scholarly journals 1α,25-Dihydroxyvitamin D3 up-regulates IL-34 expression in SH-SY5Y neural cells

2017 ◽  
Vol 23 (7) ◽  
pp. 584-591 ◽  
Author(s):  
Dong Zhang ◽  
Miaomiao Li ◽  
Yang Dong ◽  
Xinhui Zhang ◽  
Xingyun Liu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Core Promoter ◽  
Active Form ◽  
Vitamin D Supplementation ◽  
Neural Cells ◽  
Dependent Manner ◽  
Dihydroxyvitamin D3 ◽  
Protective Function

Vitamin D supplementation is regarded as a novel approach to treat Alzheimer’s disease, but the underlying mechanism remains elusive. The cytokine IL-34 provides strong neuroprotective and survival signals in brain injury and neurodegeneration and could be an immunological mediator for the vitamin D-induced protection. The aim of this study was to investigate whether human IL-34 is up-regulated in neuronal cells by the hormonally active form of vitamin D, 1α,25-dihydroxyvitamin D3 [1α,25(OH)2D3]. We found that IL-34 was detectable in a variety of cell lines and its expression was strongly induced in SH-SY5Y neural cells in a dose- and time-dependent manner by 1α,25(OH)2D3 through the vitamin D receptor (VDR). Furthermore, we identified the core promoter of IL-34 gene and a VDR binding site (CGCCCT) that was required for 1α,25(OH)2D3-induced IL-34 expression. These findings suggest that the induction of IL-34 expression by 1α,25(OH)2D3 may constitute a mechanism that explains the protective function of vitamin D in Alzheimer’s disease.

Vitamin D supplementation restores suppressed synaptic plasticity in Alzheimer's disease

2013 ◽  
Vol 17 (4) ◽  
pp. 172-177 ◽  
Author(s):  
Mohsen Taghizadeh ◽  
Sayyed Alireza Talaei ◽  
Abolghasem Djazayeri ◽  
Mahmoud Salami
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Synaptic Plasticity ◽  
Vitamin D Supplementation

scholarly journals Effect of Vitamin D Supplementation on the Progression of Alzheimer’s Disease in Rats: A Mechanistic Approach

2021 ◽  
Author(s):  
Parmi Patel ◽  
Jigna Samir Shah
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Vitamin D Supplementation ◽  
Cognitive Status ◽  
Tau Proteins ◽  
Biochemical Alterations ◽  
Vitamin D Levels ◽  
The Brain

Abstract Purpose: A multifaceted treatment approach can be effective for Alzheimer's disease (AD). However, currently, it involves only symptomatic treatment with cholinergic drugs. Beneficial effects of high vitamin D levels or its intake in the prevention and treatment of cognitive disorders have been reported. Thus, the present study examined the preventive effect of vitamin D supplementation on AD progression and evaluated its impact on the accumulation or degradation of Aβ plaques. Methods: A single intraperitoneal injection of scopolamine was used to induce AD in rats. Treatment of vitamin D was provided for 21 days after the injection. Various behavioral parameters like learning, spatial memory and exploratory behavior, biochemical alterations in the brain homogenate and histology of the hippocampus were investigated. Results: Our results indicated that scopolamine-induced rats depicted cognitive deficits with high Aβ levels and hyperphosphorylated tau proteins in the brain tissue, while vitamin D supplementation could significantly improve the cognitive status and lower these protein levels. These results were supported by the histopathological and immunohistochemical staining of the hippocampal brain region. Furthermore, mechanistic analysis depicted that vitamin D supplementation improved the Aβ protein clearance by increasing the neprilysin levels. It also reduced the accumulation of Aβ plaques by lowering neuroinflammation as well as oxidative stress. Conclusion: The present findings indicate that vitamin D supplementation can delay AD progression by an increase in Aβ plaques degradation or reducing inflammation and oxidative stress.

