A Novel Perspective for Alzheimer's Disease: Vitamin D Receptor Suppression by Amyloid-β and Preventing the Amyloid-β Induced Alterations by Vitamin D in Cortical Neurons

Dursun, Erdinç; Gezen-Ak, Duygu; Yılmazer, Selma

doi:10.3233/jad-2010-101377

Cited by 166 publications

(156 citation statements)

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“…In cell based experiments, vitamin D has been shown to inhibit Aβ induced cytotoxicity and apoptosis in cultured cortical neurons [183]. In post-mortem AD brain, a decreased level of VDR mRNA has been reported in hippocampal region [184].…”

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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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

View full text Add to dashboard Cite

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“…Vitamin D may have neuroprotective properties by decreasing inflammation and oxidative stress (1,2). Vitamin D receptors have been shown to be present in brain regions that are responsible for memory development and cognitive functions (3,4) and may also be involved in plaque clearance (5,6). Vitamin D is produced in the skin by UVB sunlight, and a smaller amount of vitamin D is provided by the diet.…”

Section: Introductionmentioning

confidence: 99%

Vitamin D is not associated with incident dementia or cognitive impairment: an 18-y follow-up study in community-living old men

Olsson¹,

Byberg

Karlström³

et al. 2017

The American Journal of Clinical Nutrition

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“…In a number of studies, it has been indicated that vitamin D in the brain regulates neurotrophic factor expression, oxidative stress mechanisms and Ca 2+ homeostasis (25)(26)(27)(28)(29)(30)(31). Vitamin D may affect neuronal plasticity processes and increase neurite outgrowth when added to cultured hippocampal cells (28).…”

Section: Discussionmentioning

confidence: 99%

Changes in the expression of the vitamin D receptor and LVSCC-A1C in the rat hippocampus submitted to single prolonged stress

Tong

Peng

et al. 2014

Molecular Medicine Reports

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Abstract. Vitamin D signaling not only controls calcium (Ca 2+ ) and phosphorus uptake and transport, but also correlates with neurocognitive decline and neurodegenerative diseases. Almost all actions of Vitamin D are mediated by the transcription factor, vitamin D receptor (VDR), which has been widely identified in the central nervous system. Although previous studies have substantially advanced the understanding of the action of VDR in the brain, much remains unknown concerning how VDR relates to stress. Multiple lines of evidence indicate that the downregulation of L-type voltage-sensitive Ca 2+ -channels α-1C (LVSCC-A1C) by vitamin D in hippocampal neurons is able to reduce the influx and excitotoxic effects of Ca 2+ to neurons. Along these lines, the purpose of the present study was to analyze the relative expression of VDR in the hippocampus of rats exposed to single prolonged stress (SPS) as a putative animal model for human post-traumatic stress disorder (PTSD). Furthermore, changes in the levels of expression of LVSCC-A1C and Ca 2+ (neurotransmitter content) were examined during the onset periods of PTSD. The results revealed an increase in the expression of VDR at 1, 3 and 7 days post-stress compared with the control group. The intracellular free Ca 2+ levels in the hippocampus increased 1 day after SPS exposure, and then decreased gradually to the normal level at 14 days, consistent with the expression pattern of LVSCC-A1C. These results indicated that VDR may be involved in the pathogenesis of SPS rats, thereby providing an alternative preparation to search for optimal therapeutic strategies for PTSD. IntroductionPost-traumatic stress disorder (PTSD) is a severe anxiety disorder that may develop following exposure to any threat or injury that results in psychological trauma. Diagnostic symptoms for PTSD include re-experiencing the original trauma through flashbacks or nightmares, avoidance of stimuli associated with the trauma and increased arousal. Single-prolonged stress (SPS), an animal model of PTSD, has been extensively developed and employed in the investigation of PTSD (1-3). The three areas of the brain whose function may be altered in PTSD have been identified as the prefrontal cortex, the amygdala and the hippocampus, among which, the hippocampus is a key organ of the limbic system involved in learning and memory, as well as being a regulatory center for the stress response (4).Alterations in brain neurochemistry have been linked with neuropsychiatric disorders, including schizophrenia, Alzheimer's disease, depression and cognitive decline. Previous studies have identified a positive association between vitamin D signaling and cognitive function (5). Vitamin D may regulate neurotransmission, neuroprotection and neuroimmunomodulation as a neurosteroid hormone (5,6), in addition to its critical role in calcium (Ca 2+ ) and phosphorous regulation and skeletal mineralization (7). Hypovitaminosis D is associated with several neuropsychiatric disorders, including dementia, Parkinson's d...

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A Novel Perspective for Alzheimer's Disease: Vitamin D Receptor Suppression by Amyloid-β and Preventing the Amyloid-β Induced Alterations by Vitamin D in Cortical Neurons

Cited by 166 publications

References 0 publications

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

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

Vitamin D is not associated with incident dementia or cognitive impairment: an 18-y follow-up study in community-living old men

Changes in the expression of the vitamin D receptor and LVSCC-A1C in the rat hippocampus submitted to single prolonged stress

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