Publications by authors named "Chikako Habuchi"

Article Synopsis
  • The study investigates why older patients with schizophrenia might be prone to developing dementia, despite previous findings suggesting their Alzheimer's disease risk is similar to those without schizophrenia.
  • It involved an examination of 32 brains from older schizophrenia patients to analyze dementia-related neuropathologies and compare clinicopathological differences between those with and without dementia.
  • The results revealed two subgroups of dementia in these patients: those with known neurodegenerative diseases and those without identifiable pathology, indicating a need for more thorough research on this issue.
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Piccolo, a presynaptic cytomatrix protein, plays a role in synaptic vesicle trafficking in the presynaptic active zone. Certain single-nucleotide polymorphisms of the Piccolo-encoding gene are reported to be associated with mental disorders. However, a few studies have evaluated the relationship between Piccolo dysfunction and psychotic symptoms.

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  • GGT is a newly identified tauopathy characterized by globular accumulations of four-repeat tau proteins in both oligodendroglia and astrocytes, as well as neurons.
  • A case study of a 79-year-old man with behavioral variant frontotemporal dementia (bvFTD) showed significant brain atrophy and inclusion of globular oligodendroglial inclusions, suggesting the presence of GGT Type I.
  • The case highlights the complexity and potential overlap of GGT subtypes, particularly in relation to psychotic symptoms, indicating that subclassifying GGT can be challenging.
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  • The study explores the relationship between long-term schizophrenia and dementia symptoms, noting that while schizophrenia patients are at a higher risk for dementia, the prevalence of Alzheimer's appears similar to that of non-afflicted individuals.
  • Researchers conducted a neuropathological assessment on three schizophrenia cases that exhibited cognitive decline after prolonged illness, using various staining techniques to evaluate brain tissues.
  • Results indicated no significant pathological findings in the patients, suggesting that cognitive decline may stem from a combination of preclinical neurodegeneration and inherent vulnerabilities linked to schizophrenia, rather than clear neurodegenerative diseases.
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Article Synopsis
  • * It's noted that while cognitive decline can be an intrinsic symptom of schizophrenia in later life, complications like dementia are not well understood and require further examination.
  • * The findings emphasize the need for awareness that schizophrenic patients can also develop neurodegenerative diseases, indicating a potential dual diagnosis and the necessity for more research on the relationship between schizophrenia and dementia.
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Huntington's disease (HD) is an autosomal-dominant neurodegenerative disorder characterized by the presence of chorea, psychiatric symptoms, and dementia. Although motor symptoms are thought to be correlated with the degeneration of the striatum, there is little information regarding the neuropathological basis of psychiatric symptoms. The ventral part of the striatum is known as the nucleus accumbens (Acb) and is a region of interest as a responsible focus of psychiatric symptoms.

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The Japan Agency of Medical Research and Development (AMED) has approved the budget for the 5-year project called Establishment of the JAPAN Brain Bank Network, which commenced in 2016. This project was established with the aim of storing brain tissue samples to enable research on the etiologies and mechanisms of psychiatric diseases, which would eventually improve standards of clinical treatment for these diseases. Japanese researchers in the field of biological psychiatry have historically depended on Western brain banks, particularly from Europe and the United States, which is regrettable.

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  • The study explores the unknown biological causes of autism spectrum disorder (ASD) using a monkey model with specific genetic modifications, focusing on the ABCA13 protein, which is the largest ABC transporter protein.
  • Researchers discovered that monkeys lacking ABCA13 exhibit disorganized neuronal formation in the frontal cortex, leading to abnormalities in neuronal size and distribution.
  • The findings imply that deficits in ABCA13 may disrupt neuronal development and connectivity, potentially contributing to mental disorders like autism.
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  • Recent research indicates that schizophrenia may be linked to abnormalities in myelin-oligodendrocytes, but there has been limited investigation into this area within the brains of those with the disease.
  • This study evaluated the expression of myelin oligodendrocyte glycoprotein (MOG) in postmortem brain tissue from 10 schizophrenia patients and 9 control subjects, focusing on the superior temporal gyrus and hippocampus.
  • Results showed significantly lower MOG expression and fiber structure thickness in long-term schizophrenia patients, suggesting that these brain changes may contribute to the progression of the disorder.
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Neuropeptide Y (NPY) has been found to play a critical role in various mental functions as a neurotransmitter and is involved in the development of schizophrenia, a particularly intractable psychiatric disease whose precise etiology remains unknown. Recent molecular biological investigations have identified several candidate genes which may be associated with this disease, including disrupted-in-schizophrenia 1 (DISC1). The role of DISC1 would involve neurogenesis and neuronal migration.