Active form of vitamin D analogue mitigates neurodegenerative changes in Alzheimer’s disease in rats by targeting Keap1/Nrf2 and MAPK-38p/ERK signaling pathways

Steroids ◽  
2020 ◽  
Vol 156 ◽  
pp. 108586 ◽  
Author(s):  
Shimaa Saad El-Din ◽  
Laila Rashed ◽  
Engy Medhat ◽  
Basma Emad Aboulhoda ◽  
Ahmed Desoky Badawy ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Signaling Pathways ◽  
Active Form ◽  
Erk Signaling ◽  
Vitamin D Analogue

Effect of Memantine Treatment and Combination with Vitamin D Supplementation on Body Composition in the APP/PS1 Mouse Model of Alzheimer’s Disease Following Chronic Vitamin D Deficiency

2021 ◽  
pp. 1-14
Author(s):  
Dickson Wong ◽  
Dana N. Broberg ◽  
Jagroop Doad ◽  
Joseph U. Umoh ◽  
Miranda Bellyou ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Body Composition ◽  
Mouse Model ◽  
Vitamin D Deficiency ◽  
Vitamin D Supplementation ◽  
Whole Body ◽  
Deficient Diet ◽  
Memantine Treatment

Background: Vitamin D deficiency and altered body composition are common in Alzheimer’s disease (AD). Memantine with vitamin D supplementation can protect cortical axons against amyloid-β exposure and glutamate toxicity. Objective: To study the effects of vitamin D deprivation and subsequent treatment with memantine and vitamin D enrichment on whole-body composition using a mouse model of AD. Methods: Male APPswe/PS1dE9 mice were divided into four groups at 2.5 months of age: the control group (n = 14) was fed a standard diet throughout; the remaining mice were started on a vitamin D-deficient diet at month 6. The vitamin D-deficient group (n = 14) remained on the vitamin D-deficient diet for the rest of the study. Of the remaining two groups, one had memantine (n = 14), while the other had both memantine and 10 IU/g vitamin D (n = 14), added to their diet at month 9. Serum 25(OH)D levels measured at months 6, 9, 12, and 15 confirmed vitamin D levels were lower in mice on vitamin D-deficient diets and higher in the vitamin D-supplemented mice. Micro-computed tomography was performed at month 15 to determine whole-body composition. Results: In mice deprived of vitamin D, memantine increased bone mineral content (8.7% increase, p <  0.01) and absolute skeletal tissue mass (9.3% increase, p <  0.05) and volume (9.2% increase, p <  0.05) relative to controls. This was not observed when memantine treatment was combined with vitamin D enrichment. Conclusion: Combination treatment of vitamin D and memantine had no negative effects on body composition. Future studies should clarify whether vitamin D status impacts the effects of memantine treatment on bone physiology in people with AD.

scholarly journals VITAMIN D AND DEMENTIA

2015 ◽  
pp. 1-10
Author(s):  
T.J. Littlejohns ◽  
K. Kos ◽  
W.E. Henley ◽  
E. Kuma ◽  
D.J. Llewellyn
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Longitudinal Studies ◽  
Ventricular Volume ◽  
Vitamin D Supplementation ◽  
Small Sample ◽  
Double Blind ◽  
Cross Sectional ◽  
Increased Risk

Emerging evidence suggests that low vitamin D concentrations are potentially involved in the pathogenesis of dementia. This is of particular interest when considering the high prevalence of vitamin D deficiency in elderly adults and the urgent need to identify modifiable risk factors for dementia. Studies have found that vitamin D is implicated in procognitive and neuroprotective functions, including the reduction of Alzheimer’s disease hallmarks such as amyloid beta and phosphorylated tau. Cross-sectional studies have consistently found that vitamin D concentrations are significantly lower in individuals with Alzheimer’s disease and cognitive impairment compared to healthy controls. Longitudinal studies support an association between low vitamin D concentrations and an increased risk of dementia and cognitive decline. Neuroimaging studies are beginning to uncover the potential neurodegenerative and cerebrovascular mechanisms that underlie these associations such as white matter hyperintensities and enlarged ventricular volume, although there is currently a lack of longitudinal studies. In contrast to observational studies, findings from interventional studies have produced mixed results on the benefits of vitamin D supplementation on dementia and cognitive outcomes. Interpretation of the findings from these studies is hampered by several major methodological limitations, such as small sample sizes, inadequate doses and inclusion of participants unlikely to benefit from vitamin D supplementation. There is a need for large double-blind randomised-control trials investigating whether vitamin D supplementation can halt or delay the risk of dementia-related outcomes in individuals with low vitamin D concentrations.

