PRMT3‐Mediated H4R3me2a Promotes Primary Age‐Related Tauopathy by Driving Tau Hyperphosphorylation in Neuron Article Swipe
Haotian Liu
,
Xinnan Liu
,
Fengyuan Tian
,
Yashuang Chen
,
Jingying Li
,
Xue Wang
,
Wenying Qiu
,
Xia Wang
,
Chao Ma
,
Wei Ge
·
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1002/advs.202506044
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1002/advs.202506044
Primary age‐related tauopathy (PART) and Alzheimer's disease (AD) both exhibit 3R/4R hyperphosphorylated tau‐positive neurofibrillary tangles (NFTs) within the hippocampal–entorhinal system. Notably, PART patients show a higher degree of tau hyperphosphorylation in the entorhinal cortex (EC) than AD, yet the molecular mechanisms driving Aβ‐independent tau hyperphosphorylation in PART remain poorly understood. Herein, through transcriptomic profiling of postmortem EC tissues and in vitro and in vivo functional validation, the present study identifies protein arginine methyltransferase 3 (PRMT3) as a critical driver of tau hyperphosphorylation. Mechanistically, PRMT3‐mediated tau hyperphosphorylation is dependent on asymmetric dimethylation of histone H4 at arginine 3 (H4R3me2a), which upregulates miR‐448. Elevated miR‐448 specifically targets and suppresses IGF1R, leading to downstream GSK3β activation and subsequent tau hyperphosphorylation through PI3K/AKT/GSK3β signaling. Treatment with SGC707, a selective PRMT3 inhibitor, effectively reduces tau hyperphosphorylation and demonstrates therapeutic promise for PART and potentially other tauopathies. Collectively, this study defines the PRMT3/H4R3me2a/miR‐448 axis as a critical regulatory pathway in tau hyperphosphorylation within PART, underscoring the potential of PRMT3 inhibition as a targeted therapeutic strategy for tauopathies.
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- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1002/advs.202506044
- https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/advs.202506044
- OA Status
- gold
- References
- 74
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4410246492
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Raw OpenAlex JSON
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https://openalex.org/W4410246492Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1002/advs.202506044Digital Object Identifier
- Title
-
PRMT3‐Mediated H4R3me2a Promotes Primary Age‐Related Tauopathy by Driving Tau Hyperphosphorylation in NeuronWork title
- Type
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articleOpenAlex work type
- Language
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enPrimary language
- Publication year
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2025Year of publication
- Publication date
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2025-05-08Full publication date if available
- Authors
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Haotian Liu, Xinnan Liu, Fengyuan Tian, Yashuang Chen, Jingying Li, Xue Wang, Wenying Qiu, Xia Wang, Chao Ma, Wei GeList of authors in order
- Landing page
-
https://doi.org/10.1002/advs.202506044Publisher landing page
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https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/advs.202506044Direct link to full text PDF
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YesWhether a free full text is available
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goldOpen access status per OpenAlex
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https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/advs.202506044Direct OA link when available
- Concepts
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Tauopathy, Neuroscience, Primary (astronomy), Hyperphosphorylation, Neuron, Chemistry, Biology, Cell biology, Medicine, Physics, Disease, Neurodegeneration, Internal medicine, Phosphorylation, AstronomyTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
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74Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.this | 143 |
| abstract_inverted_index.vivo | 64 |
| abstract_inverted_index.with | 122 |
| abstract_inverted_index.3R/4R | 11 |
| abstract_inverted_index.PART, | 158 |
| abstract_inverted_index.PRMT3 | 126, 163 |
| abstract_inverted_index.other | 140 |
| abstract_inverted_index.study | 69, 144 |
