Evidence map›Paper›PMID 34835929›Full record

ReviewNutrients2021

Role of Vitamin D in Cognitive Dysfunction: New Molecular Concepts and Discrepancies between Animal and Human Findings.

Zsolt Gáll, Orsolya Székely

Open access · goldAbstract readReview
In one paragraph

Review in Nutrients, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 3 pooled it
12.6field-weighted citation impact, top 1% 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

72 citing papers in PubMed, 3 syntheses or guidelines pooled it, 126 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Vitamin D Status and Its Association with Multiple Intelligence among Arab Adolescents.International journal of environmental research and public health · 2021
    Trial
  5. Review
  6. Article
  7. Article
  8. Epigenetic Mechanisms of Vitamin D in the Aging Process: A Narrative Review.International journal of molecular sciences · 2026
    Review
  9. Article
  10. Article
  11. Vitamin DNeurochemical research · 2026
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Journal of clinical practice and research · 2025
    Article
  19. Review
  20. Article

12 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

2 authors at 2 institutions in 1 country.

Zsolt GállDepartment of Pharmacology and Clinical Pharmacy, George Emil Palade University of Medicine, Pharmacy, Science and Technology of Trgu Mureș, 540142 Trgu Mureș, Romania.ORCID 0000-0002-9091-277X
Orsolya SzékelyDepartment of Nephrology/Internal Medicine, Mures County Clinical Hospital, 540103 Trgu Mureș, Romania.
Spitalul Clinic Judetean Mures · ROUniversitatea de Medicină, Farmacie, Științe și Tehnologie „George Emil Palade” din Târgu Mureș · RO

Funding

Romanian Ministry of Education and Research, CNCS - UEFISCDI PN-III-P1-1.1-PD-2019-0507
6 · The paper itself

Abstract

purpose of reviewincreasing evidence suggests that besides the several metabolic, endocrine, and immune functions of 1alpha,25-dihydroxyvitamin D (1,25(OH)2D), the neuronal effects of 1,25(OH)2D should also be considered an essential contributor to the development of cognition in the early years and its maintenance in aging. The developmental disabilities induced by vitamin D deficiency (VDD) include neurological disorders (e.g., attention deficit hyperactivity disorder, autism spectrum disorder, schizophrenia) characterized by cognitive dysfunction. On the other hand, VDD has frequently been associated with dementia of aging and neurodegenerative diseases (e.g., Alzheimer's, Parkinson's disease). RECENT

findingsvarious cells (i.e., neurons, astrocytes, and microglia) within the central nervous system (CNS) express vitamin D receptors (VDR). Moreover, some of them are capable of synthesizing and catabolizing 1,25(OH)2D via 25-hydroxyvitamin D 1alpha-hydroxylase (CYP27B1) and 25-hydroxyvitamin D 24-hydroxylase (CYP24A1) enzymes, respectively. Both 1,25(OH)2D and 25-hydroxyvitamin D were determined from different areas of the brain and their uneven distribution suggests that vitamin D signaling might have a paracrine or autocrine nature in the CNS. Although both cholecalciferol and 25-hydroxyvitamin D pass the blood-brain barrier, the influence of supplementation has not yet demonstrated to have a direct impact on neuronal functions. So, this review summarizes the existing evidence for the action of vitamin D on cognitive function in animal models and humans and discusses the possible pitfalls of therapeutic clinical translation.

Indexed as

25-Hydroxyvitamin D3 1-alpha-HydroxylaseAnimalsBlood-Brain BarrierBrainCognitive DysfunctionDisease Models, AnimalHumansNeurogliaReceptors, CalcitriolSignal TransductionVitamin DVitamin D3 24-HydroxylaseVitamin D Deficiency1,25-dihydroxyvitamin D25-hydroxyvitamin D25-Hydroxyvitamin D3 1-alpha-HydroxylaseReceptors, CalcitriolVitamin DVitamin D3 24-Hydroxylasebrain developmentcentral nervous systemcognitive functionvitamin Dvitamin D deficiency

Identifiers

PMID34835929
PMCPMC8620681
OpenAlexW3205305359

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.