Traumatic brain injury and hippocampal neurogenesis: Functional implications

Redell, John B.; Maynard, Mark E.; Underwood, Erica L.; Vita, Sydney M.; Dash, Pramod K.; Kobori, Nobuhide

doi:10.1016/j.expneurol.2020.113372

Cited by 55 publications

(34 citation statements)

References 119 publications

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“…Specifically, the number of FJC+ neurons determined in DG was twice as many as those in the CA1 region ( Figure 5 ). Clearly, such immature neuron loss can compromise hippocampal neurogenesis [ 60 ], particularly when associated with neuroinflammation [ 23 , 43 ], which can contribute to the memory and learning impairments that occur following a TBI.…”

Section: Discussionmentioning

confidence: 99%

“…Increasing evidence indicates that post-TBI dissemination of brain inflammation extends beyond the peri-lesion site to remote brain regions [ 22 ]. Excessively activated microglia and astrocytes in the ipsilateral and contralateral hippocampus can persist for more than a week after a TBI and drive neurodegenerative processes that include impaired neurogenesis and reparative mechanisms [ 23 ]. In large part, neuroinflammatory processes across the brain, and particularly in the hippocampus, are driven by TNF-α-responsive genes [ 24 ].…”

Section: Introductionmentioning

confidence: 99%

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3,6′-Dithiopomalidomide Ameliorates Hippocampal Neurodegeneration, Microgliosis and Astrogliosis and Improves Cognitive Behaviors in Rats with a Moderate Traumatic Brain Injury

Huang

Tsai

Yang

et al. 2021

IJMS

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Traumatic brain injury (TBI) is a leading cause of disability and mortality worldwide. It can instigate immediate cell death, followed by a time-dependent secondary injury that results from disproportionate microglial and astrocyte activation, excessive inflammation and oxidative stress in brain tissue, culminating in both short- and long-term cognitive dysfunction and behavioral deficits. Within the brain, the hippocampus is particularly vulnerable to a TBI. We studied a new pomalidomide (Pom) analog, namely, 3,6′-dithioPom (DP), and Pom as immunomodulatory imide drugs (IMiD) for mitigating TBI-induced hippocampal neurodegeneration, microgliosis, astrogliosis and behavioral impairments in a controlled cortical impact (CCI) model of TBI in rats. Both agents were administered as a single intravenous dose (0.5 mg/kg) at 5 h post injury so that the efficacies could be compared. Pom and DP significantly reduced the contusion volume evaluated at 24 h and 7 days post injury. Both agents ameliorated short-term memory deficits and anxiety behavior at 7 days after a TBI. The number of degenerating neurons in the CA1 and dentate gyrus (DG) regions of the hippocampus after a TBI was reduced by Pom and DP. DP, but not Pom, significantly attenuated the TBI-induced microgliosis and DP was more efficacious than Pom at attenuating the TBI-induced astrogliosis in CA1 and DG at 7D after a TBI. In summary, a single intravenous injection of Pom or DP, given 5 h post TBI, significantly reduced hippocampal neurodegeneration and prevented cognitive deficits with a concomitant attenuation of the neuroinflammation in the hippocampus.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

3,6′-Dithiopomalidomide Ameliorates Hippocampal Neurodegeneration, Microgliosis and Astrogliosis and Improves Cognitive Behaviors in Rats with a Moderate Traumatic Brain Injury

Huang

Tsai

Yang

et al. 2021

IJMS

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“…TBI and stroke alter hippocampal neurogenesis in murine models ( 29 , 30 ). Though hippocampal neurogenesis is recognized as an important component of cognitive recovery from TBI and stroke, there is not a direct correlation between increased neurogenesis and recovery.…”

Section: Hippocampal Neurogenesismentioning

confidence: 99%

Psychedelics for Brain Injury: A Mini-Review

Khan

Carter²,

Aggarwal

et al. 2021

Front. Neurol.

