Evidence map›Paper›PMID 29036814›Full record

ArticleJournal of Alzheimer's disease : JAD2017

Curcumin Ameliorates Neuroinflammation, Neurodegeneration, and Memory Deficits in p25 Transgenic Mouse Model that Bears Hallmarks of Alzheimer's Disease.

Jeyapriya Raja Sundaram, Charlene Priscilla Poore, Noor Hazim Bin Sulaimee, Tej Pareek, Wei Fun Cheong, Markus R Wenk, Harish C Pant, Sally A Frautschy, Chian-Ming Low, Sashi Kesavapany

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 2 pooled it
4.8field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 2 syntheses or guidelines pooled it, 99 citations in OpenAlex.

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  8. Asiatic Acid AttenuatesInternational journal of molecular sciences · 2026
    Article
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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

10 authors at 4 institutions in 2 countries.

Jeyapriya Raja SundaramNeurobiology and Ageing Program, Centre for Life Sciences, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Charlene Priscilla PooreNeurobiology and Ageing Program, Centre for Life Sciences, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Noor Hazim Bin SulaimeeNeurobiology and Ageing Program, Centre for Life Sciences, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Tej PareekDepartment of Pediatrics, Case Western Reserve University, Cleveland, OH, USA.
Wei Fun CheongNeurobiology and Ageing Program, Centre for Life Sciences, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Markus R WenkNeurobiology and Ageing Program, Centre for Life Sciences, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Harish C PantNational Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.
Sally A FrautschyDepartment of Neurology, University of California, Los Angeles, CA, USA.
Chian-Ming LowNeurobiology and Ageing Program, Centre for Life Sciences, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Sashi KesavapanyNeurobiology and Ageing Program, Centre for Life Sciences, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
National University of Singapore · SGCase Western Reserve University · USGeriatric Research Education and Clinical Center · USNational Institute of Neurological Disorders and Stroke · US

Funding

Preclinical Pharmacogenomics and Synaptic Biomarkers for Alzheimer's DiseaseR01AT006816 · NCCIH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI COLE, GREGORY M, FRAUTSCHY, SALLY ANN · 2011 to 2015
$1.9M
Modulation of tau pathogenesis by high dietary fat, gender and ApoE isoformR21AG050269 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FRAUTSCHY, SALLY ANN · 2016 to 2017
$347k
Mechanisms for NSAID Alzheimer PreventionI01BX000542 · VA · VA GREATER LOS ANGELES HEALTHCARE SYSTEM · PI COLE, GREGORY M · 2009 to 2013
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Polyphenolic Interventions for tau Pathogenesis in Alzheimers ModelsI01BX001257 · VA · VA GREATER LOS ANGELES HEALTHCARE SYSTEM · PI FRAUTSCHY, SALLY ANN · 2013 to 2016
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Curcumin and Yoga Exercise Effects in Veterans at Risk for Alzheimer's DiseaseI01RX000669 · VA · VA GREATER LOS ANGELES HEALTHCARE SYSTEM · PI FRAUTSCHY, SALLY ANN · 2015 to 2015
–
BLRD VA I01 BX000542BLRD VA I01 BX001257BLRD VA I01 BX003485NCCIH NIH HHS R01 AT006816NIA NIH HHS R21 AG050269RRD VA I01 RX000669
6 · The paper itself

Abstract

Several studies have indicated that neuroinflammation is indeed associated with neurodegenerative disease pathology. However, failures of recent clinical trials of anti-inflammatory agents in neurodegenerative disorders have emphasized the need to better understand the complexity of the neuroinflammatory process in order to unravel its link with neurodegeneration. Deregulation of Cyclin-dependent kinase 5 (Cdk5) activity by production of its hyperactivator p25 is involved in the formation of tau and amyloid pathology reminiscent of Alzheimer's disease (AD). Recent studies show an association between p25/Cdk5 hyperactivation and robust neuroinflammation. In addition, we recently reported the novel link between the p25/Cdk5 hyperactivation-induced inflammatory responses and neurodegenerative changes using a transgenic mouse that overexpresses p25 (p25Tg). In this study, we aimed to understand the effects of early intervention with a potent natural anti-inflammatory agent, curcumin, on p25-mediated neuroinflammation and the progression of neurodegeneration in p25Tg mice. The results from this study showed that curcumin effectively counteracted the p25-mediated glial activation and pro-inflammatory chemokines/cytokines production in p25Tg mice. Moreover, this curcumin-mediated suppression of neuroinflammation reduced the progression of p25-induced tau/amyloid pathology and in turn ameliorated the p25-induced cognitive impairments. It is widely acknowledged that to treat AD, one must target the early-stage of pathological changes to protect neurons from irreversible damage. In line with this, our results demonstrated that early intervention of inflammation could reduce the progression of AD-like pathological outcomes. Moreover, our data provide a rationale for the potential use of curcuminoids in the treatment of inflammation associated neurodegenerative diseases.

Indexed as

Alzheimer DiseaseAnimalsAnti-Inflammatory AgentsAstrocytesBrainCalcium-Calmodulin-Dependent Protein Kinase Type 2CurcuminHumansInflammationMemory DisordersMice, Inbred C57BLMice, Inbred CBAMice, TransgenicNerve DegenerationNeuroimmunomodulationNeuroprotective AgentsAnti-Inflammatory AgentsCalcium-Calmodulin-Dependent Protein Kinase Type 2Camk2a protein, mouseCurcuminNeuroprotective AgentsNootropic AgentsAmyloidCdk5curcuminneurodegenerationneuroinflammationp25tau

Identifiers

PMID29036814
PMCPMC8092919
OpenAlexW2761591067

What OpenQuestion holds

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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.