ArticleEMBO molecular medicine2012
A myelin gene causative of a catatonia-depression syndrome upon aging.
Article in EMBO molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
61 citing papers in PubMed, 2 syntheses or guidelines pooled it, 131 citations in OpenAlex.
- Unraveling the mystery of white matter in depression: A translational perspective on recent advances.Brain and behavior · 2022Pooled it
- Going Back to Kahlbaum's Psychomotor (and GABAergic) Origins: Is Catatonia More Than Just a Motor and Dopaminergic Syndrome?Schizophrenia bulletin · 2020Pooled it
- An activity-modulated transport route across myelin (TRAM) for motor-driven organelle transfer in oligodendrocytes.Nature neuroscience · 2026Article
- A Novel Variant in the MYT1L Gene Shared by Three Individuals with Neuropsychiatric and Neurodevelopmental Manifestations in a Family.Indian journal of psychological medicine · 2026Article
- Organ-specific proteomic aging clocks predict disease and longevity across diverse populations.Nature aging · 2026Article
- Oligodendrocyte lineage cells dysfunction in depression: early life stress, adolescent vulnerability and the emerging role of lipid metabolism.Translational psychiatry · 2025Review
- Transcriptional dynamics of the oligodendrocyte lineage and its regulation by the brain erythropoietin system.Nature communications · 2025Article
- Deciphering white matter microstructural alterations in catatonia according to ICD-11: replication and machine learning analysis.Molecular psychiatry · 2025Article
- Nanobodies against the myelin enzyme CNPase as tools for structural and functional studies.Journal of neurochemistry · 2025Article
- Oligodendrocytes: Myelination, Plasticity, and Axonal Support.Cold Spring Harbor perspectives in biology · 2024Review
- Bioenergetics of Axon Integrity and Its Regulation by Oligodendrocytes and Schwann Cells.Molecular neurobiology · 2024Review
- Catatonia.Nature reviews. Disease primers · 2024Review
- Perinatal loss of galactosylceramidase in both oligodendrocytes and microglia is crucial for the pathogenesis of Krabbe disease in mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Nanobodies against the myelin enzyme CNPase as tools for structural and functional studies.bioRxiv : the preprint server for biology · 2024Article
- Interaction between Oligodendrocytes and Interneurons in Brain Development and Related Neuropsychiatric Disorders.International journal of molecular sciences · 2024Review
- HomozygousGenes · 2024Article
- Clinically approved immunomodulators ameliorate behavioral changes in a mouse model of hereditary spastic paraplegia type 11.Frontiers in neuroscience · 2024Article
- Molecular and immunological origins of catatonia.Schizophrenia research · 2024Article
- Uncovering oligodendrocyte enhancers that control Cnp expression.Human molecular genetics · 2023Article
- The stability of the myelinating oligodendrocyte transcriptome is regulated by the nuclear lamina.Cell reports · 2023Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe mental illnesses have been linked to white matter abnormalities, documented by postmortem studies. However, cause and effect have remained difficult to distinguish. CNP (2',3'-cyclic nucleotide 3'-phosphodiesterase) is among the oligodendrocyte/myelin-associated genes most robustly reduced on mRNA and protein level in brains of schizophrenic, bipolar or major depressive patients. This suggests that CNP reduction might be critical for a more general disease process and not restricted to a single diagnostic category. We show here that reduced expression of CNP is the primary cause of a distinct behavioural phenotype, seen only upon aging as an additional 'pro-inflammatory hit'. This phenotype is strikingly similar in Cnp heterozygous mice and patients with mental disease carrying the AA genotype at CNP SNP rs2070106. The characteristic features in both species with their partial CNP 'loss-of-function' genotype are best described as 'catatonia-depression' syndrome. As a consequence of perturbed CNP expression, mice show secondary low-grade inflammation/neurodegeneration. Analogously, in man, diffusion tensor imaging points to axonal loss in the frontal corpus callosum. To conclude, subtle white matter abnormalities inducing neurodegenerative changes can cause/amplify psychiatric diseases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.