Effects of ovarian hormone loss on neuritic plaques and autophagic flux in the brains of adult female APP/PS1 double-transgenic mice

Yao, Qiuhui; Feng, Min; Yang, Bo; Long, Zhimin; Luo, Shifang; Luo, Min; He, Guiqiong; Wang, Kejian

doi:10.1093/abbs/gmy032

Cited by 14 publications

(8 citation statements)

References 63 publications

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“…All of these molecular phenotypes would suggest a generalized, dysfunctional phenotype in this brain region. The latter finding is consistent with earlier work that shows OVX increases Aβ(1–40) in a transgenic mouse model of AD (57), highlighting a possible protective effect of female sex hormones or ER-α signaling against Aβ(1–40) accumulation. There is emerging interest in the interactive role and clinical utility of Aβ variants such as the 38-/40-mers and their processing in the pathogenesis of multiple dementia phenotypes (58–61).…”

Section: Discussionsupporting

confidence: 92%

Female Sex Hormones and Cardiac Pressure Overload Independently Contribute to the Cardiogenic Dementia Profile in Yucatan Miniature Swine

Hayward

LeBlanc

Emter

et al. 2019

Front. Cardiovasc. Med.

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Post-menopausal women with heart failure (HF) frequently exhibit cardiogenic dementia. Using a pre-clinical swine model of post-menopausal HF, we recently demonstrated that experimental menopause (ovariectomy; OVX) and HF (6-month cardiac pressure overload/aortic banding; AB) independently altered cerebral vasomotor control and together impaired cognitive function. The purpose of this study was to examine the prefrontal cortex and hippocampus tissues from these animals to assess whether OVX and HF are associated with neurologic alterations that may contribute to cardiogenic dementia. We hypothesized that OVX and HF would independently alter neuronal cell signaling in swine with post-menopausal cardiogenic dementia. Immunoblot analyses revealed OVX was associated with reduced estrogen receptor-α in both brain regions and HF tended to exacerbate OVX-induced deficits in the hippocampus. Further, OVX was associated with a reduction in the ratio of phosphorylated:total Akt and ERK in the hippocampus as well as decreased total Akt and synaptophysin in the prefrontal cortex. In contrast, HF was associated with a trend toward reduced phosphorylated:total ERK in the prefrontal cortex. In addition, HF was associated with decreased β-amyloid (1–38) in the prefrontal cortex and increased β-amyloid (1–38) in the hippocampus. Regional brain lipid analysis revealed OVX tended to increase total, saturated, and monounsaturated fatty acid content in the prefrontal cortex, with the greatest magnitude of change occurring in the AB-OVX group. The data from this study suggest that OVX and HF are independently associated with regional-specific neurologic changes in the brain that contribute to the cardiogenic dementia profile in this model. This pre-clinical swine model may be a useful tool for better understanding post-menopausal cardiogenic dementia pathology and developing novel therapies.

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Section: Discussionsupporting

confidence: 92%

Female Sex Hormones and Cardiac Pressure Overload Independently Contribute to the Cardiogenic Dementia Profile in Yucatan Miniature Swine

Hayward

LeBlanc

Emter

et al. 2019

Front. Cardiovasc. Med.

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“…In the study of the short-term and long-term effects of estrogen deprivation in the OVX model, autophagy-related proteins showed a gradual decrease. The change in autophagy throughout the process of memory impairment after OVX was not clarified through these studies either (15). Obviously, the progressive change in memory and autophagy-related protein requires further study.…”

Section: Introductionmentioning

confidence: 86%

Effects of estrogen deprivation on memory and expression of related proteins in ovariectomized mice

