*The Role of Vitamin C in Preventing Some Neurodegenerative Diseases: Alzheimer's, Parkinson's… DOI: http://dx.doi.org/10.5772/intechopen.112185*

nitrogen-based radical species or oxygen generated during normal metabolism. It has been suggested to effectively clear superoxide in neurons in vivo [6]. VC with antioxidant properties plays a role in the structure of the nervous system, memory, and the learning process. It has been reported that p38, a member of the MAP kinase family, plays an important role in the early stages of VC- and laminin-induced myelination. Therefore, the main effect of VC on myelination is likely to be due to the preservation of the structural integrity of the basal lamina [4]. VC, due to its involvement in the synthesis and modulation of biogenic amines, has been recognized as a potential adjuvant for anxiolytic, antiepileptic, antipsychotic, and antidepressant drugs. Its redox capacity is believed to delay the onset of neurodegeneration in brain tissue by mitigating oxidative stress associated with aging. However, high doses of VC consumption have been reported to reverse or reduce neurodegeneration. Endogenous deficiency of VC in the brain leads to oxidative stress and neurodegeneration. The interaction between VC and oxidative protein folding in the brain, as well as its impact on the initiation and progression of neurodegeneration, remains unclear. The neuroprotective function of VC stems from its ability to attenuate neurotoxicity [2, 3]. VC safeguards neurons against oxidative stress, promotes their differentiation and maturation, and regulates the synthesis or release of neuroregulatory factors such as serotonin, catecholamines, and glutamate [10, 12, 18]. In a study on VC deficiency, a decrease of up to 1% in plasma and liver, and up to 30% in brain cells compared to the control group was observed [18]. Various nutrients, including VC, have been implicated in cognitive function. VC also stimulates the production of brain-derived neurotrophic factor, facilitates nerve development, reduces lipid peroxidation through collagen production, and decreases proinflammatory cytokines by binding to nuclear factor kappa β. Plasma VC is transported to the cerebrospinal fluid (CSF) predominantly through the choroid plexus via an active transport mechanism, resulting in CSF concentrations 2.5–4 times higher than in plasma. From there, it diffuses to the extracellular fluid, maintaining consistent VC levels in the CSF and providing a source for neuronal uptake. Despite significant fluctuations in plasma ascorbate levels, CSF concentrations remain relatively stable [8]. VC is recognized as highly important for the homeostasis and proper functioning of the central nervous system (CNS). Its pivotal role in the synthesis of catecholamines suggests that VC is a critical factor influencing the optimal performance of the CNS [3].
