Several risk factors for Vitamin C deficiency have been identified, including disease, smoking, and inadequate dietary intake, but also pregnancy and genetics have been shown to affect Vitamin C levels. Based on Vitamin C’s involvement in important processes in the brain, there is reason to believe that these could be adversely affected by a deficiency. The functions of Vitamin C include its antioxidant function of upholding redox balance, and thus reducing the effects of oxidative stress in the brain. But vitamin C also has other important functions in the brain. These include modulation of the cholinergic, catecholinergic, and glutamergic systems of the brain. Vitamin C supports the general development of neurons ( nerve cells in the brain) through maturation, differentiation and myelin formation. Vitamin C is involved in several processes in the vascular system including helping maintain integrity and function of blood vessels, e.g., nitric oxide synthase, which regulates vessel relaxation through production of nitric oxide.
Vitamin C deficiency appears to pose numerous threats to cognitive function. The involvement of vitamin C in vessel integrity, antioxidant balance and neuromodulation in the brain has prompted investigations into the effect of the vitamin on the developing brain, in aging and in stroke. In the developing brain, neuronal density and maturation is compromised by Vitamin C deficiency, giving rise to decreased brain volume. In the aging brain deficiency affects ACh release and may impair cognitive function through reduced signal transduction but also through amyloid β deposition resulting in generation of reactive oxygen species and increased neuronal impairment in people suffering from Alzheimer’s disease. In stroke, Vitamin C deficiency may result in decreased vessel integrity through decreased nitric oxide synthase generation and impaired synthesis of mature collagen; potentially leading to increased plaque formation and incidence of stroke. Furthermore, an increase in infarct area may result from oxidative damage causing increased neuronal death.
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