Neurological Manifestations of Hypovitaminosis

Abstract

SUMMARY AND CONCLUSION H ypovitaminosis has been associated with many neurological conditions. However, an actual mechanism of attack for each of the conditions has yet to be solidified. Retinoic acid receptors (RARs: RARα, β and γ) and their ligands (retinoids), such as the endogenous RAR ligand all-trans-retinoic acid (RA) are taking into account knowledge about PD, ALS and other neurodegenerative diseases. Many studies on pattern formation have confirmed the importance of retinoids in spinal cord and brain development. These findings prompted detailed analyses of RARs in brain and extensive studies of RAR signaling pathways in neurological diseases. When it comes to neurological concerns, the vitamins B1 (thiamine), B2 (riboflavin), B3 (niacin), biotin, B6 (pyridoxine), folic acid and B12 (cobalamin) are especially important. These B group vitamins have specific effects on brain cell functions and their deficiency leads to different neurological and psychological problems. Vitamin B12 deficiency is not very common in young adults but older people are more prone to this condition. Various studies have shown that cobalamin deficiency is more common in patients with Alzheimer’s disease, Parkinson’s disease and various conditions causing dementia. But a causal relationship between vitamin B12 deficiency and these diseases remains inconclusive. However, most of the studies that relate hyperhomocysteinemia with Alzheimer’s disease and other causes of dementia report positive results. This means that elevated levels of homocysteine in the blood increase the risk of these diseases. There also exists controversy in the reports of studies that evaluate an association between vitamin B12 deficiency and Multiple Sclerosis. That ascorbate is important for neuronal maturation and function, as well as for protection of the brain against oxidant stress is well supported by the evidence presented in this review. There is further evidence to support the potential for vitamin C as a therapeutic avenue for Alzheimer's disease. Orally administered ascorbate protected the CA1 area of the hippocampus against oxidative stress and cytokine release induced by injection of fibrillar β-amyloid. Scopolamine is often used as a pharmacological model for Alzheimer's disease. As noted earlier, ascorbate blocked or attenuated the effects of scopolamine in several different types of studies. Furthermore, ascorbate has been shown to be an effective acetylcholinesterase inhibitor, the most common form of treatment used for Alzheimer's disease. These results may seem contradictory, since scopolamine can also inhibit acetylcholinesterase, however, the net effect of vitamin C appears to be a boost to cholinergic system functioning, although this relationship needs further investigation. Ascorbate has been shown to improve bioavailability of levodopa (which can then be converted into dopamine) in members of an elderly Parkinson's disease population with low baseline bioavailability for levodopa. Hypovitaminosis D is associated with several neurological disorders including dementia, Parkinson's disease, multiple sclerosis, epilepsy, and schizophrenia. VDR haplotypes were detected with increased frequency in patient with Alzheimer's disease while other VDR haplotypes were detected with increased frequency, suggesting that specific haplotypes may increase or decrease risk of developing Alzheimer's. It is hypothesized that this lack of VDRs in the hippocampus prevents the proper functioning (i.e. memory) of this structure. Studies suggest that low vitamin D levels could play a role in PD. One proposed mechanism linking vitamin D to Parkinson's disease involves the Nurr 1 gene. Vitamin D deficiency is associated with decreased expression of the Nurr1 gene, a gene responsible for development of DA neurons. Based on other studies, the higher intake of vitamin D is associated with a lower risk for MS. The mechanism for this association is not fully established, however, a proposed mechanism involves inflammatory cytokines. Hypovitaminosis D is associated with an increase in proinflammatory cytokines and decrease in anti-inflammatory cytokines. The increase in these specific cytokines is associated with the degradation of the myelin sheath. More specifically, Vitamin D is involved in the down regulation of cytokine IL-6, which is a proconvulsant. [Additionally, vitamin D is associated with the up regulation of neurotrophic factors: GDNF and TN3. These neurotrophic factors are anticonvulsant. Hypovitaminosis E may cause neuromuscular problems-such as spinocerebellar ataxia and myopathies and neurological problems-may include dysarthria, absence of deep tendon reflexes, loss of vibratory sensation and proprioception, and positive Babinski sign. Many researchers have questioned whether the depletion of some vitamins actually causes these disorders or if vitamins deficiency is a symptom of these disorders. Future research is needed to fully answer these questions.