Sunlight Incidence, Vitamin D Deficiency, and Alzheimer's Disease

2018 ◽  
Vol 21 (9) ◽  
pp. 841-848 ◽  
Author(s):  
Alice Barros Câmara ◽  
Iara Dantas de Souza ◽  
Rodrigo Juliani Siqueira Dalmolin
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Vitamin D Deficiency

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 Serum Level in Elderly Patients with Alzheimer’s Disease: Preliminary Analysis from Cilento Region

2020 ◽  
Vol 14 (1) ◽  
pp. 63-67
Author(s):  
Vincenzo Pizza ◽  
Silvana Montella ◽  
Eugenio Luigi Iorio ◽  
Anna Silvestro ◽  
Anella Agresta ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Serum Level ◽  
Vitamin D Deficiency ◽  
Serum Vitamin ◽  
High Rate ◽  
Population Increase ◽  
Serum Vitamin D ◽  
The Mean

Introduction: It is estimated that 46 million people in the world live with dementia and it is estimated that this number will increase 3-fold by 2050, being a leading cause of disability worldwide and major welfare and economic problem. The aging of the general population increase these problems, especially in regions, such as Cilento (Southern Italy), where we can register higher longevity. Preserving cognitive health is one of the most important aims of the current research, also through the identification of possible preventative life-style strategies. Recent meta-analyses suggest that low serum vitamin D concentrations could be associated with Alzheimer's disease (AD) and cognitive impairment. The specific role of Vitamin D, however, is still controversial. There is a growing evidence of high rates of vitamin D deficiency in the elderly and there is still much uncertainty about the cause of AD and other forms of dementia. On the other hand, there is no definitive evidence is not conclusive and vitamin D could be involved in many other physiological and pathological mechanisms. Objective: Our aim is to investigate vitamin D serum levels in a small preliminary sample of AD patients from the Cilento area. Materials and Methods: Patients were recruited from the AD centre of the San Luca Hospital, in Vallo della Lucania (SA). We enrolled 25 consecutive patients, 13 women, and 12 men. The mean age was 78.5±8.3 years, the mean duration of the disease was 3.5±1.8 years. The average school-age of the patients was 6.1 +/- 3.5 years, the average disease age was 6.3 +/- 1.7 years, the average basal Mini-Mental Score Examination (MMSE) score was 17.6 +/- 3.6. We determined serum 25-hydroxyvitamin D (25[OH]D) in 25 consecutive AD patients. Results: The mean vitamin D serum level was 17.9+7.9 UI/ml, denoting a state of insufficiency. Among our 25 patients, only 3 had serum level above 30 UI/ml; most patients (17 out of 25) showed serum level among 10 and 30 UI, while in 5 patients, serum level was less than 10 UI. Conclusion: Our preliminary data showed that Vitamin D deficiency was, in our patients, independently associated with AD, even in a special population, high rate of centenarians, like Cilento people. However, our preliminary study has different limitations. The vitamin D deficiency has been evaluated through a single time-point of measurement (or in different periods of the year), that may be susceptible to bias. Even the differences in age and level of education should be taken into consideration. Nevertheless, these data in the Cilento region are original (there are no similar reports to our knowledge). However, our results confirm the necessity of other study, and this result is an important opportunity to introduce a modifiable risk fact and, consequently, a new treatment for AD.

Vitamin D deficiency might pose a greater risk for ApoEɛ4 non-carrier Alzheimer’s disease patients

2016 ◽  
Vol 37 (10) ◽  
pp. 1633-1643 ◽  
Author(s):  
Erdinç Dursun ◽  
Merve Alaylıoğlu ◽  
Başar Bilgiç ◽  
Haşmet Hanağası ◽  
Ebba Lohmann ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Vitamin D Deficiency

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 Vitamin D deficiency as a risk factor for dementia and Alzheimer’s disease: an updated meta-analysis

BMC Neurology ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Bingyan Chai ◽  
Fulin Gao ◽  
Ruipeng Wu ◽  
Tong Dong ◽  
Cheng Gu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Meta Analysis ◽  
Cochrane Library ◽  
Cross Sectional ◽  
Random Effects Models ◽  
Severe Vitamin ◽  
The Cochrane Library

Abstract Background We aimed to comprehensively explore the associations between serum 25(OH)D deficiency and risk of dementia and Alzheimer’s disease(AD). Methods We systematically searched Pubmed, the Cochrane Library, Embase and the reference lists of pertinent review articles for relevant articles published from database inception up until January 2019. Pooled hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated with random effects models using the Stata 12.0 statistical software package. Results Twelve prospective cohort studies and four cross-sectional studies were included in this meta-analysis. The pooled HRs of dementia and AD, respectively, were 1.32 (95%CI: 1.16, 1.52) and 1.34 (95%CI: 1.13, 1.60) for vitamin D deficiency (< 20 ng/ml). In the subgroup analyses, the pooled HRs of dementia and AD, respectively, were 1.48 (95%CI: 1.19, 1.85) and 1.51 (95%CI: 1.04, 2.18) for moderate vitamin D deficiency (10–20 ng/ml) and 1.20 (95%CI: 0.99, 1.44) and 1.36 (95%CI: 1.01, 1.84) for severe vitamin D deficiency (< 10 ng/ml). Conclusion There are significant associations between vitamin D deficiency and both dementia and AD. There are stronger associations between severe vitamin D deficiency (< 10 ng/ml) and both dementia and AD compared to moderate vitamin D deficiency (10–20 ng/ml).

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