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Patients with dementia with Lewy bodies (DLB) often experience visual hallucinations, which are related to decreased quality of life for patients and increased caregiver distress. The pathologic changes that contribute to visual hallucinations are not known, but several hypotheses implicate deficient attentional processing. The superior colliculus has a role in visual attention and planning eye movements and has been directly implicated in several models of visual hallucinations. Therefore, the present study sought to identify neurodegenerative changes that may contribute to hallucinations in DLB.

The impact of major depression in late life is considerable and set to intensify with a worldwide shift in demographic profile toward an elderly population. Although the precise neurobiological mechanisms are not fully understood, a significant body of clinical, epidemiological, and imaging data have suggested divergent pathophysiological pathways underlie depression in late life, when compared with younger patients. Neuroimaging studies have demonstrated significant increases in white matter hyperintensities in late-life depression in several key areas involved in affective circuitry. Postmortem cellular morphometry studies have played a vital role in the identification of discrete changes in the brain microstructure in depression. This review draws together such postmortem studies, which have utilized tissue from younger/mixed age and late-life depressed patients. These findings have suggested varying neuronal and glial cell pathology in depression between different age cohorts. This age-related disparity may suggest different pathophysiological basis for depression, with vascular factors playing a potentially greater role in late life.

We have previously shown delayed poststroke dementia in elderly (≥75 years old) stroke survivors is associated with medial temporal lobe atrophy; however, the basis of the structural and functional changes is unknown.

Hippocampal atrophy is widely recognized in Alzheimer disease (AD). Whether neurons within hippocampal subfields are similarly affected in other aging-related dementias, particularly after stroke, remains an open question. We investigated hippocampal CA3 and CA4 pyramidal neuron volumes and densities using 3-dimensional stereologic techniques in postmortem samples from a total of 67 subjects: poststoke demented (PSD; n = 11), nondemented stroke survivors (PSND) and PSD patients from the CogFAST (Cognitive Function After Stroke) cohort (n = 13), elderly controls (n = 12), and subjects diagnosed as having vascular dementia (n = 11), AD (n = 10), and mixed AD and vascular dementia (n = 10). We found that CA3 and CA4 neuron volumes were reduced in PSD samples compared with those in PSND samples. The CA3 and CA4 neuron volumes were positively correlated with poststroke global cognitive function but were not associated with the burden of AD pathology. There were no differences in total neuron densities in either subfield in any of the groups studied. Our results indicate that selective reductions in CA4 and to a lesser extent CA3 neuron volumes may be related to post-stroke cognitive impairment and aging-related dementias. These data suggest that CA4 neurons are vulnerable to disease processes and support our previous finding that a reduction in hippocampal neuron volume predominantly reflects vascular mechanisms as contributing to dementia after stroke.