Group 5: The cells treated with 1 µM of Aβ 1-42 + 5 µM curcumin.
![models in vitamin d video models in vitamin d video](https://m.media-amazon.com/images/I/71On6KaLbyS._AC_SX425_.jpg)
Group 4: The cells treated with 1 µM of Aβ 1-42 + 1 nM vitamin D3. Group 3: The cells treated with 1 µM of Aβ 1-42. Vitamin D3 was bought online from Amazon as 1000× stock solution:Ĭontrol Group 1: The control cells maintained in similar conditions and time without any treatment.Ĭontrol Group 2: The control cells maintained in similar conditions and time treated with 1% vehicle (ethanol). Curcumin was bought from Sigma Aldridge UK and stock solution of 10 mM was made with absolute ethanol. The cells were treated with Aβ 1-42 (Millipore Cat no. Just after plating, cells were divided into the following groups. In light of the above, this study was conducted to evaluate in detail the neuroprotective role of vitamin D, curcumin, and their combined synergistic effect on Aβ 1-42 toxicity to the primary cortical neuronal cultures. A recent study found that low-dose curcumin effectively disaggregates Aβ, as well as prevent fibril and oligomer formation, reiterating its potential use as therapy for AD. 5 - 7 Recently, curcumin has been targeted for AD therapy because of its pleiotropic effect including anti-amyloid, anti-inflammatory, and as a potent antioxidant. In addition to several lipids that contribute to generation, degradation, and aggregation of Aβ peptides, it has been reported that fat-soluble vitamin D plays an important role in the clearance of these Aβ aggregates. are more prone to aggregate and precipitate in brain parenchyma to form plaques. Cleavage by α-secretase of APP within the Aβ segment (nonamyloidogenic processing) prevents the formation of Aβ. 4 The cleavage products formed are Aβ 1-40 and Aβ 1-42. 2, 3Īβ production results from amyloidogenic processing of amyloid processing protein (APP): the sequential cleavage of APP by β and γ secretase.
#Models in vitamin d video free
This oxidative stress is mediated by the generation of excess free radicals, which has the potential to attack and react with neighboring cellular components such as proteins, lipids, and nucleic acids, resulting in cellular inflammation and Aβ deposition. Oxidative stress is one of the major contributing factors for the pathophysiology of AD.
![models in vitamin d video models in vitamin d video](https://s1.yimg.com/uu/api/res/1.2/Lba2n58JqGzAq2I3zjfPMQ--~B/Zmk9ZmlsbDtweW9mZj0wO3c9NjQwO2g9MzYwO3NtPTE7YXBwaWQ9eXRhY2h5b24-/http://media.zenfs.com/en-US/video/video.pd2upload.com/video.yahoohealth.com@081aa40d-bb3e-32d6-883b-6c0776564e71_FULL.jpg)
1 These NFTs cause shrinkage and degeneration of neurons, consequently loss of cognitive behavior. AD is a neurodegenerative disorder that is characterized by progressive loss of cognitive function, accumulation of amyloid β (Aβ) formation, and deposition of neurofibrillary tangles (NFT) in the brain cells.
![models in vitamin d video models in vitamin d video](https://i.ytimg.com/vi/onSPZ0aBUKM/hqdefault.jpg)
Alzheimer disease (AD) is the most common type of dementia, accounting for about 60-80% of all dementia cases.