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

Purpose of review: increasing 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 a...

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Autores principales: Zsolt Gáll, Orsolya Székely
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Publicado: MDPI AG 2021
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spelling oai:doaj.org-article:f2f60a67390040c2a5045c0e99c952e42021-11-25T18:33:02ZRole of Vitamin D in Cognitive Dysfunction: New Molecular Concepts and Discrepancies between Animal and Human Findings10.3390/nu131136722072-6643https://doaj.org/article/f2f60a67390040c2a5045c0e99c952e42021-10-01T00:00:00Zhttps://www.mdpi.com/2072-6643/13/11/3672https://doaj.org/toc/2072-6643Purpose of review: increasing 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 findings: various 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.Zsolt GállOrsolya SzékelyMDPI AGarticlevitamin Dvitamin D deficiencycentral nervous systemcognitive functionbrain developmentNutrition. Foods and food supplyTX341-641ENNutrients, Vol 13, Iss 3672, p 3672 (2021)
institution DOAJ
collection DOAJ
language EN
topic vitamin D
vitamin D deficiency
central nervous system
cognitive function
brain development
Nutrition. Foods and food supply
TX341-641
spellingShingle vitamin D
vitamin D deficiency
central nervous system
cognitive function
brain development
Nutrition. Foods and food supply
TX341-641
Zsolt Gáll
Orsolya Székely
Role of Vitamin D in Cognitive Dysfunction: New Molecular Concepts and Discrepancies between Animal and Human Findings
description Purpose of review: increasing 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 findings: various 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.
format article
author Zsolt Gáll
Orsolya Székely
author_facet Zsolt Gáll
Orsolya Székely
author_sort Zsolt Gáll
title Role of Vitamin D in Cognitive Dysfunction: New Molecular Concepts and Discrepancies between Animal and Human Findings
title_short Role of Vitamin D in Cognitive Dysfunction: New Molecular Concepts and Discrepancies between Animal and Human Findings
title_full Role of Vitamin D in Cognitive Dysfunction: New Molecular Concepts and Discrepancies between Animal and Human Findings
title_fullStr Role of Vitamin D in Cognitive Dysfunction: New Molecular Concepts and Discrepancies between Animal and Human Findings
title_full_unstemmed Role of Vitamin D in Cognitive Dysfunction: New Molecular Concepts and Discrepancies between Animal and Human Findings
title_sort role of vitamin d in cognitive dysfunction: new molecular concepts and discrepancies between animal and human findings
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/f2f60a67390040c2a5045c0e99c952e4
work_keys_str_mv AT zsoltgall roleofvitamindincognitivedysfunctionnewmolecularconceptsanddiscrepanciesbetweenanimalandhumanfindings
AT orsolyaszekely roleofvitamindincognitivedysfunctionnewmolecularconceptsanddiscrepanciesbetweenanimalandhumanfindings
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