Evidence map›Paper›PMID 34158119›Full record

ArticleActa neuropathologica communications2021

Equilibrative nucleoside transporter 1 inhibition rescues energy dysfunction and pathology in a model of tauopathy.

Ching-Pang Chang, Ya-Gin Chang, Pei-Yun Chuang, Thi Ngoc Anh Nguyen, Kuo-Chen Wu, Fang-Yi Chou, Sin-Jhong Cheng, Hui-Mei Chen, Lee-Way Jin, Kevin Carvalho and 6 more

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.4field-weighted citation impact, top 12% of its field
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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. ENT1 inhibition links oligodendrocyte lipid metabolism to connectivity in tauopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Adenosine and adenosine receptors in metabolic imbalance-related neurological issues.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024
    Review
  13. Review
  14. Article
  15. Article
  16. NPsychopharmacology · 2022
    Article
  17. Review
  18. 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

16 authors at 5 institutions in 4 countries.

Ching-Pang ChangInstitute of Biomedical Sciences, Academia Sinica, Nankang, Taipei, 115, Taiwan.
Ya-Gin ChangInstitute of Biomedical Sciences, Academia Sinica, Nankang, Taipei, 115, Taiwan.
Pei-Yun ChuangInstitute of Biomedical Sciences, Academia Sinica, Nankang, Taipei, 115, Taiwan.
Thi Ngoc Anh NguyenInstitute of Biomedical Sciences, Academia Sinica, Nankang, Taipei, 115, Taiwan.
Kuo-Chen WuSchool of Pharmacy, National Taiwan University, Taipei, Taiwan.
Fang-Yi ChouSchool of Pharmacy, National Taiwan University, Taipei, Taiwan.
Sin-Jhong ChengInstitute of Biomedical Sciences, Academia Sinica, Nankang, Taipei, 115, Taiwan.
Hui-Mei ChenInstitute of Biomedical Sciences, Academia Sinica, Nankang, Taipei, 115, Taiwan.
Lee-Way JinDepartment of Pathology and Laboratory Medicine, University of California Davis, Sacramento, CA, USA.
Kevin CarvalhoUniv. Lille, Inserm, CHU Lille, U1172 - LilNCog - Lille Neuroscience & Cognition, 59000, Lille, France.
Vincent HuinUniv. Lille, Inserm, CHU Lille, U1172 - LilNCog - Lille Neuroscience & Cognition, 59000, Lille, France.
Luc BuéeUniv. Lille, Inserm, CHU Lille, U1172 - LilNCog - Lille Neuroscience & Cognition, 59000, Lille, France.
Yung-Feng LiaoInstitute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan.
Chun-Jung LinSchool of Pharmacy, National Taiwan University, Taipei, Taiwan.
David BlumUniv. Lille, Inserm, CHU Lille, U1172 - LilNCog - Lille Neuroscience & Cognition, 59000, Lille, France. david.blum@inserm.fr.
Yijuang ChernInstitute of Biomedical Sciences, Academia Sinica, Nankang, Taipei, 115, Taiwan. bmychern@ibms.sinica.edu.tw.ORCID 0000-0002-5842-5429
Institute of Biomedical Sciences, Academia Sinica · TWInserm · FRNational Taiwan University · TWInstitute of Cellular and Organismic Biology, Academia Sinica · TWUniversity of California, Davis · US

Funding

UC Davis Alzheimer's Disease Core CenterP30AG010129 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI DECARLI, CHARLES · 1991 to 2020
$28.3M
NIA NIH HHS P30 AG010129
6 · The paper itself

Abstract

Tau pathology is instrumental in the gradual loss of neuronal functions and cognitive decline in tauopathies, including Alzheimer's disease (AD). Earlier reports showed that adenosine metabolism is abnormal in the brain of AD patients while consequences remained ill-defined. Herein, we aimed at investigating whether manipulation of adenosine tone would impact Tau pathology, associated molecular alterations and subsequent neurodegeneration. We demonstrated that treatment with an inhibitor (J4) of equilibrative nucleoside transporter 1 (ENT1) exerted beneficial effects in a mouse model of Tauopathy. Treatment with J4 not only reduced Tau hyperphosphorylation but also rescued memory deficits, mitochondrial dysfunction, synaptic loss, and abnormal expression of immune-related gene signatures. These beneficial effects were particularly ascribed to the ability of J4 to suppress the overactivation of AMPK (an energy reduction sensor), suggesting that normalization of energy dysfunction mitigates neuronal dysfunctions in Tauopathy. Collectively, these data highlight that targeting adenosine metabolism is a novel strategy for tauopathies.

Indexed as

AnimalsBrainDisease Models, AnimalEquilibrative Nucleoside Transporter 1HumansMiceTauopathiesEquilibrative Nucleoside Transporter 1AdenosineAlzheimer’s diseaseAMPKENT1Tauopathy

Identifiers

PMID34158119
PMCPMC8220833
OpenAlexW3173803458

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.