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Objective: Stroke and traumatic brain injury (TBI) are among the leading causes of disability. Even after engaging in rehabilitation, nearly half of patients with severe TBI requiring hospitalization are left with major disability. Despite decades of investigation, pharmacologic treatment of brain injury is still a field in its infancy. Recent clinical trials have begun into the use of psychedelic therapeutics for treatment of brain injury. This brief review aims to summarize the current state of the science's relevance to neurorehabilitation, and may act as a resource for those seeking to understand the precedence for these ongoing clinical trials.Methods: Narrative mini-review of studies published related to psychedelic therapeutics and brain injury.Results: Recent in vitro, in vivo, and case report studies suggest psychedelic pharmacotherapies may influence the future of brain injury treatment through modulation of neuroinflammation, hippocampal neurogenesis, neuroplasticity, and brain complexity.Conclusions: Historical data on the safety of some of these substances could serve in effect as phase 0 and phase I studies. Further phase II trials will illuminate how these drugs may treat brain injury, particularly TBI and reperfusion injury from stroke.

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“…This explains the site-specific or limited protein and lipid distribution in the absorption maps of the hippocampus of control group in the current study. Although moderate-severe TBI has been shown to trigger acute loss of newborn neurons besides hyper-proliferation of progenitor cell in rodents, there is no report about the alteration of hippocampal neurogenesis in mild TBI 53 . However, there are several studies showing site-specific up-regulation of non-neuronal genes which codes transcription factors such as Nuclear factor erythoid related factor 2 (NRF2), growth factors [insulin like growth factor 1 (IGF-1)] with a coincident increase in several proteins (heme-oxygenase-1, nicotinamide adenine dinucleotide phosphate-quinone-oxidoreductase 1, glutathione reductase, and catalase) in post-TBI hippocampus after 48–72 h and 1 week 52 .…”

Section: Discussionmentioning

confidence: 99%

Biomolecular changes and subsequent time-dependent recovery in hippocampal tissue after experimental mild traumatic brain injury

Ustaoğlu

Ali

Rakib

et al. 2021

Sci Rep

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Traumatic brain injury (TBI) is the main cause of disability and mortality in individuals under the age of 45 years. Elucidation of the molecular and structural alterations in brain tissue due to TBI is crucial to understand secondary and long-term effects after traumatic brain injury, and to develop and apply the correct therapies. In the current study, the molecular effects of TBI were investigated in rat brain at 24 h and 1 month after the injury to determine acute and chronic effects, respectively by Fourier transform infrared imaging. This study reports the time-dependent contextual and structural effects of TBI on hippocampal brain tissue. A mild form of TBI was induced in 11-week old male Sprague Dawley rats by weight drop. Band area and intensity ratios, band frequency and bandwidth values of specific spectral bands showed that TBI causes significant structural and contextual global changes including decrease in carbonyl content, unsaturated lipid content, lipid acyl chain length, membrane lipid order, total protein content, lipid/protein ratio, besides increase in membrane fluidity with an altered protein secondary structure and metabolic activity in hippocampus 24 h after injury. However, improvement and/or recovery effects in these parameters were observed at one month after TBI.

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Traumatic brain injury and hippocampal neurogenesis: Functional implications

Cited by 55 publications

References 119 publications

3,6′-Dithiopomalidomide Ameliorates Hippocampal Neurodegeneration, Microgliosis and Astrogliosis and Improves Cognitive Behaviors in Rats with a Moderate Traumatic Brain Injury

3,6′-Dithiopomalidomide Ameliorates Hippocampal Neurodegeneration, Microgliosis and Astrogliosis and Improves Cognitive Behaviors in Rats with a Moderate Traumatic Brain Injury

Psychedelics for Brain Injury: A Mini-Review

Biomolecular changes and subsequent time-dependent recovery in hippocampal tissue after experimental mild traumatic brain injury

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