ArticleNature neuroscience2023
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Article in Nature neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
12.3field-weighted citation impact, top 1% of its field
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 70 citations in OpenAlex.
- Exploring the role of β2-microglobulin in the relationship between physical activity and DNAm-predicted PhenoAge: Evidence from a population-based and mice single-cell RNA-sequencing study.Journal of advanced research · 2026Article
- Aberrant GRP78 Phase Transition Sustains Endothelial IRE1α Signaling and Drives Blood-Brain Barrier Failure in Cerebral Amyloid Angiopathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Tau aggregates cause reactivation of transposable DNA elements, leading to Z-RNA-ZBP1-mediated neuronal death.Nature neuroscience · 2026Article
- Molecular Mechanisms of Neurodegenerative Diseases: Emerging Biomarkers and Therapeutic Targets.Brain sciences · 2026Review
- Longitudinal Transcriptomic Analysis Reveals Systemic Effects of Risdiplam in Adults with Spinal Muscular Atrophy.Brain sciences · 2026Article
- Engineering Immune Cell to Counteract Aging and Aging-Associated Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Endothelial epigenetic senescence driven microglial activation mediates cardio-retinal neuroinflammation in heart failure.Theranostics · 2026Article
- Association between Alzheimer's disease and MHC-I antigen processing and presentation pathway: a narrative review.Frontiers in immunology · 2026Review
- Microglial RUNX1/RBM47 ablation inhibits neuronal ferroptosis via regulating the cGAS-STING-MEF2C pathway in mice with postoperative cognitive dysfunction.Communications biology · 2025Article
- Investigating the binding potential of the Melissa officinalis oil against Alzheimer's targets by molecular docking and in vitro evaluations.Scientific reports · 2025Article
- Natural Small-Molecule Bergapten Ameliorates Amyloid-β Pathology and Neuroinflammation in Alzheimer's Disease.Nutrients · 2025Article
- Molecular and neuropathological determinants of neuronal dysfunction in Alzheimer's disease.bioRxiv : the preprint server for biology · 2025Article
- Adaptive immunity in the neuroinflammation of Alzheimer's disease.Chinese medical journal · 2025Review
- CDK5-mediated hyperphosphorylation of Tau217 impairs neuronal synaptic structure and exacerbates cognitive impairment in Alzheimer's disease.Translational psychiatry · 2025Article
- Comparison of inflammatory biomarker levels in neurodegenerative proteinopathies: a case-control study.Journal of neural transmission (Vienna, Austria : 1996) · 2025Article
- Identification and Exploration of Immunity-Related Genes and Natural Products for Alzheimer's Disease Based on Bioinformatics, Molecular Docking, and Molecular Dynamics.Immunity, inflammation and disease · 2025Article
- Peripheral and central neuroimmune mechanisms in Alzheimer's disease pathogenesis.Molecular neurodegeneration · 2025Review
- CD22 modulation alleviates amyloid β-induced neuroinflammation.Journal of neuroinflammation · 2025Article
- Alzheimer's disease: insights into pathology, molecular mechanisms, and therapy.Protein & cell · 2025Review
- Cerebrospinal fluid β2-microglobulin promotes the tau pathology through microglia-astrocyte communication in Alzheimer's disease.Alzheimer's research & therapy · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 7 institutions in 2 countries.
Yini ZhaoState Key Laboratory of Cellular Stress Biology, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Qiuyang ZhengState Key Laboratory of Cellular Stress Biology, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.ORCID http://orcid.org/0000-0001-7843-3365
Yujuan HongState Key Laboratory of Cellular Stress Biology, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Yue GaoState Key Laboratory of Cellular Stress Biology, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Jiaojiao HuInterdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, China.
Maoju LangState Key Laboratory of Cellular Stress Biology, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Hongfeng ZhangState Key Laboratory of Cellular Stress Biology, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Ying ZhouNational Institute for Data Science in Health and Medicine, School of Medicine, Xiamen University, Xiamen, China.ORCID http://orcid.org/0000-0001-8276-2735
Hong LuoState Key Laboratory of Cellular Stress Biology, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.
Xian ZhangState Key Laboratory of Cellular Stress Biology, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.ORCID http://orcid.org/0000-0003-3905-0489
Hao SunState Key Laboratory of Cellular Stress Biology, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China.ORCID http://orcid.org/0000-0002-3670-2886
Xiao-Xin YanDepartment of Anatomy and Neurobiology, Central South University Xiangya Medical School, Changsha, China.
Timothy Y HuangDegenerative Diseases Program, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA, USA.ORCID http://orcid.org/0000-0002-3504-9459
Yan-Jiang WangDepartment of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, China.
Huaxi XuCenter for Brain Sciences, the First Affiliated Hospital of Xiamen University, Institute of Neuroscience, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Xiamen University, Xiamen, China.ORCID http://orcid.org/0000-0001-7031-7853
Cong LiuInterdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, China.ORCID http://orcid.org/0000-0003-3425-6672
Xin WangState Key Laboratory of Cellular Stress Biology, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Faculty of Medicine and Life Sciences, Xiamen University, Xiamen, China. wangx@xmu.edu.cn.ORCID http://orcid.org/0000-0003-2421-4639
Xiamen University · CNChinese Academy of Sciences · CNArmy Medical University · CNCentral South University · CNFirst Affiliated Hospital of Xiamen University · CNSanford Burnham Prebys Medical Discovery Institute · USShenzhen University · CN
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extensive studies indicate that β-amyloid (Aβ) aggregation is pivotal for Alzheimer's disease (AD) progression; however, cumulative evidence suggests that Aβ itself is not sufficient to trigger AD-associated degeneration, and whether other additional pathological factors drive AD pathogenesis remains unclear. Here, we characterize pathogenic aggregates composed of β
Indexed as
Alzheimer DiseaseCognition DisordersAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsBrainCognitionDisease Models, AnimalMiceMice, TransgenicPlaque, AmyloidAmyloid beta-PeptidesAmyloid beta-Protein Precursor
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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.