Abnormality of m6A mRNA methylation is involved in Alzheimer’s disease
Open accessAbstract
Alzheimer's disease (AD), the most common form of dementia, is highly prevalent in older adults. The main clinical feature is the progressive decline of memory function, which eventually leads to the decline of cognitive function. At present, the pathogenesis of AD is unclear. In the disease process, synaptic changes are the key. Recent studies have shown that the dysregulation of RNA methylation is related to many biological processes, including neurodevelopment and neurodegenerative diseases. N6-methyladenosine (m6A) is the most abundant modification in eukaryotic RNA. In this study, RNA m6A methylation was quantified in APP/PS1 transgenic mice, which is an AD mouse model, and C57BL/6 control mice, and data showed that m6A methylation was elevated in the cortex and the hippocampus of APP/PS1 transgenic mice. Next, the alterations of m6A RNA methylation in AD and in C57BL/6 mice were investigated using high-throughput sequencing. Genome-wide maps of m6A mRNA showed that the degrees of m6A methylation were higher in many genes and lower in others in AD mice. Interestingly, the expression of the m6A methyltransferase METTL3 was elevated and that of the m6A demethylase FTO was decreased in AD mice. The data were analyzed by gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, and pathways that might be related to synaptic or neuron development and growth were constructed. The related pathways and genes predicted the potential roles of the differentially expressed m6A methylation RNA in AD. Collectively, our findings demonstrate that the m6A methylation of RNA promotes the development of AD.
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m6A does not appear to accumulate in models of Aβ amyloidosis, which accumulate aggregates extracellularly.
“Interestingly, m6A does not appear to accumulate in models of Aβ amyloidosis, which accumulate aggregates extracellularly (Han et al., 2020).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Han et al., 2020
The Results section, “m6A RNA Methylation Level in the Cortex and the Hippocampus of AD” (page unavailable), reports significantly higher m6A methylation in APP/PS1 mice than in controls in both regions. The separate Results section on Aβ deposition reports increased Aβ in those mice. Thus, this paper reports m6A accumulation in an Aβ-depositing model, contrary to the cited claim. (LLM, conf=0.92)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredTotal m6A levels were reported in a previous manuscript examining m6A in an AD model utilizing over-expression of only APP, which exhibits Aβ accumulation without corresponding MAPT pathology.
“Total m6A levels were also reported in a previous manuscript examining m6A in an AD model utilizing over-expression of only APP, which is a model that exhibits Aβ accumulation without corresponding MAPT pathology (Han et al., 2020).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Han et al., 2020
The Abstract reports quantified m6A levels in an AD mouse model, and the Results report increased Aβ deposition. But Materials and Methods identifies the model as APP/PS1 double-transgenic mice, not mice overexpressing only APP. The cited passages do not establish an absence of MAPT pathology. (LLM, conf=0.90)
Experimental — accuracy not yet measuredThe absence of MAPT pathology in the APP-overexpression model produced a corresponding absence of m6A accumulation.
“Data from this manuscript suggest that the absence of MAPT pathology in this model produced a corresponding absence of m6A accumulation (Han et al., 2020).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as Han et al., 2020
The Methods (Mouse Models) identify the animals as APP/PS1 mice, not the APP-overexpression model in the claim. The Results (m6A RNA Methylation Level in the Cortex and the Hippocampus of AD) report increased m6A in those mice, but our copy does not assess MAPT pathology or whether its absence explains a lack of m6A accumulation in another model. (LLM, conf=0.76)
Experimental — accuracy not yet measured
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- Authors
- Han, M., Liu, Z., Xu, Y., Liu, X., Wang, D., Li, F., Wang, Y., & Bi, J.
- Affiliations
- Second Hospital of Shandong University (CN)
- Shandong University (CN)
- Corresponding author
- Wang, Yun
- Venue
- Frontiers in Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2020-02-28
- Volume
- 14
- Pages
- 98-98
- ISSN
- 1662-453X (ISSN-L)
- PMC
- PMC7058666
- OpenAlex
- W3008232393
- Cited by
- 286
- References
- 29
- Citations by year
- 2026: 26 · 2025: 25 · 2024: 43 · 2023: 64 · 2022: 52 · 2021: 62 · 2020: 14
- FWCI
- 16.79
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA modifications and cancer
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA regulation and disease
- Keywords
- Alzheimer's disease, N6-methyladenosine, RNA methylation, APP/PS1 mice, synaptic dysfunction, hippocampus, cortex, neurodegeneration
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