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The etiology of schizophrenia remains unknown. However, using molecular biological techniques, some candidate genes have been identified that might be associated with the disease. One of these candidate genes, disrupted-in-schizophrenia 1 (DISC1), was found in a large Scottish family with multiple mental illnesses.

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We herein report the case of a 75-year-old male who had shown many psychiatric symptoms, but whose autopsy disclosed the presence of dementia with Lewy bodies (DLB). When he was 70 years old, the patient had presented with stereotyped behavior, dietary changes, and a decline in social interpersonal conduct in clinical settings, and it was thought that these symptoms were consistent with a behavioral variant of frontotemporal dementia (bvFTD), and he lacked the core features of DLB. Nevertheless, this case was pathologically defined as the limbic type of DLB after he died at the age of 75 years.

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In recent years, MRI has revealed cortical superficial siderosis (cSS), which exhibits hemosiderin deposition in only the cortical surface. However, the associations between the histological findings and clinical symptoms of cSS remain unclear. We herein report an autopsy case of a 75-year-old Japanese man with cSS with persistent abnormal behavior according to cognitive impairment, hallucination and delusion.

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Background: The precise aetiology of schizophrenia remains unclear. The neurodevelopmental hypothesis of schizophrenia has been proposed based on the accumulation of genomic or neuroimaging studies.

Objective: In this study, we examined the catecholaminergic neuronal networks in the frontal cortices of disrupted-in-schizophrenia 1 (DISC1) knockout (KO) mice, which are considered to be a useful model of schizophrenia.

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Discrepancies between clinical and pathological diagnoses of dementia with Lewy bodies (DLB) may occur because the full disease progression remains unclear, especially during the early stage. Herein, we report the case of a 78-year-old Japanese man with hypochondriasis who had autopsy-confirmed limbic-type DLB pathology. He exhibited no core clinical features of DLB.

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Alzheimer's disease (AD) is clinically characterized by gradual onset over years with worsening of cognition. The initial and most prominent cognitive deficit is commonly memory dysfunction. However, a subset of AD cases has less hippocampal atrophy than would be expected relative to the predominance of cortical atrophy.

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The etiology of schizophrenia has been proposed to be neurodevelopmental based on neuroimaging and molecular biological studies. If there is neuronal vulnerability based on neurodevelopment failures in schizophrenic brains, then the impact of aging may have a greater effect on schizophrenic brains than on normal brains. To determine the impact of aging on schizophrenic brains, we investigated the age-related morphological changes of the cross-sectional area of the gray matter (GM) in the left Heschl's gyrus (HG) and the left superior gyrus (STG) in 22 schizophrenic and 24 age- and sex-matched normal control postmortem brains two-dimensionally.

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Important genes have been identified that are associated with susceptibility to schizophrenia. DISC1 is one of these candidate genes. The protein 14-3-3 epsilon is a DISC1-interacting molecule and is associated with axon elongation.

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Diffuse neurofibrillary tangles with calcification (DNTC) is a relatively rare presenile dementia that clinically shows overlapping symptoms of Alzheimer's disease and frontotemporal lobar degeneration (FTLD). DNTC is pathologically characterized by localized temporal or frontotemporal atrophy with massive neurofibrillary tangles, neuropil threads and Fahr's-type calcification without senile plaques. We tried to clarify the molecular basis of DNTC by immunohistochemically examining the appearance and distribution of accumulated alpha-synuclein (aSyn) and TAR DNA-binding protein of 43kDa (TDP-43) in the brains of 10 Japanese autopsy cases.

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