\u27Vitamin D and cognition in older adults\u27: updated international recommendations.

BACKGROUND: Hypovitaminosis D, a condition that is highly prevalent in older adults aged 65 years and above, is associated with brain changes and dementia. Given the rapidly accumulating and complex contribution of the literature in the field of vitamin D and cognition, clear guidance is needed for researchers and clinicians. METHODS: International experts met at an invitational summit on \u27Vitamin D and Cognition in Older Adults\u27. Based on previous reports and expert opinion, the task force focused on key questions relating to the role of vitamin D in Alzheimer\u27s disease and related disorders. Each question was discussed and voted using a Delphi-like approach. RESULTS: The experts reached an agreement that hypovitaminosis D increases the risk of cognitive decline and dementia in older adults and may alter the clinical presentation as a consequence of related comorbidities; however, at present, vitamin D level should not be used as a diagnostic or prognostic biomarker of Alzheimer\u27s disease due to lack of specificity and insufficient evidence. This population should be screened for hypovitaminosis D because of its high prevalence and should receive supplementation, if necessary; but this advice was not specific to cognition. During the debate, the possibility of \u27critical periods\u27 during which vitamin D may have its greatest impact on the brain was addressed; whether hypovitaminosis D influences cognition actively through deleterious effects and/or passively by loss of neuroprotection was also considered. CONCLUSIONS: The international task force agreed on five overarching principles related to vitamin D and cognition in older adults. Several areas of uncertainty remain, and it will be necessary to revise the proposed recommendations as new findings become available

The Effects of Vitamin D Receptor Silencing on the Expression of LVSCC-A1C and LVSCC-A1D and the Release of NGF in Cortical Neurons

Recent studies have suggested that vitamin D can act on cells in the nervous system. Associations between polymorphisms in the vitamin D receptor (VDR), age-dependent cognitive decline, and insufficient serum 25 hydroxyvitamin D(3) levels in Alzheimer's patients and elderly people with cognitive decline have been reported. We have previously shown that amyloid β (Aβ) treatment eliminates VDR protein in cortical neurons. These results suggest a potential role for vitamin D and vitamin D-mediated mechanisms in Alzheimer's disease (AD) and neurodegeneration. Vitamin D has been shown to down-regulate the L-type voltage-sensitive calcium channels, LVSCC-A1C and LVSCC-A1D, and up-regulate nerve growth factor (NGF). However, expression of these proteins when VDR is repressed is unknown. The aim of this study is to investigate LVSCC-A1C, LVSCC-A1D expression levels and NGF release in VDR-silenced primary cortical neurons prepared from Sprague-Dawley rat embryos.qRT-PCR and western blots were performed to determine VDR, LVSCC-A1C and -A1D expression levels. NGF and cytotoxicity levels were determined by ELISA. Apoptosis was determined by TUNEL. Our findings illustrate that LVSCC-A1C mRNA and protein levels increased rapidly in cortical neurons when VDR is down-regulated, whereas, LVSCC-A1D mRNA and protein levels did not change and NGF release decreased in response to VDR down-regulation. Although vitamin D regulates LVSCC-A1C through VDR, it may not regulate LVSCC-A1D through VDR.Our results indicate that suppression of VDR disrupts LVSCC-A1C and NGF production. In addition, when VDR is suppressed, neurons could be vulnerable to aging and neurodegeneration, and when combined with Aβ toxicity, it is possible to explain some of the events that occur during neurodegeneration

Neuroectodermal appendage: A case report and review

[No abstract available

Yings and Yangs of acute ethanol intoxication in experimental traumatic brain injury

Although the deleterious effects of acute alcohol intoxication on traumatic brain injury (TBI) are well known, neuroprotective features of lower doses of ethanol (EtOH) before head trauma have been reported during recent years. Inhibition of N-methyl-D-aspartate receptor (NMDA)-mediated excitotoxicity by lower doses of EtOH has been believed to be responsible for this protection. The aim of this study was to show the neuroprotective effects of low and moderate doses of EtOH and to compare their efficacy in each group. Acute EtOH intoxication at low and moderate doses was induced 40 minutes before trauma. Severe TBI was administered in Sprague-Dawley rats using an impact acceleration model. At 24 hours after trauma, all the rats were decapitated and hippocampi were evaluated under light microscopy. According to our results, red neuron formation and vacuolar degeneration in the CA1 and CA3 sectors of the hippocampi were less prominent in the lowdose and moderate-dose EtOH plus trauma groups than in the trauma only group. In addition, edema formation was less prominent in the EtOH plus trauma group. When comparing the low-dose EtOH Plus trauma and moderate-dose EtOH Plus trauma groups, an almost normal appearance of the hippocampus was noted in the moderate-dose EtOH plus trauma group. EtOH may have a neuroprotective effect when administered at a lower dose, particularly a moderate dose, and this protection may be a result of the inhibition of NMDA receptor-mediated excitotoxicity