et al., 2019). This indicates that the risk of AD was reduced with increased vitamin D levels. It is observed that low vitamin D levels is associated with increased risk of AD. Vitamin D is suspected to be a potential modulator of neurogenesis. Vitamin D has been shown to regulate neurotrophic factors and influencing neuronal pro-liferation, differentiation, survival and growth (Groves & Burne, 2017). Low vitamin D levels, or hypovitaminosis D, in AD rat models increased the number of amyloid plaques (Morello et al., 2018). Vitamin D is highly recommended to be tested before considering supplementation. At this time, there is no concrete evidence on an ideal level of serum vitamin D. However, a study done by Oudshoorn et al. (2008) suggests that there is a positive association between serum vitamin D levels and MMSE scores, with participants with serum vitamin D higher than 50nmol/L generally scoring the highest. In regards to dosing, in a double-blind randomized controlled trial of post-menopausal women with levels than 30ng/mL by Castle et al. (2020), women who took 2000IU daily found to perform better in learning and memory tests compared to the 600IU and 4000IU groups. Magnesium Another intervention in supporting neurogenesis is magne-sium. Magnesium affects many biochemical mechanisms vital for neuronal properties and synaptic plasticity, including the response of N-methyl D-aspartate (NMDA) receptors to excitatory amino acids, stability and viscosity of the cell mem-brane, and antagonism of calcium (Li et al., 2014). Magnesium is arguably often overlooked however it is cor-nerstone to our health. Magnesium levels were found to be decreased in various tissues of AD patients and negatively correlated with clinical deterioration (Li et al., 2014). More-over, Magnesium was demonstrated to modulate the traffick-ing and processing of amyloid-ß precursor protein in trans-genic mice (Li et al., 2014). Magnesium supplementation comes in many forms. One form that is more appropriate in managing cognitive decline is magnesium threonate. Magnesium threonate treatment was shown to reduce Aß-plaque, prevented synapse loss and memory decline in the transgenic mice (Li et al., 2014). Strikingly, magnesium threonate treatment was effective even when the treatment was given to the mice at the end-stage of their Alzheimer’s disease-like pathological progression (Li et al., 2014). Magnesium itself has a poor penetration across the blood brain barrier (Vink, 2016). However, magnesium threonate is a more permeable magnesium salt and is a preferred option in neurological conditions (Vink, 2016). Phosphatidylcholine and Citocholine Choline is a major constituent of all biological membranes including neurons and glial cells (Blusztain et al., 1990). Brain sample studies dating to the 1980s and 1990s showed reduced levels of phosphatidylcholine and phosphatidylethanolamine and increased levels of their metabolites, glycerophosphocho-line and glycerophosphoethanolamine, respectively, in the cerebral cortex of AD patients as compared to age-matched September/October 2021 Chiropractic and Naturopathic Doctor 7 Vitamin D One of the nutraceutical interventions to provide factors in building neural connections is vitamin D. Cross-sectional studies have consistently found that vitamin D levels are sig-nificantly low in individuals with AD and cognitive impairment compared to healthy adults. Longitudinal studies and me-ta-analysis have also exhibited an association of low vitamin D with cognitive impairment and Alzheimer’s disease (Sultan et al., 2020; Chai et al., 2019; Llewellyn et al., 2011) In another study done by Chai et al. (2019), there are sig-nificant positive associations between deficient vitamin D (defined as <20 ng/mL) and risk of developing AD. By divid-ing subgroups in the deficient vitamin D to moderate defi-ciency (10-20 ng/mL) and severe deficiency (<10 ng/mL), there was a greater association with AD in the severe deficiency group in comparison to the moderate deficiency group (Chai www.Cndoctor.ca CONTINUED ON PAGE 21
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