Evidence map›Paper›PMID 36333711›Full record

ArticleCell & bioscience2022

Salidroside reduces neuropathology in Alzheimer's disease models by targeting NRF2/SIRT3 pathway.

Yuyuan Yao, Zhichu Ren, Ruihan Yang, Yilan Mei, Yuying Dai, Qian Cheng, Chong Xu, Xiaogang Xu, Sanying Wang, Kyoung Mi Kim and 6 more

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

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  8. Salidroside mitigates cognitive deficits in AlClFrontiers in behavioral neuroscience · 2026
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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 3 countries.

Yuyuan Yao *Laboratory of Aging Neuroscience and Neuropharmacology, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing, 210009, China.
Zhichu Ren *Laboratory of Aging Neuroscience and Neuropharmacology, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing, 210009, China.
Ruihan YangLaboratory of Aging Neuroscience and Neuropharmacology, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing, 210009, China.
Yilan MeiLaboratory of Aging Neuroscience and Neuropharmacology, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing, 210009, China.
Yuying DaiLaboratory of Aging Neuroscience and Neuropharmacology, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing, 210009, China.
Qian ChengLaboratory of Aging Neuroscience and Neuropharmacology, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing, 210009, China.
Chong XuLaboratory of Aging Neuroscience and Neuropharmacology, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing, 210009, China.
Xiaogang XuZhejiang Provincial Key Lab of Geriatrics and Geriatrics, Institute of Zhejiang Province, Department of Geriatrics, Zhejiang Hospital, Hangzhou, 310030, China.
Sanying WangZhejiang Provincial Key Lab of Geriatrics and Geriatrics, Institute of Zhejiang Province, Department of Geriatrics, Zhejiang Hospital, Hangzhou, 310030, China.
Kyoung Mi KimDepartment of Biological Sciences, Chungnam National University, Daejeon, 34134, Korea.
Ji Heon NohDepartment of Biochemistry, Chungnam National University, Daejeon, 34134, Korea.
Jian ZhuDepartment of Psychology, Eastern Illinois University, Charleston, IL, 61920, USA.
Ningwei ZhaoChina Exposomics Institute, 781 Cai Lun Road, Shanghai, 200120, China.
Yong U LiuLaboratory for Neuroscience in Health and Disease, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, 510180, China.
Genxiang MaoZhejiang Provincial Key Lab of Geriatrics and Geriatrics, Institute of Zhejiang Province, Department of Geriatrics, Zhejiang Hospital, Hangzhou, 310030, China. maogenxiang@163.com.
Jian SimaLaboratory of Aging Neuroscience and Neuropharmacology, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing, 210009, China. simajian@cpu.edu.cn.ORCID http://orcid.org/0000-0002-4127-1638
China Pharmaceutical University · CNZhejiang Hospital · CNChungnam National University · KREastern Illinois University · USGuangzhou First People's Hospital · CN

Funding

National Natural Science Foundation of China 81771520National Natural Science Foundation of China 82173804
6 · The paper itself

Abstract

backgroundNeurite dystrophy is a pathologic hallmark of Alzheimer's disease (AD). However, drug discovery targeting neurite protection in AD remains largely unexplored.

methodsAβ-induced neurite and mitochondrial damage assays were used to evaluate Aβ toxicity and the neuroprotective efficacy of a natural compound salidroside (SAL). The 5×FAD transgenic mouse model of AD was used to study the neuroprotective function of SAL. To verify the direct target of SAL, we used surface plasmon resonance and cellular thermal shift assays to analyze the drug-protein interaction.

resultsSAL ameliorates Aβ-mediated neurite damage in cell culture. We further reveal that SAL represses mitochondrial damage in neurites by promoting mitophagy and maintaining mitochondrial homeostasis, dependent on an NAD-dependent deacetylase SIRT3. In AD mice, SAL protects neurite morphology, mitigates Aβ pathology, and improves cognitive function, which are all SIRT3-dependent. Notably, SAL directly binds to transcription factor NRF2, inhibits its degradation by blocking its interaction with KEAP1 ubiquitin ligase, and then advances NRF2-mediated SIRT3 transcription.

conclusionsOverall, we demonstrate that SAL, a potential anti-aging drug candidate, attenuates AD pathology by targeting NRF2/SIRT3 pathway for mitochondrial and neurite protection. Drug discovery strategies focusing on SAL may thus provide promising therapeutics for AD.

Indexed as

Alzheimer’s diseaseMitochondrial protectionNRF2SALSIRT3

Identifiers

PMID36333711
PMCPMC9636768
OpenAlexW4308296080

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.