Objective: Natural variation in ovarian steroid hormones across the female lifespan contributes to an increased risk for depressive and posttraumatic stress disorder (PTSD) symptoms in women. However, minimal work has focused on understanding the impacts of reproductive aging on the brain and behavioral health of trauma-exposed women. This systematic review examines the bidirectional relationship between trauma-related psychopathology and reproductive aging.
Method: Following PRISMA guidelines, a systematic review of PubMed, PsychInfo, and Medline databases was undertaken to identify controlled studies on how trauma history impacts psychopathology and menopause symptoms during reproductive aging.
Results: Twenty-one studies met the eligibility criteria, with only four utilizing the gold standard STRAW+ 10 criteria for defining reproductive aging stages. The peri and postmenopausal periods appear to be particularly vulnerable phases for individuals with trauma exposure. Menopause symptoms and trauma-related psychopathology symptom severity increase during reproductive aging with increases in the degree of trauma exposure. However, mechanistic insights that may explain this interaction are currently neglected in this area of research.
Conclusion: There is a significant lack of understanding regarding how reproductive aging and its related neuroendocrine changes impact the brain to influence PTSD and depression symptoms related to trauma exposure. This lack of basic understanding impedes the ability to identify, assess, and treat PTSD and depressive symptoms in trauma-exposed women most effectively, and mitigate the long-term consequences of these behavioral health symptoms on morbidity and mortality in aging women.
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http://dx.doi.org/10.1016/j.xjmad.2024.100082 | DOI Listing |
Cellular systems that govern protein folding rely on a delicate balance of functional redundancy and diversification to maintain protein homeostasis (proteostasis). Here, we use to demonstrate how both overlapping and divergent activities of two homologous endoplasmic reticulum (ER)-resident HSP70 family chaperones, HSP-3 and HSP-4, orchestrate ER proteostasis and contribute to organismal physiology. We identify tissue-, age-, and stress-specific protein expression patterns and find both redundant and distinct functions for HSP-3 and HSP-4 in ER stress resistance, reproduction, and body size regulation.
View Article and Find Full Text PDFIUBMB Life
January 2025
Department of Reproductive Medical Center, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.
Abnormality of granulosa cells (GCs) is the critical cause of follicular atresia in premature ovarian failure (POF). RIPK3 is highly expressed in GCs derived from atretic follicles. We focus on uncovering how RIPK3 contributes to ovarian GC senescence.
View Article and Find Full Text PDFVitam Horm
January 2025
Department of Zoology, Institute of Science, Banaras Hindu University, Varanasi, Uttar pradesh, India.
The discovery of Kisspeptin (Kiss) has opened a new direction in research on neuroendocrine control of reproduction in vertebrates. Belonging to the RF amide family of peptides, Kiss and its cognate receptor Gpr54 (Kissr) have a long and complex evolutionary history. Multiple forms of Kiss and Kissr are identified in non-mammalian vertebrates, with the exception of birds, and monotreme mammals.
View Article and Find Full Text PDFAging (Albany NY)
January 2025
School of Medicine, National University of La Plata (UNLP), La Plata, Argentina.
In middle-aged (MA) female rats, we have demonstrated that intrahypothalamic gene therapy for insulin-like growth factor-I (IGF-I) extends the regular cyclicity of the animals beyond 10 months (the age at which MA rats stop ovulating). Here, we implemented long-term OSKM gene therapy in the hypothalamus of young female rats. The main goal was to extend fertility in the treated animals.
View Article and Find Full Text PDFCell Biosci
January 2025
School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong S.A.R., China.
Background: Pathogenic or null mutations in WRN helicase is a cause of premature aging disease Werner syndrome (WS). WRN is known to protect somatic cells including adult stem cells from premature senescence. Loss of WRN in mesenchymal stem cells (MSCs) not only drives the cells to premature senescence but also significantly impairs the function of the stem cells in tissue repair or regeneration.
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