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Journal of Translational Neuroscience(转化神经科学电子杂志)

ISSN 2096-0689

CN 11-9363/R

Journal of Translational Neuroscience    2018, Vol. 3 Issue (2) : 1-5    https://doi.org/10.3868/j.issn.2096-0689.2018.02.001
Review
Effect of fertility history and parity on Alzheimer’s disease: a mini review from animal to human studies
Zhongrong Zhang1, Zuoli Sun1, Yuhong Li2, Rena Li1, 2, 3*
1. National Clinical Research Center for Mental Disorders & Beijing Key Laboratory of Mental Disorders, Beijing Anding Hospital, Capital Medical University, Beijing 100088, China
2. Beijing Institute for Brain Disorders, Capital Medical University, Beijing 100069, China
3. Center for Hormone Advanced Science and Education, Roskamp Institute, Sarasota, FL 34243, USA
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Abstract More women than men have Alzheimer’s disease (AD) or other dementias. There are a number of potential biological and social reasons for the sex difference in the risk of AD, such as women live longer than men on average, and estrogen depletion after menopause in women, biological or genetic variations, and education, occupation or rates of heart disease. Recent studies showed a link between reproductive history and dementia risk in women. Women with fertility history showed lower risk of dementia compared to women with no child. Other studies also suggested that women’s pregnancy history may influence AD’s risk. In this review, we will focus on the relationship between women fertility and cognition and discuss the potential role of sex hormones in the brain and cognition, especially on AD pathogenesis.
Keywords Alzheimer’s disease (AD)      fertility history      cognition      sex hormones     
Issue Date: 01 October 2018
 Cite this article:   
Zhongrong Zhang, Zuoli Sun, Yuhong Li, Rena Li. Effect of fertility history and parity on Alzheimer’s disease: a mini review from animal to human studies[J]. Journal of Translational Neuroscience,2018, 3(2): 1-5.
 URL:  
https://academic.hep.com.cn/jtn/EN/10.3868/j.issn.2096-0689.2018.02.001
https://academic.hep.com.cn/jtn/EN/Y2018/V3/I2/1
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