دورية أكاديمية
Menopause causes metabolic and cognitive impairments in a chronic cerebral hypoperfusion model of vascular contributions to cognitive impairment and dementia
| العنوان: | Menopause causes metabolic and cognitive impairments in a chronic cerebral hypoperfusion model of vascular contributions to cognitive impairment and dementia |
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| المؤلفون: | Olivia J. Gannon, Janvie S. Naik, David Riccio, Febronia M. Mansour, Charly Abi-Ghanem, Abigail E. Salinero, Richard D. Kelly, Heddwen L. Brooks, Kristen L. Zuloaga |
| المصدر: | Biology of Sex Differences, Vol 14, Iss 1, Pp 1-18 (2023) |
| بيانات النشر: | BMC |
| سنة النشر: | 2023 |
| المجموعة: | Directory of Open Access Journals: DOAJ Articles |
| مصطلحات موضوعية: | Neuroscience, Vascular, Dementia, Menopause, Cognitive impairment, Hypoperfusion, Medicine, Physiology, QP1-981 |
| الوصف: | Background The vast majority of women with dementia are post-menopausal. Despite clinical relevance, menopause is underrepresented in rodent models of dementia. Before menopause, women are less likely than men to experience strokes, obesity, and diabetes—known risk factors for vascular contributions to cognitive impairment and dementia (VCID). During menopause, ovarian estrogen production stops and the risk of developing these dementia risk factors spikes. Here, we aimed to determine if menopause worsens cognitive impairment in VCID. We hypothesized that menopause would cause metabolic dysfunction and increase cognitive impairment in a mouse model of VCID. Methods We performed a unilateral common carotid artery occlusion surgery to produce chronic cerebral hypoperfusion and model VCID in mice. We used 4-vinylcyclohexene diepoxide to induce accelerated ovarian failure and model menopause. We evaluated cognitive impairment using behavioral tests including novel object recognition, Barnes maze, and nest building. To assess metabolic changes, we measured weight, adiposity, and glucose tolerance. We explored multiple aspects of brain pathology including cerebral hypoperfusion and white matter changes (commonly observed in VCID) as well as changes to estrogen receptor expression (which may mediate altered sensitivity to VCID pathology post-menopause). Results Menopause increased weight gain, glucose intolerance, and visceral adiposity. VCID caused deficits in spatial memory regardless of menopausal status. Post-menopausal VCID specifically led to additional deficits in episodic-like memory and activities of daily living. Menopause did not alter resting cerebral blood flow on the cortical surface (assessed by laser speckle contrast imaging). In the white matter, menopause decreased myelin basic protein gene expression in the corpus callosum but did not lead to overt white matter damage (assessed by Luxol fast blue). Menopause did not significantly alter estrogen receptor expression (ERα, ERβ, or GPER1) in the ... |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| تدمد: | 2042-6410 |
| العلاقة: | https://doi.org/10.1186/s13293-023-00518-7Test; https://doaj.org/toc/2042-6410Test; https://doaj.org/article/5ab8287ee17e4496b9e92897d352f872Test |
| DOI: | 10.1186/s13293-023-00518-7 |
| الإتاحة: | https://doi.org/10.1186/s13293-023-00518-7Test https://doaj.org/article/5ab8287ee17e4496b9e92897d352f872Test |
| رقم الانضمام: | edsbas.8ED58C04 |
| قاعدة البيانات: | BASE |
Full Text Finder | تدمد: | 20426410 |
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| DOI: | 10.1186/s13293-023-00518-7 |