Abstract:
OBJECTIVE:There is clear evidence of a genetic component in major depression, and several studies indicate that neuropeptide Y (NPY) could play an important role in the pathophysiology of the disease. A well-known polymorphism encoding the substitution of leucine to proline in the signal peptide sequence of NPY (Leu7Pro variation) was previously found to protect against depression. Our study aimed at replicating this association in a large Danish population with major depression. METHOD:Leu7Pro was studied in a sample of depressed patients and ethnically matched controls, as well as psychiatric disease controls with schizophrenia. Possible functional consequences of Leu7Pro were explored in vitro. RESULTS:In contrast to previous studies, Pro7 appeared to be a risk allele for depression, being significantly more frequent in the depression sample (5.5%, n = 593; p = 0.009; odds ratio, OR: 1.46) as compared to ethnically matched controls (3.8%, n = 2912), while schizophrenia patients (4.1%, n = 503) did not differ. In vitro, the Pro7 substitution appeared to be associated with reduced levels of NPY without affecting its mRNA level. CONCLUSION:The Leu7Pro variation may increase the risk of major depression, possibly by affecting the biosynthesis of NPY.
journal_name
Acta Neuropsychiatrjournal_title
Acta neuropsychiatricaauthors
Koefoed P,Woldbye DP,Hansen TV,Eplov LF,Christiansen SH,Mors O,Kessing LV,Werge T,Kaipio K,Pesonen U,Fahmy T,Mellerup E,Jakobsen KD,Hansen ES,Knudsen GM,Bukh JD,Bock C,Lindberg C,Kristensen AS,Dam H,Nordentoft M,doi
10.1111/j.1601-5215.2011.00600.xsubject
Has Abstractpub_date
2012-04-01 00:00:00pages
81-90issue
2eissn
0924-2708issn
1601-5215pii
S0924270800026016journal_volume
24pub_type
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