The pattern and course of cognitive impairment in late-life depression

Köhler, Sebastian; Thomas, Alan; Barnett, Nicola; O’Brien, John T.

doi:10.1017/s0033291709990833

Cited by 120 publications

(117 citation statements)

References 49 publications

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“…We hypothesized that similar changes in the glutamatergic pyramidal neurons (Kirvell et al, 2010) in layers III (which largely project within the neocortex) and V (which make up the frontal circuits and connect to subcortical pathways to the basal ganglia and thalamus) (Tekin and Cummings, 2002;) may relate to executive dysfunction in dementia caused by cerebrovascular disease (Allan et al, 2011). We and others (Cotter et al, 2005;Rajkowska et al, 2005; have reported layer-specific reductions in pyramidal neurons of older depressed subjects, a syndrome postulated to have its basis in frontal vascular pathology (Alexopoulos et al, 1997;Ongur et al, 1998;Thomas et al, 2004;Kohler et al, 2010). Thus the question arises whether there is a similar global loss in post-stroke dementia, in which depression is also manifested (Altieri et al, 2012;Allan et al, 2013).…”

Section: Introductionmentioning

confidence: 84%

Pyramidal neurons of the prefrontal cortex in post-stroke, vascular and other ageing-related dementias

Foster

Oakley

Slade

et al. 2014

Brain

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Dementia associated with cerebrovascular disease is common. It has been reported that $30% of elderly patients who survive stroke develop delayed dementia (post-stroke dementia), with most cases being diagnosed as vascular dementia. The pathological substrates associated with post-stroke or vascular dementia are poorly understood, particularly those associated with executive dysfunction. Three separate yet interconnecting circuits control executive function within the frontal lobe involving the dorsolateral prefrontal cortex, anterior cingulate cortex and the orbitofrontal cortex. We used stereological methods, along with immunohistological and related cell morphometric analysis, to examine densities and volumes of pyramidal neurons of the dorsolateral prefrontal cortex, anterior cingulate cortex and orbitofrontal cortex in the frontal lobe from a total of 90 elderly subjects (age range 71-98 years). Post-mortem brain tissues from post-stroke dementia and post-stroke patients with no dementia were derived from our prospective Cognitive Function After Stroke study. We also examined, in parallel, samples from ageing controls and similar age subjects pathologically diagnosed with Alzheimer's disease, mixed Alzheimer's disease and vascular dementia, and vascular dementia. We found pyramidal cell volumes in layers III and V in the dorsolateral prefrontal cortex of post-stroke and vascular dementia and, of mixed and Alzheimer's disease subjects to be reduced by 30-40% compared to post-stroke patients with no dementia and controls. There were no significant changes in neuronal volumes in either the anterior cingulate or orbitofrontal cortices. Remarkably, pyramidal neurons within the orbitofrontal cortex were also found to be smaller in size when compared to those in the other two neocortical regions. To relate the cell changes to cognitive function, we noted significant correlations between neuronal volumes and total CAMCOG, orientation and memory scores and clinical dementia ratings. Total estimated neuronal densities were not significantly changed between patients with post-stroke dementia and post-stroke patients with no dementia groups or ageing controls in any of the three frontal regions. In further morphometric analysis of the dorsolateral prefrontal cortex, we showed that neither diffuse cerebral atrophy nor neocortical thickness explained the selective neuronal volume effects. We also noted that neurofilament protein SMI31 immunoreactivity was increased in post-stroke and vascular dementia compared with post-stroke patients with no dementia and correlated with decreased neuronal volumes in subjects with post-stroke dementia and vascular dementia. Our findings suggest selective regional pyramidal cell atrophy in the dorsolateral prefrontal cortex-rather than neuronal density changes per se-are associated with dementia and executive dysfunction in poststroke dementia and vascular dementia. The changes in dorsolateral prefrontal cortex pyramidal cells were not associated with neurofibrillary pathology suggesting...

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Section: Introductionmentioning

confidence: 84%

Pyramidal neurons of the prefrontal cortex in post-stroke, vascular and other ageing-related dementias

Foster

Oakley

Slade

et al. 2014

Brain

View full text Add to dashboard Cite

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“…State effects are expected to be present only during the clinical depressive episode, while trait effects are expected to endure after depressive symptoms have resolved. In a recent study, Koehler and colleagues [27] examined older subjects with and without MDD, and found that tests of global cognition, memory, executive functioning, and processing speed did not differ significantly when mood, remission status, or antidepressant treatment were taken into account. The authors concluded that cognitive deficits in late-life depression persist over months to years, affect multiple domains, and are a manifestation of trait rather than state effects of depression.…”

Section: Discussionmentioning

confidence: 99%

Neuropsychological Functioning in the Acute and Remitted States of Late-Life Depression

Koenig

DeLozier

Zmuda

et al. 2015

The American Journal of Geriatric Psychiatry

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“…20 As per newer studies, approximately half of the patients with late-onset depression have generalized cognitive impairment. 21 Symptoms of depression are often precursors of cognitive decline 22 and dementia 23 with senior individuals who have major depression and neurocognitive impairment likely to develop major neurocognitive impairments within a few years of onset of depression. 24,25 Symptoms of depression in early years are also a potential risk factor for disorders of dementia.…”

Section: Neurologic or Psychiatric Comorbiditiesmentioning

confidence: 99%

Rapid Depression Assessment in Geriatric Patients

Grossberg

Beck

Zaidi

2017

Clinics in Geriatric Medicine

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The pattern and course of cognitive impairment in late-life depression

Abstract: Cognitive deficits in late-life depression persist up to 4 years, affect multiple domains and are related to trait rather than state effects. Differences in severity and course between early and late onset depression suggest different pathogenic processes.

Cited by 120 publications

References 49 publications

Pyramidal neurons of the prefrontal cortex in post-stroke, vascular and other ageing-related dementias

Pyramidal neurons of the prefrontal cortex in post-stroke, vascular and other ageing-related dementias

Neuropsychological Functioning in the Acute and Remitted States of Late-Life Depression

Rapid Depression Assessment in Geriatric Patients

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