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Homocysteinemia and Its Neurological Effects

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The Clinical Application of Homocysteine
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Abstract

Homocysteinemia causes neurological damage through a variety of molecular mechanisms. The sequelae are, therefore, varied, ranging from neural tube defects to epilepsy to apoptosis and dementia.

Folate as well as cobalamin deficiency has been implicated in neural tube defects and both have been demonstrated to mediate these abnormalities through homocysteinemia and the ensuant alterations in methylation reactions which modulate gene expressions. In addition, homocysteinemia causes vascular remodelling of the placental vasculature too, resulting in compromised blood flow to the fetus.Vascular remodelling of the cerebral vessels results in ischemic as well as hemorrhagic events.

It has been seen that homocysteinemia is involved in the pathophysiology of almost all types of neurological as well as neuropsychiatric disorders, for e.g epilepsy, parkinson’s disease, multiple sclerosis, peripheral neuropathy, Down’s syndrome, schizophrenia, depression, bipolar disorder, etc. Hence, in these situations, it must be ascertained whether or not the patient has high circulating levels of homocysteine, and, if yes, then modulators of homocysteine may be included in their management.

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Notes

  1. 1.

    Leucovorin is a formyl derivative of tetrahydrofolate and is easily converted to the reduced folate derivatives. It, therefore, functions as the vitamin in absence or deficiency of the latter and allows for some purine/pyrimidine syntheses and, thus, DNA synthesis. Hence, it circumvents the effects of folate deficiency.

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Bhargava, S. (2018). Homocysteinemia and Its Neurological Effects. In: The Clinical Application of Homocysteine. Springer, Singapore. https://doi.org/10.1007/978-981-10-7632-9_5

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