Vitamin D and Alzheimer's Disease: Is There a Link?

Pogge, Elizabeth

doi:10.4140/tcp.n.2010.440

Cited by 30 publications

(21 citation statements)

References 31 publications

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“…There are several lines of evidence that an increase in extracellular actin in the CSF, vitamin D deficiency, neuroendothelial disruption, and immune dysfunction are commonly associated with AD pathology. [42][43][44][45] Interestingly, DBP is known to act as an actin scavenger, a vitamin D transporter, a growth factor for endothelial cells, an immunmodulator, and a macrophage activator. 10,46 Therefore, it is possible that DBP may improve the synaptic loss and inhibit memory deficits through the regulation of other pathological mediators of AD.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D-binding protein interacts with Aβ and suppresses Aβ-mediated pathology

et al. 2012

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The level of vitamin D-binding protein (DBP) is increased in the cerebrospinal fluid of patients with Alzheimer's disease (AD), suggesting a relationship with its pathogenesis. In this study, we investigated whether and how DBP is related to AD using several different approaches. A pull-down assay and a surface plasmon resonance binding assay indicated direct interactions between purified DBP and amyloid beta (Ab), which was confirmed in the brain of AD patients and transgenic AD model mice by immunoprecipitation assay and immunohistochemical double-staining method. Moreover, atomic force microscopic examination revealed that DBP reduced Ab aggregation in vitro. DBP also prevented Ab-mediated death in cultured mouse hippocampal HT22 cell line. Finally, DBP decreased Ab-induced synaptic loss in the hippocampus and rescued memory deficits in mice after injection of Ab into the lateral ventricle. These results provide converging evidence that DBP attenuates the harmful effects of Ab by a direct interaction, and suggest that DBP is a promising therapeutic agent for the treatment of AD.

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Section: Discussionmentioning

confidence: 99%

Vitamin D-binding protein interacts with Aβ and suppresses Aβ-mediated pathology

et al. 2012

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“…Some studies have suggested a link between vitamin D deficiency and cognitive impairment and dementia, particularly in the elderly (8,9). Vitamin D, also known as calciferol, is a steroid hormone that can be obtained from dietary sources as both vitamin D2 and D3.…”

Section: Introductionmentioning

confidence: 99%

Effect of vitamin intake on cognitive decline in older adults: Evaluation of the evidence

Krause

Roupas

2015

The Journal of nutrition, health and aging

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“…LOAD is a complex disorder, caused by a combination of genetic and environmental risk factors, all of which alter risk for AD without alone being necessary or sufficient for the development of the disorder. Age is the most significant environmental risk factor for LOAD, and other factors which have been implicated in increasing or decreasing LOAD risk, affecting age of onset, or affecting disease progression include educational status, head injury, hypertension, high cholesterol and vitamin intake (Dosunmu et al 2007;Pogge 2010). …”

Section: Late Onset Admentioning

confidence: 99%

“…Age is by far the most significant environmental risk factor for late onset AD, with risk increasing dramatically as aging occurs. Other factors include educational status, head injury, exercise, hypertension, and vitamin intake (Dosunmu et al 2007;Dangour et al 2010;Pogge 2010), although what effect modifications of these risk exposures could have on public health remains to be determined (Dangour et al 2010). …”

Section: Preventionmentioning

confidence: 99%

P2‐030: Investigating the Role of Clu, Picalm, and Cr1 in Alzheimer's Disease

Lord

Turton

Braae

et al. 2014

Alzheimer's & Dementia

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In 2009, two large genome wide association studies (GWAS) found associations between common single nucleotide polymorphisms (SNPs) at three loci (CLU, PICALM and CR1) and Alzheimer's disease (AD) risk. The causal variants underlying these associations and how these impact on AD susceptibility remain unclear. Target enrichment and next generation sequencing (NGS) were used to completely resequence the three associated loci in 96 AD patients in an attempt to uncover potentially causative and rare variants that may explain the observed association signals. A pipeline was developed for the handling of pooled NGS data following a comparison of several different combinations of programs. 33 exonic SNPs were found within the three genes, along with over 1000 non-coding variants. To identify the variants most likely to be affecting AD risk, a two pronged approach was adopted. The variants were imputed in a large case-control cohort (2067 cases, 7376 controls) to test for association with AD, and the likely functional consequences of the variants were assessed using in silico resources. Several of the analysed variants showed suggestive or significant association with AD in the imputed data, and/or were predicted to have consequences on the function or regulation of the genes, suggesting avenues for future research in AD genetics. The whole method of pooled, targeted NGS and prioritisation using imputed data for association testing and in silico resources for functional analysis represents a new strategy for tracking down the illusive causation of GWAS signals. PublicationsNext generation sequencing of CLU, PICALM and CR1: pitfalls and potential solutions. Lord J,

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Vitamin D and Alzheimer's Disease: Is There a Link?

Cited by 30 publications

References 31 publications

Vitamin D-binding protein interacts with Aβ and suppresses Aβ-mediated pathology

Vitamin D-binding protein interacts with Aβ and suppresses Aβ-mediated pathology

Effect of vitamin intake on cognitive decline in older adults: Evaluation of the evidence

P2‐030: Investigating the Role of Clu, Picalm, and Cr1 in Alzheimer's Disease

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