ReviewMolecular psychiatry2019
Protein misassembly and aggregation as potential convergence points for non-genetic causes of chronic mental illness.
Review in Molecular psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 62 citations in OpenAlex.
- Network-Based Spreading of Gray Matter Changes Across Different Stages of Psychosis.JAMA psychiatry · 2023Trial
- Assessment of Aggregation- and Condensation-Prone Regions of Proteins Involved in Neurodegenerative, Neurological and Mental-State Diseases.Biomolecules · 2026Article
- Biological factors contributing to divergent cortical abnormalities in adolescent and adult psychiatric disorders.Translational psychiatry · 2026Article
- Widespread synaptic density loss in schizophrenia follows molecular and network architecture.Molecular psychiatry · 2026Article
- Epigenetic Evidence Implies Disturbed Proteostasis and Potentially Protein Aggregation in Suicidality.Biomolecules · 2026Review
- Levels of aggregation of proteins related to mental illness, assayed by insolubility, vary across the brains of individuals.Scientific reports · 2026Article
- Transdiagnostic prevention in youth mental health, Part I: rationale, shared risk factors.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Review
- Epigenetic and Transcriptomic Alterations of Protein Aggregation-Linked Genes in Suicide: A Pilot Study.Genes · 2025Article
- Novel Insights into Schizophrenia Treatment: Comprehensive Analysis Unveiling FGFR1 as a Promising Druggable Gene.Molecular neurobiology · 2025Article
- Protein aggregation identified in olfactory neuronal cells is associated with cognitive impairments in a subset of living schizophrenia patients.Molecular psychiatry · 2025Article
- Tracing the aggregation pathway of the scaffold protein DISC1: Structural implications for chronic mental illnesses.Journal of structural biology: X · 2025Article
- TransgenicCurrent issues in molecular biology · 2024Article
- Regulated cell death and its role in Alzheimer's disease and amyotrophic lateral sclerosis.Acta neuropathologica · 2024Review
- Proteome analysis of the prefrontal cortex and the application of machine learning models for the identification of potential biomarkers related to suicide.Frontiers in psychiatry · 2024Article
- Which Severe Mental Illnesses Most Increase the Risk of Developing Dementia? Comparing the Risk of Dementia in Patients with Schizophrenia, Major Depressive Disorder and Bipolar Disorder.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2023Article
- Article
- Co-Expression Network Analysis Identifies Molecular Determinants of Loneliness Associated with Neuropsychiatric and Neurodegenerative Diseases.International journal of molecular sciences · 2023Article
- Mapping the Domain Structure and Aggregation Propensity of Proteins Using a Gateway Plasmid Vector System.Methods in molecular biology (Clifton, N.J.) · 2023Article
- TRIOBP-1 Protein Aggregation Exists in Both Major Depressive Disorder and Schizophrenia, and Can Occur through Two Distinct Regions of the Protein.International journal of molecular sciences · 2022Article
- Molecular origin of somatostatin-positive neuron vulnerability.Molecular psychiatry · 2022Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic mental illnesses (CMI), such as schizophrenia or recurrent affective disorders, are complex conditions with both genetic and non-genetic elements. In many other chronic brain conditions, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and frontotemporal dementia, sporadic instances of the disease are more common than gene-driven familial cases. Yet, the pathology of these conditions can be characterized by the presence of aberrant protein homeostasis, proteostasis, resulting in misfolded or aggregated proteins in the brains of patients that predominantly do not derive from genetic mutations. While visible deposits of aggregated protein have not yet been detected in CMI patients, we propose the existence of more subtle protein misassembly in these conditions, which form a continuum with the psychiatric phenotypes found in the early stages of many neurodegenerative conditions. Such proteinopathies need not rely on genetic variation. In a similar manner to the established aberrant neurotransmitter homeostasis in CMI, aberrant homeostasis of proteins is a functional statement that can only partially be explained by, but is certainly complementary to, genetic approaches. Here, we review evidence for aberrant proteostasis signatures from post mortem human cases, in vivo animal work, and in vitro analysis of candidate proteins misassembled in CMI. The five best-characterized proteins in this respect are currently DISC1, dysbindin-1, CRMP1, TRIOBP-1, and NPAS3. Misassembly of these proteins with inherently unstructured domains is triggered by extracellular stressors and thus provides a converging point for non-genetic causes of CMI.
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