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      Bilateral Common Carotid Artery Stenosis in Mice: A Model of Chronic Cerebral Hypoperfusion-Induced Vascular Cognitive Impairment

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          Abstract

          Vascular cognitive impairment (VCI) is a syndrome defined as cognitive decline caused by vascular disease and is associated with various types of dementia. Chronic cerebral hypoperfusion (CCH) is one of the major contributors to VCI. Among the various rodent models used to study CCH-induced VCI, we have found the mouse bilateral common carotid artery stenosis (BCAS) model to be highly suitable. Here, we introduce the BCAS model of C57BL/6J mice generated using microcoils with an internal diameter of 0.18 mm. To produce the mouse BCAS model, the bilateral common carotid arteries are isolated from the adhering tissues and vagus nerves and twined around the microcoils. This model shows cognitive impairment and white matter lesions preceding neuronal dysfunction around postoperative day 28, which is similar to the human clinical picture. Overall, the mouse BCAS model will continue to be useful in studying CCH-induced VCI.

          Key features

          • This mouse BCAS model requires approximately 4 weeks to show phenotypes such as cognitive impairment and white matter injury.

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          Most cited references14

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          The overlap between vascular disease and Alzheimer’s disease – lessons from pathology

          Johannes Attems, Kurt A Jellinger (2014)
          Recent epidemiological and clinico-pathological data indicate considerable overlap between cerebrovascular disease (CVD) and Alzheimer’s disease (AD) and suggest additive or synergistic effects of both pathologies on cognitive decline. The most frequent vascular pathologies in the aging brain and in AD are cerebral amyloid angiopathy and small vessel disease. Up to 84% of aged subjects show morphological substrates of CVD in addition to AD pathology. AD brains with minor CVD, similar to pure vascular dementia, show subcortical vascular lesions in about two-thirds, while in mixed type dementia (AD plus vascular dementia), multiple larger infarcts are more frequent. Small infarcts in patients with full-blown AD have no impact on cognitive decline but are overwhelmed by the severity of Alzheimer pathology, while in early stages of AD, cerebrovascular lesions may influence and promote cognitive impairment, lowering the threshold for clinically overt dementia. Further studies are warranted to elucidate the many hitherto unanswered questions regarding the overlap between CVD and AD as well as the impact of both CVD and AD pathologies on the development and progression of dementia.
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            Vascular Cognitive Impairment.

            Martin Dichgans, Didier Leys (2017)
            Cerebrovascular disease typically manifests with stroke, cognitive impairment, or both. Vascular cognitive impairment refers to all forms of cognitive disorder associated with cerebrovascular disease, regardless of the specific mechanisms involved. It encompasses the full range of cognitive deficits from mild cognitive impairment to dementia. In principle, any of the multiple causes of clinical stroke can cause vascular cognitive impairment. Recent work further highlights a role of microinfarcts, microhemorrhages, strategic white matter tracts, loss of microstructural tissue integrity, and secondary neurodegeneration. Vascular brain injury results in loss of structural and functional connectivity and, hence, compromise of functional networks within the brain. Vascular cognitive impairment is common both after stroke and in stroke-free individuals presenting to dementia clinics, and vascular pathology frequently coexists with neurodegenerative pathology, resulting in mixed forms of mild cognitive impairment or dementia. Vascular dementia is now recognized as the second most common form of dementia after Alzheimer's disease, and there is increasing awareness that targeting vascular risk may help to prevent dementia, even of the Alzheimer type. Recent advances in neuroimaging, neuropathology, epidemiology, and genetics have led to a deeper understanding of how vascular disease affects cognition. These new findings provide an opportunity for the present reappraisal of vascular cognitive impairment. We further briefly address current therapeutic concepts.
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              White matter lesions and glial activation in a novel mouse model of chronic cerebral hypoperfusion.

              Masunari Shibata, Ryo Ohtani, Masafumi Ihara … (2004)
              Cerebrovascular white matter (WM) lesions are closely associated with cognitive impairment and gait disorders in the elderly. We have successfully established a mouse model of chronic cerebral hypoperfusion that may provide new strategies for the molecular analysis of cerebrovascular WM lesions. Adult C57Bl/6 male mice were subjected to bilateral common carotid artery stenosis (BCAS) using external microcoils with varying inner diameters from 0.16 to 0.22 mm. Cerebral blood flow (CBF) in the frontal cortices was measured by laser-Doppler flowmetry at 2 hours and at 1, 3, 7, 14, and 30 days after BCAS. The brains were then removed and examined at 30 days with histological stains and immunohistochemistry for markers of microglia and astroglia. At 2 hours, the CBF values (ratio to the preoperative value) did not change in the 0.22 mm group but decreased significantly to 77.3+/-13.4% in the 0.20 mm group, 67.3+/-18.5% in the 0.18 mm group, and 51.4+/-11.5% in the 0.16 mm group. At day 1, the CBF began to recover in all groups but remained significantly lower until 14 days in comparison to the control group. In the 0.20 mm and 0.18 mm groups, WM lesions occurred after 14 days without any gray matter involvement. These lesions were the most intense in the corpus callosum adjacent to the lateral ventricle but were mild in the anterior commissure and optic tract. In contrast, 4 of 5 mice developed some gray matter changes in the 0.16 mm group. The proliferation of activated microglia and astroglia was observed in the WM beyond 3 days after BCAS. WM lesions were successfully induced after chronic cerebral hypoperfusion with relative preservation of the visual pathway. These features in this mouse model are appropriate for cognitive assessment and genetic analysis, and it may provide a powerful tool to understand the pathophysiology of WM lesions.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Bio Protoc
                Journal ID (iso-abbrev): Bio Protoc
                Journal ID (publisher-id): Bio Protoc
                Journal ID (publisher-id): Bio-Protoc
                Title: Bio-protocol
                Publisher: Bio-Protocol (1075 Lorne Way, Sunnyvale, CA 94087, USA )
                ISSN (Electronic): 2331-8325
                Publication date (Electronic): 05 July 2024
                Publication date Collection: 05 July 2024
                Volume: 14
                Issue: 13
                Electronic Location Identifier: e5022
                Affiliations
                [1 ]Department of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan
                [2 ]Department of Clinical Pharmacology and Pharmacotherapy, School of Pharmaceutical Sciences, Wakayama Medical University, Wakayama, Japan
                Author notes
                Article
                Publisher ID: e5022 Publisher ID: 5022
                DOI: 10.21769/BioProtoc.5022
                PMC ID: 11238111
                SO-VID: 3c883199-4543-4bc9-a3a2-82cee04360e2
                Copyright © ©Copyright : © 2024 The Authors; This is an open access article under the CC BY icense
                License:

                This is an open access article under the CC BY license ( https://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 25 March 2024
                Date revision received : 30 April 2024
                Date accepted : 11 June 2024
                Categories
                Subject: Methods Article
                Subject: Biology
                Subject: Clinical Protocols

                Keywords: bilateral common carotid artery stenosis (bcas),vascular cognitive impairment (vci),chronic cerebral hypoperfusion (cch),white matter injury,microcoil,vagus nerve
                Data availability:
                Keywords: bilateral common carotid artery stenosis (bcas), vascular cognitive impairment (vci), chronic cerebral hypoperfusion (cch), white matter injury, microcoil, vagus nerve

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