Evidence map›Paper›PMID 41051385›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Uric Acid Functions as an Endogenous Modulator of Microglial Function and Amyloid Clearance in Alzheimer's Disease.

De Xie, Qiuyang Zheng, Jiaming Lv, Qian Zhang, Zhiwei Cui, Shuai Huang, Wei Yu, Binyang Chen, Wanling Que, Shanpan Fu and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

19 authors.

De XieDepartment of Internal Medicine, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.ORCID https://orcid.org/0000-0002-2127-0558
Qiuyang ZhengState Key Laboratory of Cellular Stress Biology, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Shenzhen Research Institute, Xiamen University, Xiamen, Fujian, 361102, China.
Jiaming LvDepartment of Internal Medicine, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Qian ZhangDepartment of Internal Medicine, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Zhiwei CuiThe First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China.
Shuai HuangDepartment of Internal Medicine, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Wei YuDepartment of Internal Medicine, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Binyang ChenDepartment of Internal Medicine, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Wanling QueDepartment of Internal Medicine, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Shanpan FuDepartment of Internal Medicine, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Yuemei XiDepartment of Internal Medicine, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Jiayu ChenDepartment of Internal Medicine, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Xueling YeDepartment of Internal Medicine, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Shuyi ChenDepartment of Internal Medicine, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Hairong ZhaoDepartment of Internal Medicine, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Tetsuya YamamotoDepartment of Health Evaluation Center, Osaka Gyoumeikan Hospital, Osaka, 554-0012, Japan.
Hidenori KoyamaDepartment of Diabetes, Endocrinology and Clinical Immunology, Hyogo College of Medicine, Nishinomiya, Hyogo, 663-8501, Japan.
Xin WangState Key Laboratory of Cellular Stress Biology, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Shenzhen Research Institute, Xiamen University, Xiamen, Fujian, 361102, China.
Jidong ChengDepartment of Internal Medicine, Xiang'an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.ORCID https://orcid.org/0000-0002-5909-5759

Funding

Alzheimer's Disease Neuroimaging Initiative - SupplementU01AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI WEINER, MICHAEL W · 2004 to 2015
$121.0M
DOD ADNI W81XWH-12-2-0012Fujian Provincial Industry-University-Research Collaborative Innovation Project Plan 2022Y4007National Natural Science Foundation of China 82260163National Natural Science Foundation of China 82271451National Natural Science Foundation of China 82370895Natural Science Foundation of Fujian Province 2020J01018NIA NIH HHS U01 AG024904
6 · The paper itself

Abstract

Epidemiological studies have linked uric acid (UA), the end product of purine metabolism in humans, with reduced Alzheimer's disease (AD) risk. Decreased serum UA levels are observed in AD patients versus age-matched controls, while upstream purine metabolites remained unchanged. In 5×FAD mice, two months of UA supplementation improved cognitive function and reduced amyloid plaque burden. Mechanistically, UA enhances microglial amyloid-β (Aβ) phagocytosis and induces transcriptional reprogramming in AD mouse microglia, characterized by upregulated phagocytic pathways and attenuated inflammatory responses. UA treatment restored the recycling of Aβ receptors CD36 and TREM2 in microglia, enhanced lysosomal biogenesis, and facilitated Aβ degradation. These findings identify UA as a critical endogenous modulator of microglial Aβ processing and suggest exploring UA supplementation as a therapeutic strategy for AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesMicrogliaUric AcidAnimalsDisease Models, AnimalHumansMaleMiceMice, TransgenicPhagocytosisPlaque, AmyloidAmyloid beta-PeptidesUric AcidAlzheimer's diseaseamyloid‐βmicrogliauric acid

Identifiers

PMID41051385
PMCPMC12752628

What OpenQuestion holds

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Registered trials

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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.