Subarachnoid Hemorrhage Induces Sub-acute and Early Chronic Impairment in Learning and Memory in Mice

Regnier-Golanov, Angelique; Gulinello, Maria; Hernandez, Magda S; Golanov, Eugene V.; Britz, Gavin W.

doi:10.1007/s12975-022-00987-9

Cited by 12 publications

(6 citation statements)

References 101 publications

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“…The expression levels of IL-1β and IL-18 were signi cantly decreased while the expression levels of IL-10 were increased in the SAH + WBV group than that in the SAH group. In addition to the EBI within 72 h after SAH, the impairment of learning and memory function is also one of the important factors affecting the prognosis of patients with SAH [27]. In this study, less neuronal loss of hippocampus in CA1, CA3, and DG regions was found in the SAH + WBV group compared with the SAH group, which suggested that WBV treatment contributes to the increased number of neurons in the hippocampus after SAH.…”

Section: Discussionsupporting

confidence: 50%

Whole-body vibration protects against early brain injury and neuroinflammation after experimental subarachnoid hemorrhage

Wang

Ding

Zhang

et al. 2022

Preprint

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Whole body vibration (WBV), as a form of physical stimulation through mechanical vibration, has been proved to have neuroprotective effects on a variety of central nervous system (CNS) diseases. However, whether WBV plays a neuroprotective role in early brain injury (EBI) after subarachnoid hemorrhage (SAH) has not been well demonstrated. Herein, we focused on investigating the potential mechanism of the therapeutic effects of WBV on SAH-induced mice. The endovascular perforation was performed to induce SAH in C57BL/6J male mice. The mice were exposed to WBV twice a day at a frequency of 30 Hz for 20 days. The curative actions of WBV were assessed using the modified Garcia scale and the beam balance scoring system, along with measuring brain water content 24 h after SAH induction. TUNEL staining was performed to observe the apoptotic cells. Immunofluorescence staining was used to evaluate the expression of astrocytes and microglia in mice's cerebral cortex. Additionally, the ELISA assay was performed to detect inflammatory cytokines, such as IL-10, IL-18, and IL-1β. Western blot was conducted to explore the expression analysis of apoptosis-associated proteins (cleaved Caspase-3). Morris Water Maze (MWM) test and rotarod test were used to evaluate the long-term neurological function of mice. Nissl staining was used to evaluate the loss of neurons in the hippocampus of mice. Our study illustrated that WBV can reduce brain water content without significantly affecting the weight of mice. Also, the TUNEL-positive cell counts of the cerebral cortex of mice in the SAH+WBV group were significantly reduced compared with that in the SAH group. The protein level of cleaved Caspase-3 in the SAH+WBV group was also decreased than that in the SAH group. Immunofluorescence staining showed that WBV suppressed the high expression of GFAP and Iba-1 caused by SAH. MWM assay and rotarod test revealed that the long-term neurological dysfunction of mice following SAH was attenuated by WBV treatment compared with SAH-induced mice, which may be closely related to the low level of neuronal loss in the hippocampal regions. Our research demonstrated that WBV treatment can reduce EBI and neuroinflammation and improve the long-term neurological dysfunction of mice after SAH, which provides a new possibility for clinical treatment of SAH in the future.

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Section: Discussionsupporting

confidence: 50%

Whole-body vibration protects against early brain injury and neuroinflammation after experimental subarachnoid hemorrhage

Wang

Ding

Zhang

et al. 2022

Preprint

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“…For single blood injection models into the prechiasmatic cistern or cisterna magna, neurocognitive de cits have only been observed up to 2-week after ictus (Table 1) [12,22,23], which limits translatability to the human condition. For the endovascular perforation mouse model, disparate results have been reported with one laboratory noting signi cant neurocognitive de cits one month post-ictus [24] and two other laboratories showing no or minimal neurocognitive de cits one month post-ictus [25] [26]. Important advantages of our mouse model of SAH compared with existing methods are summarized in Table 1.…”

Section: Discussionmentioning

confidence: 99%

“…For prechiasmatic injection and cisterna magna injections mouse models, neurocognitive de cits have only been demonstrated up to 2-week after ictus (Table 1) [12,22,23]. For the endovascular perforation mouse model, disparate results have been reported with Regnier-Golanov et al reporting signi cant neurocognitive de cits 1-month after ictus using a battery of behavioral tests including Morris Water Maze [24], while Milner et al showed no neurocognitive de cits 1-month after ictus as assessed by Morris Water Maze [25] and Fanizzi et al showed minimal long-term neurobehavioral de cits 1month after ictus using a battery of behavioral tests including Morris Water Maze [26]. Development of a mouse model of SAH that produces robust and consistent long-term neurocognitive de cits is highly desirable, as it would accelerate experiments, lower costs, and leverage the tremendous power of genetically manipulated mice.…”

Section: Introductionmentioning

confidence: 99%

Development and validation of prechiasmatic mouse model of subarachnoid hemorrhage to measure long-term neurobehavioral impairment

