No abstract

This investigation concerns the mental changes associated with Lewy bodies. Lewy bodies are inclusion bodies found in nerve cells and are characteristic of idiopathic Parkinson's disease. It has also been suggested that they may occur as a normal ageing change. Previous literature concerning the psychiatric symptoms of Lewy body disease is reviewed. Dementia and parkinsonism‐associated depression have been previously recognized. For this study the psychiatric histories of two groups of autopsied mental hospital patients were compared; one group with Lewy bodies, and one group without Lewy bodies. There were 212 autopsies. Of these, 15 had Lewy bodies and 197 did not. Clinical and neuropathological descriptions of those with Lewy bodies are given. Findings are also presented in tabulated form, and the groups are compared statistically. Clinical diagnosis of Parkinson's disease and admission with a paranoid diagnosis were the findings most associated with Lewy bodies. It is suggested that paranoia may sometimes be an early symptom of Lewy body disease. The problem of patients with psychosis who subsequently develop idiopathic Parkinson's disease is discussed. Such patients could be misidentified and mistreated because of being diagnosed as drug‐induced parkinsonism.

This study concerns differences between Alzheimer's disease in the old and the young. Literature differentiating Alzheimer's disease from ‘senile dementia’ is reviewed. Two groups of mental hospital patients with Alzheimer brain changes at autopsy are compared. They comprised the 17 oldest and 17 youngest of the 56 ptients with definite Alzheimer changes in a series of 212 consecutive autopsies. The younger group had been first hospitalized at later ages than the older group, and were more likely to have been demented at admission. The older group had mostly been diagnosed as schizophrenic (mainly paranoid) on admission. Neuropathologically the younger group showed more severe Alzheimer changes of all kinds. The changes in the older group tended to be limited to the hippocampus, whereas in the younger group they showed extension into the frontal and occipital cortex and were also found in subcortical gray matter. Lipofuscin was more abundant in the older group, so that a discrepancy between very severe Alzheimer changes and less abundant lipofuscin characterizes the younger cases.

The essential role of the Reelin gene (RELN) during brain development makes it a prominent candidate in human epigenetic studies of Schizophrenia. Previous literature has reported differing levels of DNA methylation (DNAm) in patients with psychosis. Therefore, this study aimed to (1) examine and compare RELN DNAm levels in subjects at different stages of psychosis cross-sectionally, (2) analyse the effect of antipsychotics (AP) on DNAm, and (3) evaluate the effectiveness and applicability of RELN promoter DNAm as a possible biological-based marker for symptom severity in psychosis.. The study cohort consisted of 56 healthy controls, 87 ultra-high risk (UHR) individuals, 26 first-episode (FE) psychosis individuals and 30 chronic schizophrenia (CS) individuals. The Positive and Negative Syndrome Scale (PANSS) was used to assess Schizophrenia severity. After pyrosequencing selected CpG sites of peripheral blood, the Average mean DNAm levels were compared amongst the 4 subgroups. Our results showed differing levels of DNAm, with UHR having the lowest (7.72 ± 0.19) while the CS had the highest levels (HC: 8.78 ± 0.35; FE: 7.75 ± 0.37; CS: 8.82 ± 0.48). Significantly higher Average mean DNAm levels were found in CS subjects on AP (9.12 ± 0.61) compared to UHR without medication (UHR(−)) (7.39 ± 0.18). A significant association was also observed between the Average mean DNAm of FE and PANSS Negative symptom factor (R2 = 0.237, ß = −0.401, *p = 0.033). In conclusion, our findings suggested different levels of DNAm for subjects at different stages of psychosis. Those subjects that took AP have different DNAm levels. There were significant associations between FE DNAm and Negative PANSS scores. With more future experiments and on larger cohorts, there may be potential use of DNAm of the RELN gene as one of the genes for the biological-based marker for symptom severity in psychosis.