Amyloid brain plaque both prevented and removed by high vitamin D (in mice)
Vitamin D Improves Neurogenesis and Cognition in a Mouse Model of Alzheimer’s Disease
Mol Neurobiol. 2018; 55(8): 6463–6479. doi: 10.1007/s12035-017-0839-1
François Féron francois.feron@univ-amu.fr, Pascal Millet pascal.millet@univ-amu.fr.
Maria Morello morello@uniroma2.it; Véréna Landel, landel.verena@gmail.com; Emmanuelle Lacassagne, emmanuelle.lacassagne@gmail.com; Kevin Baranger. kevin.baranger@univ-amu.fr, Cedric Annweiler, Cedric.Annweiler@chu-angers.fr
1. # Prevented plaque from transgenic mice with high dose vitamin D at 1-6 months
More brain cells with early high dose
1. # Removed plaque from transgenic mice with high dose vitamin D at 4-9 months
Plaque decreased with high dose later in life
1. Life Extension Magazine winter edition covered this study
"Vitamin D Removes Amyloid Brain Plaque"
LEF Magazine continues to recommend 50-80 ng level of vitamin D via 5,000 to 8,000 IU
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1. Additional mouse and Vitamin D studies in VitaminDWiki include
* Colitis treated by activated vitamin D getting into the colon via emulsion (mice) – July 2018
* Multiple Sclerosis varies with race and sex in mice too – July 2018
* Traffic pollution increases asthma unless supplement with Vitamin D (mice) June 2018
* Vitamin D in breast milk increased later spacial learning in adult mice – April 2018
* Ischemic strokes half as large if had good level of vitamin D (mice) – Feb 2018
* Mice designed to get diabetes often failed to get diabetes if they had lots of vitamin D during their lives – Feb 2014
* Smoking caused more breathing problems in those (mice) with low vitamin D – Sept 2015
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1. Overview Alzheimer's-Cognition and Vitamin D starts with
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1. Cognitive category starts with the following
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* Dementia surprisingly associated with low vitamin D (should not a surprise) – Aug 2014 has the following
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1. See also web
* The End of Alzheimer's and Dementia if adjust Vitamin D, B-12, Iron, Omega-3, etc.
* Two items on Dr. Bredesen's book The End of Alzheimer's
* [100 Simple Things You Can Do to Prevent Alzheimer's and Age-Related Memory Loss](https://www.amazon.com/Simple-Things-Prevent-Alzheimers-Age-Related-ebook/dp/B003JTHY1C/ref=sr_1_1?ie=UTF8&qid;=1543763356&sr;=8-1&keywords;=100+Simple+Things+We+Can+Do+to+Prevent+Alzheimer%E2%80%99s) 2010
📄 Download the PDF from VitaminDWiki
The impairment of hippocampal neurogenesis at the early stages of Alzheimer’s disease (AD) is believed to support early cognitive decline. Converging studies sustain the idea that vitamin D might be linked to the pathophysiology of AD and to hippocampal neurogenesis. Nothing being known about the effects of vitamin D on hippocampal neurogenesis in AD, we assessed them in a mouse model of AD. In a previous study, we observed that dietary vitamin D supplementation in female AD-like mice reduced cognitive decline only when delivered during the symptomatic phase. With these data in hand, we wondered whether the consequences of vitamin D administration on hippocampal neurogenesis are stage-dependent. Male wild-type and transgenic AD-like mice (5XFAD model) were fed with a diet containing either no vitamin D (0VD) or a normal dose of vitamin D (NVD) or a high dose of vitamin D (HVD), from month 1 to month 6 (preventive arm) or from month 4 to month 9 (curative arm). Working memory was assessed using the Y-maze, while amyloid burden, astrocytosis, and neurogenesis were quantified using immunohistochemistry. In parallel, the effects of vitamin D on proliferation and differentiation were assayed on primary cultures of murine neural progenitor cells. Improved working memory and neurogenesis were observed when high vitamin D supplementation was administered during the early phases of the disease, while a normal dose of vitamin D increased neurogenesis during the late phases. Conversely, an early hypovitaminosis D increased the number of amyloid plaques in AD mice while a late hypovitaminosis D impaired neurogenesis in AD and WT mice. The observed in vivo vitamin D-associated increased neurogenesis was partially substantiated by an augmented in vitro proliferation but not an increased differentiation of neural progenitors into neurons. Finally, a sexual dimorphism was observed. Vitamin D supplementation improved the working memory of males and females, when delivered during the pre-symptomatic and symptomatic phases, respectively. Our study establishes that (i) neurogenesis is improved by vitamin D in a male mouse model of AD, in a time-dependent manner, and (ii) cognition is enhanced in a gender-associated way. Additional pre-clinical studies are required to further understand the gender- and time-specific mechanisms of action of vitamin D in AD. This may lead to an adaptation of vitamin D supplementation in relation to patient’s gender and age as well as to the stage of the disease.