vitamin-d-2 and Neurodegenerative-Diseases

vitamin-d-2 has been researched along with Neurodegenerative-Diseases* in 3 studies

Reviews

1 review(s) available for vitamin-d-2 and Neurodegenerative-Diseases

Article	Year
[Vitamin D supplemention in the elderly]. Deutsche medizinische Wochenschrift (1946), 2011, Volume: 136, Issue:48 Topics: Accidental Falls; Aged; Cholecalciferol; Depressive Disorder; Dose-Response Relationship, Drug; Ergocalciferols; Humans; Neurodegenerative Diseases; Nutritional Requirements; Osteoporotic Fractures; Risk Factors; Vitamin D; Vitamin D Deficiency	2011

Other Studies

2 other study(ies) available for vitamin-d-2 and Neurodegenerative-Diseases

Article	Year
Vitamin D2 suppresses amyloid-β 25-35 induced microglial activation in BV2 cells by blocking the NF-κB inflammatory signaling pathway. Life sciences, 2016, Sep-15, Volume: 161 Present emerging world is emphasizing the implication of vitamin D deficiency associated with development of inflammation and neurodegenerative disorder like Alzheimer's disease (AD). The chief neuropathological hallmark of AD is aggregation of amyloid-beta (Aβ) peptides surrounding microglial cells in human brain. Microglial activation plays a key role in inflammatory response and neuronal injury. Naturally abundant vitamin D2 (VD2) exhibiting anti-inflammatory activities are yet to explore more. This study has investigated the inhibitory effect of VD2 on inflammatory activities of BV2 microglial cells.. Cellular compatibility of VD2 and Aβ25-35 protein in treated BV2 microglial cells were measured by CCK-8 assay. Induction of iNOS, COX-2 and NF-κB signaling cascade were measured by western blotting, whereas pro-inflammatory cytokines were measured by ELISA. In addition, generation of ROS was detected by fluorescence intensity.. Morphological observations showed that Aβ25-35 induced BV2 cells stimulation noticeably got reduced in VD2 pre-treated group at 24h time period. Anti-inflammatory activities of VD2 was observed demonstrating the inhibition of up-regulated iNOS and COX-2 protein expression further confirmed by attenuating the activated microglia released pro-inflammatory cytokines IL-1β, IL-6, TNF- α and ROS, while blocking the phosphorylation of NF-κB p65 in nucleus by preventing IκB-α degradation and phosphorylation in cytosol.. The present study revealed that VD2 blocked the phosphorylation of NF-κB inflammatory signaling pathway in Aβ25-35 induced activated BV2 microglial cells by suppressing ROS generation and inflammatory cytokines. Our finding suggests that vitamin D2 has therapeutic potential against inflammation and Alzheimer's disease. Topics: Amyloid beta-Peptides; Animals; Cell Line, Transformed; Ergocalciferols; Humans; Mice; Microglia; Neurodegenerative Diseases; NF-kappa B; Peptide Fragments; Reactive Oxygen Species; Signal Transduction	2016
[Fortuitous discovery of Fahr's syndrome after seizures]. Revue neurologique, 2015, Volume: 171, Issue:12 Topics: Basal Ganglia Diseases; Calcinosis; Calcium; Epilepsy, Tonic-Clonic; Ergocalciferols; Humans; Male; Middle Aged; Neurodegenerative Diseases; Seizures; Syndrome; Tomography, X-Ray Computed; Treatment Outcome	2015

Article

Year

Vitamin D2 suppresses amyloid-β 25-35 induced microglial activation in BV2 cells by blocking the NF-κB inflammatory signaling pathway.

Life sciences, 2016, Sep-15, Volume: 161

Present emerging world is emphasizing the implication of vitamin D deficiency associated with development of inflammation and neurodegenerative disorder like Alzheimer's disease (AD). The chief neuropathological hallmark of AD is aggregation of amyloid-beta (Aβ) peptides surrounding microglial cells in human brain. Microglial activation plays a key role in inflammatory response and neuronal injury. Naturally abundant vitamin D2 (VD2) exhibiting anti-inflammatory activities are yet to explore more. This study has investigated the inhibitory effect of VD2 on inflammatory activities of BV2 microglial cells.. Cellular compatibility of VD2 and Aβ25-35 protein in treated BV2 microglial cells were measured by CCK-8 assay. Induction of iNOS, COX-2 and NF-κB signaling cascade were measured by western blotting, whereas pro-inflammatory cytokines were measured by ELISA. In addition, generation of ROS was detected by fluorescence intensity.. Morphological observations showed that Aβ25-35 induced BV2 cells stimulation noticeably got reduced in VD2 pre-treated group at 24h time period. Anti-inflammatory activities of VD2 was observed demonstrating the inhibition of up-regulated iNOS and COX-2 protein expression further confirmed by attenuating the activated microglia released pro-inflammatory cytokines IL-1β, IL-6, TNF- α and ROS, while blocking the phosphorylation of NF-κB p65 in nucleus by preventing IκB-α degradation and phosphorylation in cytosol.. The present study revealed that VD2 blocked the phosphorylation of NF-κB inflammatory signaling pathway in Aβ25-35 induced activated BV2 microglial cells by suppressing ROS generation and inflammatory cytokines. Our finding suggests that vitamin D2 has therapeutic potential against inflammation and Alzheimer's disease.

Topics: Amyloid beta-Peptides; Animals; Cell Line, Transformed; Ergocalciferols; Humans; Mice; Microglia; Neurodegenerative Diseases; NF-kappa B; Peptide Fragments; Reactive Oxygen Species; Signal Transduction

2016

[Fortuitous discovery of Fahr's syndrome after seizures].

Revue neurologique, 2015, Volume: 171, Issue:12

Topics: Basal Ganglia Diseases; Calcinosis; Calcium; Epilepsy, Tonic-Clonic; Ergocalciferols; Humans; Male; Middle Aged; Neurodegenerative Diseases; Seizures; Syndrome; Tomography, X-Ray Computed; Treatment Outcome

2015