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Healy and colleagues1 recently reported that dopamine β-hydroxylase (DBH) activity could mediate predisposition to Parkinson’s disease through its role in catalysing the conversion of dopamine to noradrenaline (norepinephrine). By studying a promoter variant (−1021 C/T) in the DBH gene which has been shown to influence plasma DBH activity, they showed that homozygosity for the low DBH expressing T allele was protective against Parkinson’s disease, and proposed that lower levels of DBH protein might lead to increased ratios of dopamine to noradrenaline.1 In Alzheimer’s disease, significant reductions in noradrenergic neurones within locus coeruleus, as well as reduced brain noradrenaline levels, have often been reported.2 In addition, there is a causative link between reduced noradrenaline content and the potentiation of β-amyloid (Aβ) induced cortical inflammation.3 We hypothesised that relative noradrenaline deficiency associated with homozygosity for the (−1021) DBH T allele might lead to increased risk for Alzheimer’s disease, either through an independent effect or through interaction with the proinflammatory interleukin (IL) 1A and IL6 genes.
The study involved 266 patients …
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