ArticleCurrent Alzheimer research2012
Allopregnanolone increases the number of dopaminergic neurons in substantia nigra of a triple transgenic mouse model of Alzheimer's disease.
Article in Current Alzheimer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 41 citations in OpenAlex.
- Allopregnanolone pleiotropic action in neurons and astrocytes: calcium signaling as a unifying mechanism.Frontiers in endocrinology · 2023Article
- EndogenousNeural regeneration research · 2022Review
- Nmnat1 Modulates Mitochondrial Oxidative Stress by Inhibiting Caspase-3 Signaling in Alzheimer's Disease.Journal of molecular neuroscience : MN · 2021Article
- The mechanistic link between selective vulnerability of the locus coeruleus and neurodegeneration in Alzheimer's disease.Acta neuropathologica · 2021Review
- Allopregnanolone Improves Locomotor Activity and Arousal in the Aged CGG Knock-in Mouse Model of Fragile X-Associated Tremor/Ataxia Syndrome.Frontiers in neuroscience · 2021Article
- [Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020Article
- Retracted: Allopregnanolone restores the tyrosine hydroxylase-positive neurons and motor performance in a 6-OHDA-injected mouse model.CNS neuroscience & therapeutics · 2020Article
- 1,25(OH)International journal of molecular sciences · 2020Article
- GABA-A receptor modulating steroids in acute and chronic stress; relevance for cognition and dementia?Neurobiology of stress · 2020Article
- Mitochondria modulatory effects of new TSPO ligands in a cellular model of tauopathies.Journal of neuroendocrinology · 2020Article
- Allopregnanolone Modulates GABAAR-Dependent CaMKIIδ3 and BDNF to Protect SH-SY5Y Cells Against 6-OHDA-Induced Damage.Frontiers in cellular neuroscience · 2019Article
- TSPO Ligands Boost Mitochondrial Function and Pregnenolone Synthesis.Journal of Alzheimer's disease : JAD · 2019Article
- Neurosteroid Metabolites of Gonadal Steroid Hormones in Neuroprotection: Implications for Sex Differences in Neurodegenerative Disease.Frontiers in molecular neuroscience · 2018Review
- Monoaminergic neuropathology in Alzheimer's disease.Progress in neurobiology · 2017Review
- Neurotrophic natural products: chemistry and biology.Angewandte Chemie (International ed. in English) · 2014Review
- Allopregnanolone and neurogenesis in the nigrostriatal tract.Frontiers in cellular neuroscience · 2014Review
- Age-related changes in neuroactive steroid levels in 3xTg-AD mice.Neurobiology of aging · 2013Article
- Neurosteroids as regenerative agents in the brain: therapeutic implications.Nature reviews. Endocrinology · 2013Review
- Neuroregeneration and dementia: new treatment options.Journal of molecular psychiatry · 2013Review
- Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
More than a third of Alzheimer's disease (AD) patients show nigrostriatal pathway disturbances, resulting in akinesia (inability to initiate movement) and bradykinesia (slowness of movement). The high prevalence of this dysfunction of dopaminergic neuron in the nigrostriatal pathway in AD suggests that the risk factors for AD appear also significant risk factors for substantia nigra pars compacta (SNpc) lesions. Previously, we have demonstrated that allopregnanolone (APα) promotes neurogenesis and improves the cognitive function in a triple transgenic mouse model of AD (3xTgAD). In this study, we sought to exam 1) the SNpc lesions in 3xTgAD mice and 2) the impact of APα on promoting the regeneration of new dopaminergic neurons in SNpc of the 3xTgAD mice. The number of Nissl-stained total neurons, tyrosine hydroxylase (TH) positive neurons, and BrdU/TH double positive newly formed neurons were analyzed with unbiased stereology. In the SNpc of 3xTgAD mice, TH positive neurons was 47+- 18 % (p = 0.007), total neurons was 62 +-11.6 % (p = 0.016), of those in the SNpc of non-Tg mice, respectively. APα treatment increased the TH positive neurons in the SNpc of 3xTgAD mice to 93.2 +- 18.5 (p = 0.021 vs. 3xTgAD vehicle) and the total neurons to 84.9+- 6.6 (p = 0.046 vs. 3xTgAD vehicle) of non-Tg mice. These findings indicate that there is a loss of neurons, specifically the TH positive neurons in SNpc of 3xTgAD mice, and that APα reverses the lesion in SNpc of 3xTgAD by increasing the formation of new TH neurons.
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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.