Evidence map›Paper›PMID 41700129›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2026

Astrocytic PYGM attenuates tau pathology by promoting lactate-mediated neuroprotection.

Jing Cao, Jian Meng, Yiqing Chen, Ziqian Tang, Yong Wang, Kun Li, Xian Zhang, Hong Luo, Huihui Li, Zhanxiang Wang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2026. 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. Article
  2. Astrocytic PYGM attenuates tau pathology by promoting lactate-mediated neuroprotection.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    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

11 authors.

Jing CaoXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, China.
Jian MengXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, China.
Yiqing ChenXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, China.
Ziqian TangXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, China.
Yong WangXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, China.
Kun LiXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, China.
Xian ZhangXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, China.
Hong LuoXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, China.
Huihui LiXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, China.
Zhanxiang WangXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, China.
Yun-Wu ZhangXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, China.ORCID https://orcid.org/0000-0002-7152-7630

Funding

Changping Laboratory 2025B-07-39Fujian Provincial Natural Science Foundation of China 2023J011624Nanqiang Outstanding Young Talents Program from Xiamen University 0070/X2450216National Natural Science Foundation of China 82130039National Natural Science Foundation of China 82371420National Natural Science Foundation of China U21A20361Natural Science Foundation of Xiamen Municipality, China 3502Z202373012Postdoctoral Fellowship Program of China Postdoctoral Science Foundation GZB20230385Scientific Research Project for Health and Hygiene of Fujian Province 2023ZQNZD018State Key Laboratory of Vaccines for Infectious DiseasesXiang An Biomedicine Laboratory 2023XAKJ0102054
6 · The paper itself

Abstract

introductionTauopathies are characterized by hyperphosphorylated tau accumulation and neurodegeneration. Although astrocytic metabolism is known to support neuronal health, the role of astrocytic glycogen metabolism, particularly the glycogenolytic enzyme PYGM (glycogen phosphorylase, muscle associated), in tauopathies remains unclear.

methodsWe analyzed PYGM expression in the brains of frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U) patients and tau

resultsPYGM expression increased in the brains of FTLD-U patients and the astrocytes of PS19 mice. Astrocytic PYGM deficiency impaired mouse cognition, exacerbated tauopathy-related phenotypes in male PS19 mice, and disrupted astrocyte-neuron metabolic coupling. PYGM overexpression and lactate supplementation attenuated tauopathy-related phenotypes in male PS19 mice. DISCUSSION: Astrocytic PYGM supports neuronal health by sustaining lactate-mediated astrocyte-neuron metabolic coupling. Enhancing astrocytic glycogenolysis may be beneficial in tauopathies.

Indexed as

AstrocytesGlycogen PhosphorylaseLactic AcidNeuroprotectionTauopathiesAnimalsBrainDisease Models, AnimalHumansMaleMiceMice, TransgenicNeuronstau ProteinsGlycogen PhosphorylaseLactic Acidtau Proteinsastrocyteglycogen metabolismlactatePYGMtautauopathy

Identifiers

PMID41700129
PMCPMC12910249

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.