ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2020
Allopregnanolone Reverses Bioenergetic Deficits in Female Triple Transgenic Alzheimer's Mouse Model.
Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Neurosteroid-Mediated Neuroprotection via mTORC1/AMPK/BDNF Signaling Pathway in Alzheimer's Disease.Molecular neurobiology · 2026Review
- Etifoxine drives macrophage M2 polarization via Schwann cell-derived progesterone activation of PPARγ to accelerate peripheral nerve repair.Frontiers in cellular neuroscience · 2026Article
- Accelerated midlife endocrine and bioenergetic brain aging in APOE4 females.Frontiers in aging neuroscience · 2025Article
- Establishment of a graphene quantum dot (GQD) based steroid binding assay for the nuclear progesterone receptor (pgr).Biochemistry and biophysics reports · 2024Article
- Establishment of a steroid binding assay for goldfish membrane progesterone receptor (mPR) by coupling with graphene quantum dots (GQDs).Fish physiology and biochemistry · 2024Article
- Biochemical Profiling of Urine Metabolome in Premature Infants Based on LC-MS Considering Maternal Influence.Nutrients · 2024Article
- Brain-derived neuerotrophic factor and related mechanisms that mediate and influence progesterone-induced neuroprotection.Frontiers in endocrinology · 2024Review
- Potential association between COVID-19 and neurological disorders: analysis of common genes and therapeutics.Frontiers in neurology · 2024Article
- Exploring the potential anti-Alzheimer disease mechanisms of Alpiniae Oxyphyliae Fructus by network pharmacology study and molecular docking.Metabolic brain disease · 2023Article
- Allopregnanolone pleiotropic action in neurons and astrocytes: calcium signaling as a unifying mechanism.Frontiers in endocrinology · 2023Article
- Allopregnanolone: An overview on its synthesis and effects.Journal of neuroendocrinology · 2022Review
- Progesterone and Allopregnanolone Neuroprotective Effects in the Wobbler Mouse Model of Amyotrophic Lateral Sclerosis.Cellular and molecular neurobiology · 2022Review
- Review
- From Menopause to Neurodegeneration-Molecular Basis and Potential Therapy.International journal of molecular sciences · 2021Review
- Natural products targeting mitochondria: emerging therapeutics for age-associated neurological disorders.Pharmacology & therapeutics · 2021Review
- Insights into Disease-Associated Tau Impact on Mitochondria.International journal of molecular sciences · 2020Review
- Progesterone in the Brain: Hormone, Neurosteroid and Neuroprotectant.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Previously, we reported that the neurosteroid allopregnanolone (Allo) promoted neural stem cell regeneration, restored cognitive function, and reduced Alzheimer's Disease (AD) pathology in the triple transgenic Alzheimer's mouse model (3xTgAD). To investigate the underlying systems biology of Allo action in AD models in vivo, we assessed the regulation of Allo on the bioenergetic system of the brain. Outcomes of these analysis indicated that Allo significantly reversed deficits in mitochondrial respiration and biogenesis and key mitochondrial enzyme activity and reduced lipid peroxidation in the 3xTgAD mice in vivo. To explore the mechanisms by which Allo regulates the brain metabolism, we conducted targeted transcriptome analysis. These data further confirmed that Allo upregulated genes involved in glucose metabolism, mitochondrial bioenergetics, and signaling pathways while simultaneously downregulating genes involved in Alzheimer's pathology, fatty acid metabolism, and mitochondrial uncoupling and dynamics. Upstream regulatory pathway analysis predicted that Allo induced peroxisome proliferator-activated receptor gamma (PPARG) and coactivator 1-alpha (PPARGC1A) pathways while simultaneously inhibiting the presenilin 1 (PSEN 1), phosphatase and tensin homolog (PTEN), and tumor necrosis factor (TNF) pathways to reduce AD pathology. Collectively, these data indicate that Allo functions as a systems biology regulator of bioenergetics, cholesterol homeostasis, and β-amyloid reduction in the brain. These systems are critical to neurological health, thus providing a plausible mechanistic rationale for Allo as a therapeutic to promote neural cell function and reduce the burden of AD pathology.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.