A voxel- and source-based morphometry analysis of grey matter volume differences in very-late-onset schizophrenia-like psychosis.

BACKGROUND: Very-late-onset schizophrenia-like psychosis (VLOSLP) is associated with significant burden. Its clinical importance is increasing as the global population of older adults rises, yet owing to limited research in this population, the neurobiological underpinnings of VLOSP remain insufficiently clarified. Here we address this knowledge gap using novel morphometry techniques to investigate grey matter volume (GMV) differences between VLOSLP and healthy older adults, and their correlations with neuropsychological scores. METHODS: In this cross-sectional study, we investigated whole-brain GMV differences between 35 individuals with VLOSLP (mean age 76.7, 26 female) and 36 healthy controls (mean age 75.7, 27 female) using whole-brain voxel-based morphometry (VBM) and supplementary source-based morphometry (SBM) on high resolution 3D T1-weighted MRI images. Additionally, we investigated relationships between GMV differences and cognitive function assessed with an extensive neuropsychological battery. RESULTS: VBM showed lower GMV in the thalamus, left inferior frontal gyrus and left insula in patients with VLOSLP compared to healthy controls. SBM revealed lower thalamo-temporal GMV in patients with VLOSLP. Processing speed, selective attention, mental flexibility, working memory, verbal memory, semantic fluency and confrontation naming were impaired in patients with VLOSLP. Correlations between thalamic volumes and memory function were significant within the group of individuals with VLOSLP, whereas no significant associations remained in the healthy controls. CONCLUSIONS: Lower GMV in the thalamus and fronto-temporal regions may be part of the underlying neurobiology of VLOSLP, with lower thalamic GMV contributing to memory impairment in the disorder.

Ghosts from the past? The association between childhood interpersonal trauma, attachment and anxiety and depression in late life.

Objectives: Research suggests that vulnerability for anxiety and depression in late life results from a complex interaction between (neuro)biological and environmental factors. In this context, there is growing evidence for the role of childhood trauma on vulnerability for both anxiety and depression throughout the course of life, mainly through its effects on attachment as a biologically based neurodevelopmental stress regulation system. Yet, the impact of childhood trauma on depression and anxiety in late life specifically remains unclear. The current study therefore aims to investigate the association between retrospectively reported childhood interpersonal trauma, attachment dimensions and levels of anxiety and depression in late life.Method: A sample of 81 community dwelling older adults completed measures of early and current adversity, attachment dimensions, and levels of anxiety and depression.Results: The occurrence and frequency of childhood trauma, but not later negative adult life events, was associated with late life anxiety and depression. Both attachment anxiety and avoidance were related to anxiety and depression. Only attachment anxiety affected the association between childhood trauma, and emotional neglect in particular, and late life anxiety and depression.Conclusion: Childhood trauma may be associated with anxiety and depression in late life. Part of this association is probably indirect, via the effect of insecure attachment and high levels of attachment anxiety in particular.

The neuropsychology and neurobiology of late-onset schizophrenia and very-late-onset schizophrenia-like psychosis: A critical review.

OBJECTIVE: The current review discusses neuropsychological profiles and the longitudinal course of cognitive dysfunction in Late Onset Schizophrenia (LOS) and Very-late-onset schizophrenia-like psychosis (VLOSLP), and attempts to clarify its neurobiological underpinnings. METHOD: A systematic literature search resulted in 29 publications describing original research on the neuropsychology of LOS/VLOSLP and 46 studies focussing on neurobiology. RESULTS: Although mildly progressive cognitive impairment is usually present, only a subgroup of LOS/VLOSLP develops dementia during a 10-year follow-up succeeding the onset of psychosis. This coincides with the absence of neuropathological evidence for neurodegeneration in many cases. Cognitive deterioration is characterized by deficits in (working) memory, language, psychomotor speed and executive functioning. Underlying neurobiological changes encompass white matter pathology, increased ventricle-to-brain ratio (VBR) with coinciding atrophy and hypo-metabolism of frontal, temporal and subcortical areas. CONCLUSIONS: Multiple changes in neurobiology and cognition contributing to LOS/VLOSLP may reflect stress-related accelerated brain aging rather than neurodegenerative pathology. Their involvement in the onset of illness, however, might be inversely proportional to pre-existing (psychosocial and/or genetic) vulnerability to psychosis.