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Late-onset depression: genetic, vascular and clinical contributions

Published online by Cambridge University Press:  17 December 2001

I. HICKIE ,
E. SCOTT ,
S. NAISMITH ,
P. B. WARD ,
K. TURNER ,
G. PARKER ,
P. MITCHELL  and
K. WILHELM
I. HICKIE
Affiliation:
From the School of Psychiatry, University of New South Wales, Sydney, Australia
E. SCOTT
Affiliation:
From the School of Psychiatry, University of New South Wales, Sydney, Australia
S. NAISMITH
Affiliation:
From the School of Psychiatry, University of New South Wales, Sydney, Australia
P. B. WARD
Affiliation:
From the School of Psychiatry, University of New South Wales, Sydney, Australia
K. TURNER
Affiliation:
From the School of Psychiatry, University of New South Wales, Sydney, Australia
G. PARKER
Affiliation:
From the School of Psychiatry, University of New South Wales, Sydney, Australia
P. MITCHELL
Affiliation:
From the School of Psychiatry, University of New South Wales, Sydney, Australia
K. WILHELM
Affiliation:
From the School of Psychiatry, University of New South Wales, Sydney, Australia
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Abstract

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Background. Neuropsychiatric research needs to examine the relationships between aetiological, genotypic and clinical risk factors and behavioural phenotypes. These relationships can now be examined in older patients with depressive disorders.

Methods. Key behavioural features, clinical and vascular risk factors and putative genotypes for late-onset neurodegenerative disorders and/or vascular 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 homozygous or heterozygous forms of the C677T mutation of the methylenetetrahydrofolate 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 associated with depression, late-onset depression, cognitive impairment, or psychomotor change. Patients with apolipoprotein E epsilon 4 were less likely to have psychotic forms of depression.

Conclusions. Patients with late-onset depression had an increased rate of the 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 assisted by currently-available preventative strategies.

Type
Original Article
Information
Psychological Medicine , Volume 31 , Issue 8 , November 2001 , pp. 1403 - 1412
Copyright
© 2001 Cambridge University Press