ArticleTranslational neurodegeneration2013
Effects of 17-allylamino-17-demethoxygeldanamycin (17-AAG) in transgenic mouse models of frontotemporal lobar degeneration and Alzheimer's disease.
Article in Translational neurodegeneration, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- Pharmacokinetics, Dose-Proportionality, and Tolerability of Intravenous Tanespimycin (17-AAG) in Single and Multiple Doses in Dogs: A Potential Novel Treatment for Canine Visceral Leishmaniasis.Pharmaceuticals (Basel, Switzerland) · 2024Article
- HSF1 and Its Role in Huntington's Disease Pathology.Advances in experimental medicine and biology · 2023Review
- Hsp90: From Cellular to Organismal Proteostasis.Cells · 2022Review
- Effects of Deferasirox in Alzheimer's Disease and Tauopathy Animal Models.Biomolecules · 2022Article
- Impact of Heat Shock Proteins in Neurodegeneration: Possible Therapeutical Targets.Annals of neurosciences · 2022Review
- TRAP1 in Oxidative Stress and Neurodegeneration.Antioxidants (Basel, Switzerland) · 2021Review
- Expanding the role of proteasome homeostasis in Parkinson's disease: beyond protein breakdown.Cell death & disease · 2021Review
- Molecular Dysfunctions of Mitochondria-Associated Membranes (MAMs) in Alzheimer's Disease.International journal of molecular sciences · 2020Review
- Mechanistic Insights into the Role of Molecular Chaperones in Protein Misfolding Diseases: From Molecular Recognition to Amyloid Disassembly.International journal of molecular sciences · 2020Review
- HSP70 and HSP90 in neurodegenerative diseases.Neuroscience letters · 2020Review
- Heat Shock Proteins in Alzheimer's Disease: Role and Targeting.International journal of molecular sciences · 2018Review
- Promoting the clearance of neurotoxic proteins in neurodegenerative disorders of ageing.Nature reviews. Drug discovery · 2018Review
- Clusterin protects neurons against intracellular proteotoxicity.Acta neuropathologica communications · 2017Article
- Enhanced tau pathology via RanBP9 and Hsp90/Hsc70 chaperone complexes.Human molecular genetics · 2017Article
- Hsp90 regulation of fibroblast activation in pulmonary fibrosis.JCI insight · 2017Article
- The entangled ER-mitochondrial axis as a potential therapeutic strategy in neurodegeneration: A tangled duo unchained.Cell calcium · 2016Review
- Behind the curtain of tauopathy: a show of multiple players orchestrating tau toxicity.Cellular and molecular life sciences : CMLS · 2016Review
- Mapping neuroinflammation in frontotemporal dementia with molecular PET imaging.Journal of neuroinflammation · 2015Review
- NeuroTransDB: highly curated and structured transcriptomic metadata for neurodegenerative diseases.Database : the journal of biological databases and curation · 2015Article
- Targeting Hsp90 and its co-chaperones to treat Alzheimer's disease.Expert opinion on therapeutic targets · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD), the most common dementia, is characterized by potentially neurotoxic aggregation of Aβ peptide and tau protein, and their deposition as amyloid plaques and neurofibrillary tangles (NFTs). Tau aggregation also occurs in other common neurodegenerative diseases. Frontotemporal dementia (FTD) can be caused by tau mutations that increase the susceptibility of tau to hyperphosphorylation and aggregation, which may cause neuronal dysfunction and deposition of NFTs. 17-allylamino-17-demethoxygeldanamycin (17-AAG) is a potent inhibitor of heat shock protein 90 (Hsp90), a cytosolic chaperone implicated in the proper folding and functions of a repertoire of client proteins. 17-AAG binds to Hsp90 and enhances degradation of Hsp90 client protein. We sought to determine whether 17-AAG can reduce Aβ and tau pathology in the brains of AD and FTD model mice expressing Aβ or P301L mutant tau, respectively. Mice were randomized to receive 25, 5, or 0 mg/kg 17-AAG thrice weekly from age eight to 11 months. Analysis was performed by rotarod test on motor function, on the area occupied by plaques in hippocampus or NFTs in medulla tissue sections, and on mortality. A high dose of 17-AAG tended to decrease NFTs in male mice (p = 0.08). Further studies are required to confirm the effect of 17-AAG in diseases of tau aggregation.
Identifiers
What OpenQuestion holds
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.