Late-onset depression: genetic, vascular and clinical contributions

Citation
I. Hickie et al., Late-onset depression: genetic, vascular and clinical contributions, PSYCHOL MED, 31(8), 2001, pp. 1403-1412
Citations number
58
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Psychiatry,"Clinical Psycology & Psychiatry","Neurosciences & Behavoir
Journal title
PSYCHOLOGICAL MEDICINE
ISSN journal
0033-2917 → ACNP
Volume
31
Issue
8
Year of publication
2001
Pages
1403 - 1412
Database
ISI
SICI code
0033-2917(200111)31:8<1403:LDGVAC>2.0.ZU;2-U
Abstract
Background. Neuropsychiatric research needs to examine the relationships be tween aetiological, genotypic and clinical risk factors and behavioural phe notypes. These relationships can now be examined in older patients with dep ressive disorders. Methods. Key behavioural features, clinical and vascular risk factors and p utative genotypes for late-onset neurodegenerative disorders and/or vascula r disease were recorded in 78 older patients with depression (mean age = 54 (.)9 years, S.D. = 14(.)1) and 22 healthy control subjects (mean age 55(.)5 years, S.D. = 9(.)6). Results. Two or more vascular risks were more common in older patients (65 % v. 26 % of control subjects, P < 0(.)01), and in patients with late-onset disorders (82 % v. 57 % in patients with early-onset disorders, P < 0(.)05 ). Patients with late-onset depression had a higher prevalence of the homoz ygous or heterozygous forms of the C677T mutation of the methylenetetrahydr ofolate reductase enzyme (MTHFR)(74 % v. 48 % in patients with early-onset disorders, P < 0(.)05). In a multivariate model, only presence of the MTHFR gene mutation predicted late-onset depression (odds ratio = 3(.)8, 95 % CI = 1(.)1-12(.)9). Neither apolipoprotein E epsilon 4 or epsilon 2 was assoc iated with depression, late-onset depression, cognitive impairment, or psyc homotor change. Patients with apolipoprotein E epsilon 4 were less likely t o have psychotic forms of depression. Conclusions. Patients with late-onset depression had an increased rate of t he C677T MTHFR gene mutation and other vascular risk factors. This suggests that a proportion of these patients may have genetically-determined and/or other vascular aetiologies. Patients at risk of these disorders may be ass isted by currently-available preventative strategies.