Evidence map›Paper›PMID 26910813›Full record

ArticleMolecular neurobiology2017

Curcumin Ameliorates Memory Decline via Inhibiting BACE1 Expression and β-Amyloid Pathology in 5×FAD Transgenic Mice.

Kunmu Zheng, Xiaoman Dai, Nai'an Xiao, Xilin Wu, Zhen Wei, Wenting Fang, Yuangui Zhu, Jing Zhang, Xiaochun Chen

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 4 pooled it
–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

57 citing papers in PubMed, 4 syntheses or guidelines pooled it.

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  14. Neuroprotective synergy of curcumin andFrontiers in pharmacology · 2025
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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

9 authors.

Kunmu ZhengDepartment of Neurology and Geriatrics, Fujian Institute of Geriatrics, Affiliated Union Hospital of Fujian Medical University, 29 Xinquan Road, Fuzhou, Fujian, 350001, People's Republic of China.
Xiaoman DaiDepartment of Neurology and Geriatrics, Fujian Institute of Geriatrics, Affiliated Union Hospital of Fujian Medical University, 29 Xinquan Road, Fuzhou, Fujian, 350001, People's Republic of China.
Nai'an XiaoKey Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, 29 Xinquan Road, Fuzhou, 350001, China.
Xilin WuKey Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, 29 Xinquan Road, Fuzhou, 350001, China.
Zhen WeiKey Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, 29 Xinquan Road, Fuzhou, 350001, China.
Wenting FangKey Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, 29 Xinquan Road, Fuzhou, 350001, China.
Yuangui ZhuDepartment of Neurology and Geriatrics, Fujian Institute of Geriatrics, Affiliated Union Hospital of Fujian Medical University, 29 Xinquan Road, Fuzhou, Fujian, 350001, People's Republic of China.
Jing ZhangDepartment of Neurology and Geriatrics, Fujian Institute of Geriatrics, Affiliated Union Hospital of Fujian Medical University, 29 Xinquan Road, Fuzhou, Fujian, 350001, People's Republic of China. drzj@163.com.
Xiaochun ChenDepartment of Neurology and Geriatrics, Fujian Institute of Geriatrics, Affiliated Union Hospital of Fujian Medical University, 29 Xinquan Road, Fuzhou, Fujian, 350001, People's Republic of China. chenxc998@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common dementia and the trigger of its pathological cascade is widely believed to be the overproduction and accumulation of β-amyloid protein (Aβ) in the affected brain. However, effective AD remedies are still anxiously awaited. Recent evidence suggests that curcumin may be a potential agent for AD treatment. In this study, we used 5×FAD transgenic mice as an AD model to investigate the effects of curcumin on AD. Our results showed that curcumin administration (150 or 300 mg/kg/day, intragastrically, for 60 days) dramatically reduced Aβ production by downregulating BACE1 expression, preventing synaptic degradation, and improving spatial learning and memory impairment of 5×FAD mice. These findings suggest that curcumin is a potential candidate for AD treatment.

Indexed as

Amyloid beta-PeptidesAmyloid Precursor Protein SecretasesAnimalsAnti-Inflammatory Agents, Non-SteroidalAspartic Acid EndopeptidasesCurcuminGene ExpressionMaleMemory DisordersMiceMice, Inbred C57BLMice, TransgenicPeptide FragmentsAmyloid beta-Peptidesamyloid beta-protein (1-42)Amyloid Precursor Protein SecretasesAnti-Inflammatory Agents, Non-SteroidalAspartic Acid EndopeptidasesBace1 protein, mouseCurcuminPeptide FragmentsAlzheimer’s disease (AD)Curcuminβ-Amyloid protein (Aβ)β-Site amyloid precursor protein cleavage enzyme 1 (BACE1)

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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.