et al. 2020

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Background: The ovariectomized (OVX) rodent model is most widely used for studying the influence of estrogen deprivation on memory. However, the results of these studies are inconsistent, in that the memory of OVX rodents shows either impairment or no change. These inconsistent outcomes increase the difficulty of researching neurochemical mechanisms and evaluating drug efficacy. One possible explanation for these discrepancies might be that the time point for memory examination after OVX varies considerably among studies. The aim of our study was to investigate the effects of estrogen deprivation on memory and the expression of memory-related proteins at different times after OVX.Methods: Novel object recognition (NOR), step-through passive avoidance (STPA) and the Morris water maze (MWM) were performed to evaluate the memory performance of mice at different times after OVX.The expressions of BDNF, TrkB, ULK1 and LC3II/LC3I in the hippocampus were also assessed to explore the relevant mechanisms.Results: After OVX, a significant memory impairment was found in the STPA test at 4 weeks. In the NOR and MWM tests, however, memory deficits were not observed until 8 weeks post-OVX. Interestingly, at 8 weeks, a memory rebound was found in the STPA test. In the hippocampus, the levels of BDNF and TrkB in OVX mice were markedly decreased at 4 and 8 weeks. Subsequently, a significant decrease in the ULK1 and LC3II/LC3I level in OVX mice was observed at 8 weeks.Conclusions: Memory impairment in mice was observed as early as 4 weeks after OVX, although there was a possibility of memory rebound with the prolongation of estrogen deprivation. Eight weeks of estrogen deprivation would be more likely to induce hippocampus-dependent memory impairment. This progressive impairment of memory might be due to the downregulation of the BDNF/TrkB signaling pathway at the early post-OVX stage, while the decrease of autophagy level in the later stage might also contribute to these progressive alterations. The underlying relationship between the BDNF/TrkB signaling pathway and autophagy in this progressive impairment of memory requires further study.

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“…Este modelo animal é capaz de replicar a neurobiologia e comportamentos clínicos observados na DA, porém, se observa proeminência dos déficits aos 11 meses, em camundongos. É visto que para melhor reprodutibilidade animais precisam ser APP/PS1, pois a mutação APP isolada não afeta os marcadores para neurogênese e PS1 mostra-se com declínio cognitivo, sem a reprodutibilidade esperada (YAO et al, 2018).…”

Section: Modelo Animal Duplo Transgênicounclassified

Métodos Experimentais Para Estudos Não Clínicos Da Doença De Alzheimer

2022

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Os autores se responsabilizam publicamente por esta obra, garantindo que o mesmo é de autoria própria, assumindo integral responsabilidade diante de terceiros, quer de natureza moral ou patrimonial, em razão de seu conteúdo, declarando que o trabalho é original, livre de plágio e que não infringe quaisquer direitos de propriedade intelectual de terceiros. Os autores declaram não haver qualquer interesse comercial ou irregularidade que comprometa a integridade desta obra. SUMÁRIOAPRESENTAÇÃO CAPÍTULO 1 PRINCIPAIS MODELOS ANIMAIS DE INDUÇÃO DA DOENÇA DE ALZHEIMER Modelo animal triplo transgênico Modelo animal duplo transgênico Modelo por infusão intracerebroventricular (i.c.v.) Peptídeo β-amiloide Lipopolissacarídeo (LPS) Estreptozotocina Indução por Alumínio Indução da DA em neurônios do hipocampo (Cultura celular) CAPÍTULO 2 PROTOCOLOS PARA ANÁLISE DOS MODELOS EXPERIMENTAIS Protocolo de avaliação em campo aberto Labirinto Aquático de Morris (Morris Water Maze) Teste de suspensão pela cauda Teste labirinto em cruz elevado Teste de realocação de objetos Avaliação do estresse oxidativo Atividade da enzima acetilcolinesterase (AchE) Captação de glutamato Fator de necrose tumora (TNF-a) Micróglia ativada Interleucinas 1a, 2, 6, 18 Óxido nítrico Prostaglandina E2 Estrutura química da prostaglandina E 2 Proteína quimiotática de Monócitos (MCP-1) Fator estimulador de colônia (G-CSF) CAPÍTULO 3 ZEBRAFISH COMO MODELO NEUROFARMACOLÓGICO DA DOENÇA DE ALZHEIMER Zebrafish como modelo para DA Zebrafish como modelo neurogenético Estudos de drogas neuroespecíficas usando o modelo de zebrafish REFERÊNCIAS SOBRE OS AUTORES

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Effects of ovarian hormone loss on neuritic plaques and autophagic flux in the brains of adult female APP/PS1 double-transgenic mice

Cited by 14 publications

References 63 publications

Female Sex Hormones and Cardiac Pressure Overload Independently Contribute to the Cardiogenic Dementia Profile in Yucatan Miniature Swine

Female Sex Hormones and Cardiac Pressure Overload Independently Contribute to the Cardiogenic Dementia Profile in Yucatan Miniature Swine

Effects of estrogen deprivation on memory and expression of related proteins in ovariectomized mice

Métodos Experimentais Para Estudos Não Clínicos Da Doença De Alzheimer

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