Reproductive Markers in Alzheimer's Disease Progression: A Mini Review
Huitong Ding1,2*, Sanskruti Madan1, Rhoda Au1,2,3,4,5,6, P. Murali Doraiswamy7, Chunyu Liu2,8
1Department of Anatomy and Neurobiology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA
2The Framingham Heart Study, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA
3Department of Epidemiology, Boston University School of Public Health, Boston, MA, USA
4Department of Medicine, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA
5Slone Epidemiology Center, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA
6Departments of Neurology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA
7Neurocognitive Disorders Program, Departments of Psychiatry and Medicine, and the Duke Institute for Brain Sciences, Duke University School of Medicine, Durham, NC, USA
8Department of Biostatistics, Boston University School of Public Health, Boston, MA, USA
Accumulating evidence suggests that reproductive markers, such as age at menarche, are associated with cognitive function and the risk of developing Alzheimer's disease (AD). These reproductive markers offer promising potential for predicting the risk of AD, underscoring the necessity for sex-specific considerations in understanding and managing this neurodegenerative disorder. This review first discusses recent findings on reproductive markers in AD progression, and further points out the direction for future research to unravel the complex interplay between reproductive health and cognitive health. We advocate for the incorporation of sex heterogeneity into AD precision medicine to tailor sex-specific diagnostic and intervention approaches.
DOI: 10.29245/2572.942X/2024/2.1300 View / Download PdfInteractions between genetic and environmental factors and schizophrenia: Insights from KPNA1-deficient mice
Hirotaka Nomiya1, Masami Yamada1,2*
1Department of Cell Biology and Biochemistry, Division of Medicine, Faculty of Medical Sciences, University of Fukui, Matsuoka Shimoaizuki, Eiheiji-cho, Yoshida-gun, Fukui, Japan
2Life Science Innovation Center, University of Fukui, Bunkyo, Fukui-City, Fukui, Japan
The interactions between genetic and environmental factors (G x E interactions) play a crucial role in the pathogenesis of schizophrenia. The administration of phencyclidine, a psychotropic drug, to Kpna1-deficient mice induces behavioral abnormalities resembling schizophrenia. In the nucleus accumbens of these mice, the expressions of dopamine receptors, an RNA editing enzyme, and cytoplasmic dynein demonstrate gene-environment interaction-dependent alterations. Kpna1-deficient mice may be useful as a gene-environment interaction model for schizophrenia and provide insights into its pathogenesis. Further, changes in gene expression in the nucleus accumbens may be involved in the development of schizophrenia.
DOI: 10.29245/2572.942X/2024/2.1299 View / Download Pdf