scholarly journals The non-genomic vitamin D pathway links β-amyloid to autophagic apoptosis in Alzheimer's disease

2021 ◽  
Author(s):  
Rai-Hua Lai ◽  
Yueh-Ying Hsu ◽  
Feng-Shiun Shie ◽  
Mei-Hsin Chen ◽  
Jyh-Lyh Juang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Cognitive Impairment ◽  
Vitamin D Deficiency ◽  
Epidemiological Studies ◽  
Vitamin D Supplementation ◽  
Adult Brain ◽  
Plasma Vitamin ◽  
Vitamin D Levels

Vitamin D is an important hormonal molecule, which exerts genomic and non-genomic actions in maintaining brain development and adult brain health. Many epidemiological studies have associated vitamin D deficiency with Alzheimer's disease (AD). Nevertheless, the underlying signaling pathway through which this occurs remains to be characterized. We were intrigued to find that although vitamin D levels are significantly low in AD patients, their hippocampal vitamin D receptor (VDR) levels are inversely increased in the cytosol of the brain cells, and colocalized with Aβ plaques, gliosis and autophagosomes, suggesting that a non-genomic form of VDR is implicated in AD. Mechanistically, Aβ induces the conversion of nuclear heterodimer of VDR/RXR heterodimer into a cytoplasmic VDR/p53 heterodimer. The cytosolic VDR/p53 complex mediates the Aβ induced autophagic apoptosis. Reduction of p53 activity in AD mice reverses the VDR/RXR formation and rescues AD brain pathologies and cognitive impairment. In line with the impaired genomic VDR pathway, the transgenic AD mice fed a vitamin D sufficient diet exhibit lower plasma vitamin D levels since early disease phases, raising the possibility that vitamin D deficiency may actually be an early manifestation of AD. Despite the deficiency of vitamin D in AD mice, vitamin D supplementation not only has no benefit but lead to exacerbated Aβ depositions and cognitive impairment. Together, these data indicate that the impaired genomic vitamin D pathway links Aβ to induce autophagic apoptosis, and suggest that VDR/p53 pathway could be targeted for the treatment of AD.

scholarly journals Low Vitamin D and Its Association with Cognitive Impairment and Dementia

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Sadia Sultan ◽  
Uzma Taimuri ◽  
Shatha Abdulrzzaq Basnan ◽  
Waad Khalid Ai-Orabi ◽  
Afaf Awadallah ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Cognitive Impairment ◽  
Behavioral Problems ◽  
Small Sample Size ◽  
Vitamin D Supplementation ◽  
Small Sample ◽  
Vitamin D Levels ◽  
Prevention And Treatment

Vitamin D is a neurosteroid hormone that regulates neurotransmitters and neurotrophins. It has anti-inflammatory, antioxidant, and neuroprotective properties. It increases neurotrophic factors such as nerve growth factor which further promotes brain health. Moreover, it is also helpful in the prevention of amyloid accumulation and promotes amyloid clearance. Emerging evidence suggests its role in the reduction of Alzheimer’s disease hallmarks such as amyloid-beta and phosphorylated tau. Many preclinical studies have supported the hypothesis that vitamin D leads to attentional, behavioral problems and cognitive impairment. Cross-sectional studies have consistently found that vitamin D levels are significantly low in individuals with Alzheimer’s disease and cognitive impairment compared to healthy adults. Longitudinal studies and meta-analysis have also exhibited an association of low vitamin D with cognitive impairment and Alzheimer’s disease. Despite such evidence, the causal association cannot be sufficiently answered. In contrast to observational studies, findings from interventional studies have produced mixed results on the role of vitamin D supplementation in the prevention and treatment of cognitive impairment and dementia. The biggest issue of the existing RCTs is their small sample size, lack of consensus over the dose, and age of initiation of vitamin D supplements to prevent cognitive impairment. Therefore, there is a need for large double-blind randomized control trials to assess the benefits of vitamin D supplementation in the prevention and treatment of cognitive impairment.

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