Dataset Information

Tooth loss, cognitive impairment and chronic cerebral ischemia.

ABSTRACT:

Background/purpose

Vascular factor is an important risk factor in the process of cognitive impairment or dementia. Tooth loss could cause impairments of spatial learning and memory in mice, and nitric oxide (NO) and its synthase might be involved in the process. The objectives of this study were to investigate and compare the behavioral impairments between the Wistar rats with tooth loss and those with chronic ischemia and to determine the changes in nitric oxide (NO) and its synthases under those two conditions.

Materials and methods

The Morris water maze was used to test the spatial learning and memory abilities in the Wistar rats 8 weeks after the molar extraction procedure and the occlusion of 2 blood vessels to produce cerebral ischemia. The changes in NO and its synthases were evaluated using the Griess assay, Western blotting, and immunohistochemistry.

Results

Similar impairments in the spatial learning and memory of Wistar rats were found after tooth loss and the induction of cerebral ischemia. The levels of NO and iNOS in the rat hippocampus increased, and the levels of eNOS decreased. Conclusion: For Wistar rats, the results of cognitive impairments related to tooth loss and those that occur due to chronic cerebral ischemia were statistically not significant and that NO, iNOS and eNOS in the hippocampus are involved in both cases.

SUBMITTER: Pang Q

PROVIDER: S-EPMC7109480 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

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Publications

Tooth loss, cognitive impairment and chronic cerebral ischemia.

Pang Qian Q Wu Qianqian Q Hu Xingxue X Zhang Jianjun J Jiang Qingsong Q

Journal of dental sciences 20191019 1

<h4>Background/purpose</h4>Vascular factor is an important risk factor in the process of cognitive impairment or dementia. Tooth loss could cause impairments of spatial learning and memory in mice, and nitric oxide (NO) and its synthase might be involved in the process. The objectives of this study were to investigate and compare the behavioral impairments between the Wistar rats with tooth loss and those with chronic ischemia and to determine the changes in nitric oxide (NO) and its synthases u ...[more]

PMID: 32257004

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Project description:Lipocalin 2 (LCN2) is a pleiotropic molecule that is induced in the central nervous system (CNS) in several acute and chronic pathologies. The acute induction of LCN2 evolved as a beneficial process, aimed at combating bacterial infection through the sequestration of iron from pathogens, while the role of LCN2 during chronic, non-infectious disease remains unclear, and recent studies suggest that LCN2 is neurotoxic. However, whether LCN2 is sufficient to induce behavioral and cognitive alterations remains unclear. In this paper, we sought to address the role of cerebral LCN2 on cognition in both acute and chronic settings. We demonstrate that LCN2 is robustly induced in the CNS during both acute and chronic inflammatory conditions, including LPS-based sepsis and cancer cachexia. In vivo, LPS challenge results in a global induction of LCN2 in the central nervous system, while cancer cachexia results in a distribution specific to the vasculature. Similar to these in vivo observations, in vitro modeling demonstrated that both glia and cerebral endothelium produce and secrete LCN2 when challenged with LPS, while only cerebral endothelium secrete LCN2 when challenged with cancer-conditioned medium. Chronic, but not short-term, cerebral LCN2 exposure resulted in reduced hippocampal neuron staining intensity, an increase in newborn neurons, microglial activation, and increased CNS immune cell infiltration, while gene set analyses suggested these effects were mediated through melanocortin-4 receptor independent mechanisms. RNA sequencing analyses of primary hippocampal neurons revealed a distinct transcriptome associated with prolonged LCN2 exposure, and ontology analysis was suggestive of altered neurite growth and abnormal spatial learning. Indeed, LCN2-treated hippocampal neurons display blunted neurite processes, and mice exposed to prolonged cerebral LCN2 levels experienced a reduction in spatial reference memory as indicated by Y-maze assessment. These findings implicate LCN2 as a pathologic mediator of cognitive decline in the setting of chronic disease.

Project description:ObjectiveCurrently, most models of vascular cognitive impairment are established by occluding the carotid arteries uni- or bilaterally to reduce the cerebral blood flow mimicking chronic cerebral hypoxia. Due to the sudden blood flow interruption, a gradual narrowing of the carotid artery cannot be completely imitated. This paper aims to establish a bilateral carotid stenosis model with mild cognitive dysfunction and mild white matter changes to simulate patients with vascular predementia.MethodsAged Wistar rats (18 months old) underwent either bilateral common carotid artery stenosis (BCAS) or occlusion (BCAO) surgery or a sham operation (control group). The cerebral blood flow in the frontal cortex was measured using Doppler flowmetry. Thirty days after surgery, cognitive function impairments were determined with the Morris water maze; cerebral magnetic resonance imaging was performed to detect changes in fractional anisotropy to assess white matter injuries, and histological studies were performed.ResultsThe aged rats in the BCAS group showed a more gradual cerebral blood flow reduction and a lower mortality rate (11%) compared to rats in the BCAO group. The water maze test revealed a more marginal impairment affecting spatial learning and memory in rats with BCAS than in rats with BCAO. Diffusion tensor imaging detected white matter injuries in the hippocampus and cerebral cortex of BCAS rats. Particularly, a small portion of nerve fibers of the lateral somatosensory cortex was significantly different between rats of the BCAO and BCAS groups. In the BCAS group, the microscopic structure of the hippocampal CA1 region changed slightly after 30 days and sustained a slight mitochondrial crista crack. Fluorescence staining indicated that the number of GFAP-positive cells was increased in rat brains of the BCAS group, and this phenomenon was even more pronounced in the BCAO group. The hnRNPA2/B1 and GABAAR-α1 expression levels were significantly decreased in the hippocampus of rats with BCAS compared to those of controls.ConclusionSevere bilateral carotid stenosis induced mild cognitive dysfunction and slight structural changes in the brains of aged rats. Thus, a chronic cerebral hypoperfusion model was successfully established.

Dataset Information

Tooth loss, cognitive impairment and chronic cerebral ischemia.

Background/purpose

Materials and methods

Results

Publications

Tooth loss, cognitive impairment and chronic cerebral ischemia.

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