Abstract
Since the era of Gaupp who introduced the concept of atheroscletic depressive disorder,
the concept of late-life depression has been correlated with cerebrovascular comorbidities,
microvascular lesions, frontal cortical and subcortical gray and white matter hyperintensities.
The predominant neuropsychological deficits concern the domains of planning, organization
and abstraction, with executive dysfunction being the predominant finding. MRI studies
reveal a higher prevalence of white matter lesions in elderly patients with depression.
Molecular mechanisms underlying the disease still remain unclear. Hyperhomocysteinemia
has been associated with depression through its toxicity to neurons and blood vessels.
Endothelial dysfunction is another possible mechanism referring to the loss of vasodilatation
capacity. Inflammatory phenomena, such as increased peripheral leucocytes, elevated
CRP and cytokine levels, could play a role in endothelial dysfunction. In this review
we will briefly combine findings from neurobiological, epidemiological, structural
and post-mortem data. A more complex model in late-life depression combining different
modalities could be an elucidating approach to the disease's etiopathogeny in the
future.
Keywords
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Article info
Publication history
Published online: June 11, 2012
Accepted:
May 23,
2012
Received in revised form:
May 21,
2012
Received:
February 28,
2012
Identification
Copyright
© 2012 Elsevier B.V. Published by Elsevier Inc. All rights reserved.