Evidence map›Paper›PMID 24849345›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

1α,25-Dihydroxyvitamin D3 reduces cerebral amyloid-β accumulation and improves cognition in mouse models of Alzheimer's disease.

Matthew R Durk, Kyung Han, Edwin C Y Chow, Rosemary Ahrens, Jeffrey T Henderson, Paul E Fraser, K Sandy Pang

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 1 pooled it
7.5field-weighted citation impact, top 2% 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

76 citing papers in PubMed, 1 synthesis or guideline pooled it, 150 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Vitamin DNeurochemical research · 2026
    Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. The Moderating Effect of Serum Vitamin D on the Relationship between Beta-amyloid Deposition and Neurodegeneration.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2024
    Article
  13. Review
  14. Review
  15. Review
  16. Journal of Alzheimer's disease reports · 2024
    Article
  17. Review
  18. Review
  19. Review
  20. Review

16 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Matthew R DurkDepartment of Pharmaceutical Sciences, Leslie Dan Faculty of Pharmacy, Toronto, Ontario, Canada, M5S 3M2.
Kyung HanTanz Centre for Research in Neurodegenerative Diseases, Krembil Discovery Tower, Toronto, Ontario, Canada, M5T 2S8.
Edwin C Y ChowDepartment of Pharmaceutical Sciences, Leslie Dan Faculty of Pharmacy, Toronto, Ontario, Canada, M5S 3M2.
Rosemary AhrensTanz Centre for Research in Neurodegenerative Diseases, Krembil Discovery Tower, Toronto, Ontario, Canada, M5T 2S8.
Jeffrey T HendersonDepartment of Pharmaceutical Sciences, Leslie Dan Faculty of Pharmacy, Toronto, Ontario, Canada, M5S 3M2.
Paul E FraserDepartment of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada, M5S 3H2, and Tanz Centre for Research in Neurodegenerative Diseases, Krembil Discovery Tower, Toronto, Ontario, Canada, M5T 2S8.
K Sandy PangDepartment of Pharmaceutical Sciences, Leslie Dan Faculty of Pharmacy, Toronto, Ontario, Canada, M5S 3M2, ks.pang@utoronto.ca.
Discovery Centre · CAUniversity of Toronto · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

We demonstrate a role of the vitamin D receptor (VDR) in reducing cerebral soluble and insoluble amyloid-β (Aβ) peptides. Short-term treatment of two human amyloid precursor protein-expressing models, Tg2576 and TgCRND8 mice, with 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3], the endogenous active ligand of VDR, resulted in higher brain P-glycoprotein (P-gp) and lower soluble Aβ levels, effects negated with coadministration of elacridar, a P-gp inhibitor. Long-term treatment of TgCRND8 mice with 1,25(OH)2D3 during the period of plaque formation reduced soluble and insoluble plaque-associated Aβ, particularly in the hippocampus in which the VDR is abundant and P-gp induction is greatest after 1,25(OH)2D3 treatment, and this led to improved conditioned fear memory. In mice fed a vitamin D-deficient diet, lower cerebral P-gp expression was observed, but levels were restored on replenishment with VDR ligands. The composite data suggest that the VDR is an important therapeutic target in the prevention and treatment of Alzheimer's disease.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsCerebral CortexCognition DisordersConditioning, PsychologicalGene Expression RegulationHumansMaleMiceMice, Inbred C57BLMice, TransgenicMutationVitamin DVitaminsAmyloid beta-PeptidesAmyloid beta-Protein Precursordihydroxy-vitamin D3Vitamin DVitaminsAlzheimer'samyloid betablood-brain barrierP-glycoproteinvitamin D receptor

Identifiers

PMID24849345
PMCPMC6608194
OpenAlexW1994221276

What OpenQuestion holds

Textmetadata
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.