| abstract_inverted_index.vitro | 61 |
| abstract_inverted_index.which | 99 |
| abstract_inverted_index.(NFTs) | 16 |
| abstract_inverted_index.(PART) | 4 |
| abstract_inverted_index.GSK3β | 112 |
| abstract_inverted_index.IGF1R, | 108 |
| abstract_inverted_index.cortex | 34 |
| abstract_inverted_index.degree | 27 |
| abstract_inverted_index.driver | 79 |
| abstract_inverted_index.higher | 26 |
| abstract_inverted_index.poorly | 49 |
| abstract_inverted_index.remain | 48 |
| abstract_inverted_index.within | 17, 157 |
| abstract_inverted_index.(PRMT3) | 75 |
| abstract_inverted_index.Herein, | 51 |
| abstract_inverted_index.Primary | 1 |
| abstract_inverted_index.SGC707, | 123 |
| abstract_inverted_index.defines | 145 |
| abstract_inverted_index.disease | 7 |
| abstract_inverted_index.driving | 42 |
| abstract_inverted_index.exhibit | 10 |
| abstract_inverted_index.histone | 93 |
| abstract_inverted_index.leading | 109 |
| abstract_inverted_index.pathway | 153 |
| abstract_inverted_index.present | 68 |
| abstract_inverted_index.promise | 135 |
| abstract_inverted_index.protein | 71 |
| abstract_inverted_index.reduces | 129 |
| abstract_inverted_index.system. | 20 |
| abstract_inverted_index.tangles | 15 |
| abstract_inverted_index.targets | 105 |
| abstract_inverted_index.through | 52, 118 |
| abstract_inverted_index.tissues | 58 |
| abstract_inverted_index.Abstract | 0 |
| abstract_inverted_index.Elevated | 102 |
| abstract_inverted_index.Notably, | 21 |
| abstract_inverted_index.arginine | 72, 96 |
| abstract_inverted_index.critical | 78, 151 |
| abstract_inverted_index.patients | 23 |
| abstract_inverted_index.strategy | 169 |
| abstract_inverted_index.targeted | 167 |
| abstract_inverted_index.Treatment | 121 |
| abstract_inverted_index.dependent | 88 |
| abstract_inverted_index.miR‐448 | 103 |
| abstract_inverted_index.molecular | 40 |
| abstract_inverted_index.potential | 161 |
| abstract_inverted_index.profiling | 54 |
| abstract_inverted_index.selective | 125 |
| abstract_inverted_index.tauopathy | 3 |
| abstract_inverted_index.activation | 113 |
| abstract_inverted_index.asymmetric | 90 |
| abstract_inverted_index.downstream | 111 |
| abstract_inverted_index.entorhinal | 33 |
| abstract_inverted_index.functional | 65 |
| abstract_inverted_index.identifies | 70 |
| abstract_inverted_index.inhibition | 164 |
| abstract_inverted_index.inhibitor, | 127 |
| abstract_inverted_index.mechanisms | 41 |
| abstract_inverted_index.miR‐448. | 101 |
| abstract_inverted_index.postmortem | 56 |
| abstract_inverted_index.regulatory | 152 |
| abstract_inverted_index.signaling. | 120 |
| abstract_inverted_index.subsequent | 115 |
| abstract_inverted_index.suppresses | 107 |
| abstract_inverted_index.(H4R3me2a), | 98 |
| abstract_inverted_index.Alzheimer's | 6 |
| abstract_inverted_index.effectively | 128 |
| abstract_inverted_index.potentially | 139 |
| abstract_inverted_index.therapeutic | 134, 168 |
| abstract_inverted_index.understood. | 50 |
| abstract_inverted_index.upregulates | 100 |
| abstract_inverted_index.validation, | 66 |
| abstract_inverted_index.demonstrates | 133 |
| abstract_inverted_index.specifically | 104 |
| abstract_inverted_index.tauopathies. | 141, 171 |
| abstract_inverted_index.underscoring | 159 |
| abstract_inverted_index.Collectively, | 142 |
| abstract_inverted_index.age‐related | 2 |
| abstract_inverted_index.dimethylation | 91 |
| abstract_inverted_index.tau‐positive | 13 |
| abstract_inverted_index.transcriptomic | 53 |
| abstract_inverted_index.PI3K/AKT/GSK3β | 119 |
| abstract_inverted_index.neurofibrillary | 14 |
| abstract_inverted_index.Mechanistically, | 83 |
| abstract_inverted_index.PRMT3‐mediated | 84 |
| abstract_inverted_index.Aβ‐independent | 43 |
| abstract_inverted_index.methyltransferase | 73 |
| abstract_inverted_index.hyperphosphorylated | 12 |
| abstract_inverted_index.hyperphosphorylation | 30, 45, 86, 117, 131, 156 |
| abstract_inverted_index.hyperphosphorylation. | 82 |
| abstract_inverted_index.PRMT3/H4R3me2a/miR‐448 | 147 |
| abstract_inverted_index.hippocampal–entorhinal | 19 |
| cited_by_percentile_year | |
| countries_distinct_count | 1 |
| institutions_distinct_count | 10 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.6700000166893005 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.16245924 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |