Vitamin D in Relation to Cognitive Impairment, Cerebrospinal Fluid Biomarkers, and Brain Volumes

Hooshmand, Babak; Lökk, Johan; Solomon, Alina; Mangialasche, Francesca; Miralbell, Júlia; Spulber, Gabriela; Annerbo, Sylvia; Andreasen, Niels; Winblad, Bengt; Cedazo-Minguez, Ángel; Wahlund, Lars‐Olof; Kivipelto, Miia

doi:10.1093/gerona/glu022

Cited by 73 publications

(50 citation statements)

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“…Age-related cognitive decline has been largely explained by the role of vascular pathology [37]. Alternatively, a recent Swedish study reported a positive association between plasma 25(OH)D levels and concentrations of cerebrospinal fluid Aβ 1-42 and brain volumes, which partly accounted for the significant link between reduced plasma 25(OH)D and cognitive impairment [38]. …”

Section: Discussionmentioning

confidence: 99%

Midlife Dietary Vitamin D Intake and Subsequent Performance in Different Cognitive Domains

et al. 2014

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Background/Aims: We evaluated the cross-time association between midlife dietary vitamin D intake and subsequent cognitive performance in a French general-population sample. Methods: Data from participants in both the SU.VI.MAX trial (1994-2002) and the SU.VI.MAX 2 observational study (2007-2009) were used. Dietary intake was estimated at baseline from 6 or more 24-hour records. Cognitive performance was evaluated 13 years later with a comprehensive neuropsychological battery. Parameter estimates of cognitive performance according to quartiles (Q) of vitamin D intake were estimated via ANCOVA. Results: In a sample of 1,990 aging adults, principal component analyses yielded two cognitive factors - for episodic/semantic memory and short-term memory/executive function; however, neither one displayed associations with dietary vitamin D intake. Midlife vitamin D intake was significantly and positively associated with scores on the forward digit span task measuring short-term memory (fully adjusted model: mean difference, Q4 vs. Q1 = 1.95; 95% CI 0.37-3.53; p_trend = 0.03). No significant interaction with either sex or lifetime sun exposure was found. Conclusions: Midlife vitamin D intake exhibited a cross-time and domain-specific association with cognition in the context of aging. Further investigations in this area of prevention are warranted given the rapidly expanding elderly population and the absence of curative treatment for dementia.

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Section: Discussionmentioning

confidence: 99%

Midlife Dietary Vitamin D Intake and Subsequent Performance in Different Cognitive Domains

et al. 2014

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“…A large population based prospective studies of Danish subjects over a follow up period of 30 years has concluded that 25-hydroxy vitamin D3 deficiency increases the risk of AD [181]. Other studies have shown that plasma vitamin D is an important determinant of cognitive status, CSF Aβ42 level and brain volume in patients of AD, MCI and subjective cognitive impairment [182].…”

Section: Vitamin Dmentioning

confidence: 99%

Metabolic Risk Factors of Sporadic Alzheimer's Disease: Implications in the Pathology, Pathogenesis and Treatment

Chakrabarti¹,

Khemka²,

Banerjee³

et al. 2015

Aging and disease

112

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Alzheimer's disease (AD), the major cause of dementia among the elderly world-wide, manifests in familial and sporadic forms, and the latter variety accounts for the majority of the patients affected by this disease. The etiopathogenesis of sporadic AD is complex and uncertain. The autopsy studies of AD brain have provided limited understanding of the antemortem pathogenesis of the disease. Experimental AD research with transgenic animal or various cell based models has so far failed to explain the complex and varied spectrum of AD dementia. The review, therefore, emphasizes the importance of AD related risk factors, especially those with metabolic implications, identified from various epidemiological studies, in providing clues to the pathogenesis of this complex disorder. Several metabolic risk factors of AD like hypercholesterolemia, hyperhomocysteinemia and type 2 diabetes have been studied extensively both in epidemiology and experimental research, while much less is known about the role of adipokines, proinflammatory cytokines and vitamin D in this context. Moreover, the results from many of these studies have shown a degree of variability which has hindered our understanding of the role of AD related risk factors in the disease progression. The review also encompasses the recent recommendations regarding clinical and neuropathological diagnosis of AD and brings out the inherent uncertainty and ambiguity in this area which may have a distinct impact on the outcome of various population-based studies on AD-related risk factors.

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confidence: 97%

“…Additionally, reduced risk of cognitive impairment, higher concentrations of CSF Aβ1-42 and greater brain volumes (e.g. white matter and structures belonging to medial temporal lobe) were found in patients attending a memory clinic who had higher serum 25(OH)D [8].A biological rationale for the effect of vitamin D on cognitive performance is plausible. Vitamin D receptors have been located in many brain regions (including the hippocampus) [9] associated with cognitive functions that decline with the development of dementia.…”

mentioning

confidence: 99%

“…Vitamin D correlates negatively with cerebral ventricle size, suggesting that it contributes to brain atrophy [10]. It has been suggested that the anti-ischaemic, anti-inflammatory and anti-oxidant roles of vitamin D are neuroprotective and vasoprotective [8,11]. In addition, various functions of vitamin D in neurotransmitter metabolism, particularly in the dopaminergic system, have been proposed [9].…”

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confidence: 99%

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Vitamin D and Cognition: Are There Any Cautions Against Intervention Trials for Older Adults?

Jager¹

2014

Vitam Miner

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EditorialVitamin D has long been known as the sunshine vitamin, as it is synthesized in the skin from 7-dehydrocholesterol in the presence of sunlight. It is known for its role in strengthening bones through metabolic processing of calcium. The main circulating metabolite form of vitamin D is 25-hydroxyvitamin D (25(OH)D); this is processed mainly via the liver and kidneys to the active form, 1,25(OH) 2 D, which is water soluble. Extra-renal cells can also produce 1,25(OH) 2 D. Blood levels are controlled by the parathyroid hormone, growth factors, cytokines and calcium [1]. Deficiencies of vitamin D are linked to conditions such as rickets in children and osteoporosis, falls and fractures in older adults, as well as some psychiatric conditions such as depression and seasonal affective disorder (SAD) [2].Surveys suggest that up to a third of the populations in the Western World may be D vitamin deficient, depending on the lower limit for normal serum levels [3]. Levels vary seasonally, although exposure to sunshine is not absolutely necessary, if dietary sources and supplements are sufficient. Sources of vitamin D3include oily fish, eggs, fish oils such as cod liver oil and liver. Vegan sources include lichen for vitamin D3, cholecalciferol, and mushrooms and alfalfa for D2, ergocalciferol. Vitamin D3 supplementation has been shown to be more efficacious than D2 in increasing levels of serum 25(OH)D, possibly due to more rapid clearance of vitamin D(2), or other mechanisms [ 4] . Fortification of milk, milk products, and flour may also supplement intake in certain countries. Older adults are more prone to deficiency due to thinning of the skin and decreasing amounts of dehydrocholesterol, accompanied by less absorption of sunlight and conversion to the active form. Low dietary intake and poorer absorption by the gut, limited sunlight exposure and limited physical activity may also contribute to deficiency.Health claims for vitamin D supplements include maintenance of a normal immune system and inflammatory responses, reduction in falls, fractures and osteoporosis. However, recent research has shown links between vitamin D3deficiency (25(OH)D) and increases in the incidence of hypertension, hyperlipidaemia, diabetes, myocardial infarction and stroke [3]. These conditions are associated with increased risk of neurodegenerative diseases such as vascular dementia, Alzheimer's disease (AD) and Parkinson's disease. Crosssectional and longitudinal observational studies used for a metaanalysis [5] showed associations of low 25(OH)D with cognitive impairment and decline in older adults. Generally, deficiency or low 25(OH)D was equated to serum levels below 20ng/ml, while normal levels ranged between 20-50 ng/ml. Meta-analyses have confirmed significantly lower levels of vitamin D in Alzheimer's disease patients and in those with mild cognitive impairment (MCI) compared to normal controls [6].A meta-analysis reviewed by van der Schaft et al. [7] suggested a more than doubled risk of cognitive impairment in patients with v...

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Vitamin D in Relation to Cognitive Impairment, Cerebrospinal Fluid Biomarkers, and Brain Volumes

Abstract: This study suggests that vitamin D may be associated with cognitive status, CSF Aβ(1-42) levels, and brain tissue volumes.

Cited by 73 publications

References 28 publications

Midlife Dietary Vitamin D Intake and Subsequent Performance in Different Cognitive Domains

Midlife Dietary Vitamin D Intake and Subsequent Performance in Different Cognitive Domains

Metabolic Risk Factors of Sporadic Alzheimer's Disease: Implications in the Pathology, Pathogenesis and Treatment

Vitamin D and Cognition: Are There Any Cautions Against Intervention Trials for Older Adults?

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