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• W2108083723 abstract "Familial dysautonomia (FD), a recessive neurodegenerative disease, is caused by mutations in the IKBKAP gene that result in the production of nonfunctional IKAP protein. Manifestations of FD include autonomic crises characterized by hypertension, tachycardia, diaphoresis, and vomiting. Elevated plasma levels of norepinephrine (NE) and dopamine observed during autonomic crises and an exaggerated hypertensive response to low doses of NE prompted an examination of monoamine oxidase (MAO) levels, key isoenzymes responsible for degrading biogenic and dietary monoamines, in individuals with FD. Fetal tissue homozygous for the common FD-causing mutation and peripheral blood cells of individuals with FD have reduced MAO A mRNA levels. FD-derived cells, stimulated with tocotrienols or EGCG to produce increased levels of functional IKAP, express increased amounts of MAO A mRNA transcript and protein. Administration of tocotrienol to individuals with FD results in increased expression of both functional IKAP and MAO A transcripts in their peripheral blood cells. These findings provide new insight into the pathophysiology of FD and demonstrate the value of therapeutic approaches designed to elevate cellular levels of functional IKAP and MAO A." @default.
• W2108083723 created "2016-06-24" @default.
• W2108083723 creator A5045849420 @default.
• W2108083723 creator A5090634823 @default.
• W2108083723 date "2005-10-01" @default.
• W2108083723 modified "2023-09-25" @default.
• W2108083723 title "Tocotrienols reverse IKAP and monoamine oxidase deficiencies in familial dysautonomia" @default.
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• W2108083723 doi "https://doi.org/10.1016/j.bbrc.2005.08.054" @default.
• W2108083723 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16125677" @default.
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