ArticleNeural regeneration research2013
Metabolic alteration of neuroactive steroids and protective effect of progesterone in Alzheimer's disease-like rats.
Article in Neural regeneration research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 34 citations in OpenAlex.
- Associations Between Heavy Metal Exposure from Milk and Steroid Hormones in Mothers.Biological trace element research · 2025Article
- Functional Food Nutrients, Redox Resilience Signaling and Neurosteroids for Brain Health.International journal of molecular sciences · 2024Review
- Biomaterials-based anti-inflammatory treatment strategies for Alzheimer's disease.Neural regeneration research · 2024Review
- Dihuang-Yinzi Alleviates Cognition DeficitsFrontiers in aging neuroscience · 2022Article
- Promising Intervention Approaches to Potentially Resolve Neuroinflammation And Steroid Hormones Alterations in Alzheimer's Disease and Its Neuropsychiatric Symptoms.Aging and disease · 2021Review
- Drug Repurposing for Alzheimer's Disease Based on Protein-Protein Interaction Network.BioMed research international · 2021Article
- The Role of the Effects of Autophagy on NLRP3 Inflammasome in Inflammatory Nervous System Diseases.Frontiers in cell and developmental biology · 2021Review
- Steroids and Alzheimer's Disease: Changes Associated with Pathology and Therapeutic Potential.International journal of molecular sciences · 2020Review
- Involvement of Astrocytes in Alzheimer's Disease from a Neuroinflammatory and Oxidative Stress Perspective.Frontiers in molecular neuroscience · 2017Review
- Article
- Embracing failure: What the Phase III progesterone studies can teach about TBI clinical trials.Brain injury · 2015Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A correlation between metabolic alterations of neuroactive steroids and Alzheimer's disease remains unknown. In the present study, amyloid beta (Aβ) 25-35 (Aβ25-35) injected into the bilateral hippocampus CA1 region significantly reduced learning and memory. At the biochemical level, hippocampal levels of pregnenolone were significantly reduced with Aβ25-35 treatment. Furthermore, progesterone was considerably decreased in the prefrontal cortex and hippocampus, and 17β-estradiol was significantly elevated. To our knowledge, this is the first report showing that Aβ25-35, a main etiological factor of Alzheimer's disease, can alter the level and metabolism of neuroactive steroids in the prefrontal cortex and hippocampus, which are brain regions significantly involved in learning and memory. Aβ25-35 exposure also increased the expression of inflammatory mediators, tumor necrosis factor-α and interleukin-1β. However, subcutaneous injection of progesterone reversed the upregulation of tumor necrosis factor-α and interleukin-1β in a dose-dependent manner. Concomitant with improved cognitive abilities, progesterone blocked Aβ-mediated inflammation and increased the survival rate of hippocampal pyramidal cells. We thus hypothesize that Aβ-mediated cognitive deficits may occur via changes in neuroactive steroids. Moreover, our findings provide a possible therapeutic strategy for Alzheimer's disease via neuroactive steroids, particularly progesterone.
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