dysfunction with no findings on conventional structural MR imaging. It is urgent to develop advanced imaging modalities to detect and understand the pathophysiology of blast-induced mTBI. Fluorine-18 fluorodeoxyglucose positron emission tomography (18F-FDG PET) could detect neuronal function and activity of the injured brain, while MR spectroscopy provides complementary information and assesses metabolic irregularities following injury. This study aims to investigate the effectiveness of combining 18F-FDG PET with MR spectroscopy to evaluate acute and subacute metabolic cerebral alterations caused by blast-induced mTBI. Thirty-two adult male Sprague–Dawley rats were exposed to a single blast (mTBI group) and 32 rats were not exposed to the blast (sham group), followed by 18F-FDG PET, MRI, and histological evaluation at baseline, 1–3 h, 1 day, and 7 days post-injury in three separate cohorts. 18F-FDG uptake showed a transient increase in the amygdala and somatosensory cortex, followed by a gradual return to baseline from day 1 to 7 days post-injury and a continuous rise in the motor cortex. In contrast, decreased 18F-FDG uptake was seen in the midbrain structures (inferior and superior colliculus). Analysis of MR spectroscopy showed that inflammation marker myo-inositol (Ins), oxidative stress marker glutamine + glutamate (Glx), and hypoxia marker lactate (Lac) levels markedly elevated over time in the somatosensory cortex, while the major osmolyte taurine (Tau) level immediately increased at 1–3 h and 1 day, and then returned to sham level on 7 days post-injury, which could be due to the disruption of the blood–brain barrier. Increased 18F-FDG uptake and elevated Ins and Glx levels over time were confirmed by histology analysis which showed increased microglial activation and gliosis in the frontal cortex. These results suggest that 18F-FDG PET and MR spectroscopy can be used together to reflect more comprehensive neuropathological alterations in vivo, which could improve our understanding of the complex alterations in the brain after blast-induced mTBI.

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Caffeine attenuates brain injury but increases mortality induced by high-intensity blast wave exposure

Cited by 4 publications

References 49 publications

Targeting the adenosine A2A receptor for neuroprotection and cognitive improvement in traumatic brain injury and Parkinson's disease

Targeting the adenosine A2A receptor for neuroprotection and cognitive improvement in traumatic brain injury and Parkinson's disease

Caffeine and Parkinson’s Disease: Multiple Benefits and Emerging Mechanisms

18F-FDG PET Combined With MR Spectroscopy Elucidates the Progressive Metabolic Cerebral Alterations After Blast-Induced Mild Traumatic Brain Injury in Rats

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