Evidence map›Paper›PMID 29122628›Full record

ArticleNeuropharmacology2018

A novel curcumin derivative for the treatment of diabetic neuropathy.

Daniel J Daugherty, Alexandra Marquez, Nigel A Calcutt, David Schubert

Abstract read
In one paragraph

Article in Neuropharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.7field-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

32 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Novel drugs affecting diabetic peripheral neuropathy.Iranian journal of basic medical sciences · 2024
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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

4 authors at 2 institutions in 1 country.

Daniel J DaughertyThe Salk Institute for Biological Studies, La Jolla, CA, USA. Electronic address: Schubert@salk.edu.
Alexandra MarquezDepartment of Pathology, UCSD, La Jolla, CA, USA.
Nigel A CalcuttDepartment of Pathology, UCSD, La Jolla, CA, USA.
David SchubertThe Salk Institute for Biological Studies, La Jolla, CA, USA.
Salk Institute for Biological Studies · USUniversity of California San Diego · US

Funding

TRAINING IN THE NEUROPLASTICITY OF AGINGT32AG000216 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KOO, EDWARD H. · 1992 to 2017
$8.4M
Identification of Old-Age-Associated Alzheimer's Disease Drug TargetsR01AG046153 · NIA · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI MAHER, PAMELA ANNE, SCHUBERT, DAVID R · 2014 to 2018
$2.9M
Cholinergic constraint and diabetic neuropathyR01NS081082 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CALCUTT, NIGEL A. · 2013 to 2017
$1.6M
NIA NIH HHS R01 AG046153NIA NIH HHS T32 AG000216NINDS NIH HHS R01 NS081082
6 · The paper itself

Abstract

Neuropathy is a common complication of long-term diabetes. Proposed mechanisms of neuronal damage caused by diabetes that are downstream of hyperglycemia and/or loss of insulin signaling include ischemic hypoxia, inflammation and loss of neurotrophic support. The curcumin derivative J147 is a potent neurogenic and neuroprotective drug candidate initially developed for the treatment of neurodegenerative conditions associated with aging that impacts many pathways implicated in the pathogenesis of diabetic neuropathy. Here, we demonstrate efficacy of J147 in ameliorating multiple indices of neuropathy in the streptozotocin-induced mouse model of type 1 diabetes. Diabetes was determined by blood glucose, HbA1c, and insulin levels and efficacy of J147 by behavioral, physiologic, biochemical, proteomic, and transcriptomic assays. Biological efficacy of systemic J147 treatment was confirmed by its capacity to decrease TNFα pathway activation and several other markers of neuroinflammation in the CNS. Chronic oral treatment with J147 protected the sciatic nerve from progressive diabetes-induced slowing of large myelinated fiber conduction velocity while single doses of J147 rapidly and transiently reversed established touch-evoked allodynia. Conduction slowing and allodynia are clinically relevant markers of early diabetic neuropathy and neuropathic pain, respectively. RNA expression profiling suggests that one of the pathways by which J147 imparts its protection against diabetic induced neuropathy may be through activation of the AMP kinase pathway. The diverse biological and therapeutic effects of J147 suggest it as an alternative to the polypharmaceutical approaches required to treat the multiple pathogenic mechanisms that contribute to diabetic neuropathy.

Indexed as

AMP-Activated Protein Kinase KinasesAnimalsAnti-Inflammatory Agents, Non-SteroidalC-Reactive ProteinCurcuminDiabetic NeuropathiesDisease Models, AnimalFemaleGene Expression ProfilingGene Expression RegulationGlycated HemoglobinHumansInsulinMiceNerve Tissue ProteinsNeural ConductionAMP-Activated Protein Kinase KinasesAnti-Inflammatory Agents, Non-SteroidalC-Reactive ProteinCurcuminGlycated HemoglobinInsulinNerve Tissue ProteinsProtein KinasesStreptozocinTumor Necrosis Factor-alphaAMP kinaseDiabetesInflammationJ147Neuropathy

Identifiers

PMID29122628
PMCPMC5841546
OpenAlexW2767288256

What OpenQuestion holds

Textmetadata
LicenceTDM
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.