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 [email protected], Pascal Millet [email protected].
Maria Morello [email protected]; Véréna Landel, [email protected]; Emmanuelle Lacassagne, [email protected]; Kevin Baranger. [email protected], Cedric Annweiler, [email protected]
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 monthsPlaque 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--- 1. Additional mouse and Vitamin D studies in Vitamin D Life 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--- 1. Overview Alzheimer's-Cognition and Vitamin D starts with{include}--- 1. Cognitive category starts with the following{include}* Dementia surprisingly associated with low vitamin D (should not a surprise) – Aug 2014 has the following
--- 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 Vitamin D Life
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.