Diwan,

Mehla,

Nelson

et al. 2024

Preprint

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Controllable and reproducible animal models of aneurysmal subarachnoid hemorrhage (SAH) are crucial for the systematic study of the pathophysiology and treatment of this debilitating condition. Despite the variety of animal models of SAH currently available, attempts to translate promising therapeutic strategies from preclinical studies to humans have largely failed. This failure is likely due, at least in part, to poor replication of pathology and disabilities in these preclinical models, especially the long-term neurocognitive deficits that drive poor quality of life / return to work in SAH survivors. Therefore, there is an unmet need to develop experimental models that reliably replicate the long-term clinical ramifications of SAH – especially in mice where genetic manipulations are straightforward and readily available. To address this need, we developed a standardized mouse model of SAH that reproducibly produced significant and trackable long-term neurobehavioral deficits. SAH was induced by performing double blood injections into the prechiasmatic cistern – a simple modification to the well-characterized single prechiasmatic injection mouse model of SAH. Following SAH, mice recapitulated key characteristics of SAH patients including long-term cognitive impairment as observed by a battery of behavioral testing and delayed pathophysiologic processes assayed by neuroinflammatory markers. We believe that this new SAH mouse model will be an ideal paradigm for investigating the complex pathophysiology of SAH and identifying novel druggable therapeutic targets for treating SAH-associated long-term neurocognitive deficits in patients.

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“…The hippocampus is a region responsible for cognitive function, especially memory function. Biological functions of the hippocampus can be largely impaired by subarachnoid hemorrhage, the subsequent middle cerebral artery spasm can reduce blood supply, block synaptic neurotransmission, and damage plasticity (Tariq et al, 2010 ; Regnier-Golanov et al, 2022 ). Neuroinflammation and oxidative stress in hippocampal neurons secondary to subarachnoid hemorrhage also contribute to cognitive impairment (Han et al, 2014 ; Hu et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Utilization of clinical and radiological parameters to predict cognitive prognosis in patients with mild-to-moderate traumatic brain injury

Wang¹,

Hui²,

Wang³

et al. 2023

Front. Neurosci.

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BackgroundCognitive impairment is a common sequela following traumatic brain injury (TBI). This study aimed to identify risk factors for cognitive impairment after 3 and 12 months of TBI and to create nomograms to predict them.MethodsA total of 305 mild-to-moderate TBI patients admitted to the First Affiliated Hospital with Nanjing Medical University from January 2018 to January 2022 were retrospectively recruited. Risk factors for cognitive impairment after 3 and 12 months of TBI were identified by univariable and multivariable logistic regression analyses. Based on these factors, we created two nomograms to predict cognitive impairment after 3 and 12 months of TBI, the discrimination and calibration of which were validated by plotting the receiver operating characteristic (ROC) curve and calibration curve, respectively.ResultsCognitive impairment was detected in 125/305 and 52/305 mild-to-moderate TBI patients after 3 and 12 months of injury, respectively. Age, the Glasgow Coma Scale (GCS) score, >12 years of education, hyperlipidemia, temporal lobe contusion, traumatic subarachnoid hemorrhage (tSAH), very early rehabilitation (VER), and intensive care unit (ICU) admission were independent risk factors for cognitive impairment after 3 months of mild-to-moderate TBI. Meanwhile, age, GCS score, diabetes mellitus, tSAH, and surgical treatment were independent risk factors for cognitive impairment after 12 months of mild-to-moderate TBI. Two nomograms were created based on the risk factors identified using logistic regression analyses. The areas under the curve (AUCs) of the two nomograms to predict cognitive impairment after 3 and 12 months of mild-to-moderate TBI were 0.852 (95% CI [0.810, 0.895]) and 0.817 (95% CI [0.762, 0.873]), respectively.ConclusionTwo nomograms are created to predict cognitive impairment after 3 and 12 months of TBI. Age, GCS score, >12 years of education, hyperlipidemia, temporal lobe contusion, tSAH, VER, and ICU admission are independent risk factors for cognitive impairment after 3 months of TBI; meanwhile, age, the GCS scores, diabetes mellitus, tSAH, and surgical treatment are independent risk factors of cognitive impairment after 12 months of TBI. Two nomograms, based on both groups of factors, respectively, show strong discriminative abilities.

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Subarachnoid Hemorrhage Induces Sub-acute and Early Chronic Impairment in Learning and Memory in Mice

Cited by 12 publications

References 101 publications

Whole-body vibration protects against early brain injury and neuroinflammation after experimental subarachnoid hemorrhage

Whole-body vibration protects against early brain injury and neuroinflammation after experimental subarachnoid hemorrhage

Development and validation of prechiasmatic mouse model of subarachnoid hemorrhage to measure long-term neurobehavioral impairment

Utilization of clinical and radiological parameters to predict cognitive prognosis in patients with mild-to-moderate traumatic brain injury

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