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Hippocampal volume change in depression: late- and early-onset illness compared

School of Neurology, Neurobiology and Psychiatry, University of Psychiatry, University Newcastle, Royal Victoria Infirmary, Newcastle upon Tyne

Robert Barber, MD

Institute for Ageing and Health, Newcastle General Hospital, Newcastle upon Tyne

Anil Gholkar, MD

Regional Neurosciences Centre, Newcastle General Hospital, Newcastle upon Tyne

Allan H. Young, PhD

School of Neurology, Neurobiology and Psychiatry, University of Newcastle, Royal Victoria Infirmary, Newcastle upon Tyne

John T. O’brien, DM

Wolfson Research Centre, Institute for Ageing and Health, University of Newcastle, Newcastle General Hospital, Newcastle upon Tyne, UK

Correspondence: Dr A. J. Lloyd, School of Neurology, Neurobiology and Psychiatry, University of Newcastle, Leazes Wing, Royal Victoria Infirmary, Newcastle uponTyne NE1 4LP, UK. E-mail: a.j.lloyd{at}ncl.ac.uk

Declaration of interest Funding from the Wellcome Trust and the Stanley Foundation.

Background Evidence for structural hippocampal change in depression is limited despite reports of neuronal damage due to hypercortisolaemia and vascular pathology.

Aims To compare hippocampal and white matter structural change in demographically matched controls and participants with early-onset and late-onset depression.

Method High-resolution volumetric magnetic resonance imaging (MRI) and rating of MRI hyperintensities.

Results Atotal of 51 people with depression and 39 control participants were included. Participants with late-onset depression had bilateral hippocampal atrophy compared with those with early-onset depression and controls. Hippocampal volumes did not differ between control participants and those with early-onset depression. Age of depression onset correlated (negatively) with hippocampal volume but lifetime duration of depression did not. Hyperintensity ratings did not differ between groups.

Conclusions Results suggest that acquired biological factors are of greater importance in late-than in early-onset illness and that pathological processes other than exposure to hypercortisolaemia of depression underlie hippocampal atrophy in depression of late life.

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