Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (708 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Elongated gray mass of the neostriatum located adjacent to the lateral ventricle of the brain.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Nucleus, Caudate; Caudatus; Nucleus Caudatus; Caudatus, Nucleus.
Where it fits in the MeSH classification
- Broader topics
- Neostriatum
Research landscape
PubMed indexes 10,208 records tagged with the MeSH heading “Caudate Nucleus” (counts retrieved 2026-10-29). 361 of them (3.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 7,303 records.
Reviews account for 275 records (2.7%) and meta-analyses for 15. Randomized controlled trials number 57 (0.6%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 7,303 |
| 2000-2009 | 1,357 |
| 2010-2019 | 1,187 |
| 2020 onward | 361 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 275 | 2.7% |
| Meta-analyses | 15 | 0.1% |
| Randomized controlled trials | 57 | 0.6% |
Method: PubMed query "Caudate Nucleus"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in neuroscience
Neuroscience draws on tools with different strengths: cellular and animal work can manipulate circuits directly, while human imaging and electrophysiology observe the living brain at lower resolution. Small imaging studies are prone to false positives, and findings in animals do not always carry over to people. Clinical neurology and psychiatry rely on trials and cohort studies whose outcomes are often symptom scales. Check the species, the sample size, how the outcome was measured and whether results were replicated.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Altered glutathione redox state in schizophrenia | 2006 | Research article Design not recorded in structured metadata | 262 | cc by PMID 16410648 · DOI · PMC3850558 |
| Empathic concern drives costly altruism | 2015 | Research article Design not recorded in structured metadata | 169 | cc by PMID 25462694 · DOI · PMC4275572 |
| Atypical intrinsic neural timescale in autism | 2019 | Research article Design not recorded in structured metadata | 146 | cc by PMID 30717827 · DOI · PMC6363380 |
| Cell type-specific multi-omics analysis of cocaine use disorder in the human caudate nucleus | 2025 | Research article Design not recorded in structured metadata | 8 | cc by PMID 40204703 · DOI · PMC11982542 |
Altered glutathione redox state in schizophrenia [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Altered antioxidant status has been reported in schizophrenia.
- Closing excerpt
- By contrast, lack of such correlations in schizophrenia point to a disturbance of redox coupling mechanisms in the antioxidant defense system, possibly resulting from a decreased level of GSH as well as age-related decreases of GSSG and GR activities.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (248 words)
Altered antioxidant status has been reported in schizophrenia. The glutathione (GSH) redox system is important for reducing oxidative stress. GSH, a radical scavenger, is converted to oxidized glutathione (GSSG) through glutathione peroxidase (GPx), and converted back to GSH by glutathione reductase (GR). Measurements of GSH, GSSG and its related enzymatic reactions are thus important for evaluating the redox and antioxidant status. In the present study, levels of GSH, GSSG, GPx and GR were assessed in the caudate region of postmortem brains from schizophrenic patients and control subjects (with and without other psychiatric disorders). Significantly lower levels of GSH, GPx, and GR were found in schizophrenic group than in control groups without any psychiatric disorders. Concomitantly, a decreased GSH:GSSG ratio was also found in schizophrenic group. Moreover, both GSSG and GR levels were significantly and inversely correlated to age of schizophrenic patients, but not control subjects. No significant differences were found in any GSH redox measures between control subjects and individuals with other types of psychiatric disorders. There were, however, positive correlations between GSH and GPx, GSH and GR, as well as GPx and GR levels in control subjects without psychiatric disorders. These positive correlations suggest a dynamic state is kept in check during the redox coupling under normal conditions. By contrast, lack of such correlations in schizophrenia point to a disturbance of redox coupling mechanisms in the antioxidant defense system, possibly resulting from a decreased level of GSH as well as age-related decreases of GSSG and GR activities.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 16410648 · DOI · PMC3850558
Empathic concern drives costly altruism [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Why do we self-sacrifice to help others in distress?
- Closing excerpt
- Together, this data helps identify the behavioral and neural mechanisms motivating costly altruism, while demonstrating that individual differences in empathic concern-related brain responses can predict real prosocial choice.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (161 words)
Why do we self-sacrifice to help others in distress? Two competing theories have emerged, one suggesting that prosocial behavior is primarily motivated by feelings of empathic other-oriented concern, the other that we help mainly because we are egoistically focused on reducing our own discomfort. Here we explore the relationship between costly altruism and these two sub-processes of empathy, specifically drawing on the caregiving model to test the theory that trait empathic concern (e.g. general tendency to have sympathy for another) and trait personal distress (e.g. predisposition to experiencing aversive arousal states) may differentially drive altruistic behavior. We find that trait empathic concern--and not trait personal distress--motivates costly altruism, and this relationship is supported by activity in the ventral tegmental area, caudate and subgenual anterior cingulate, key regions for promoting social attachment and caregiving. Together, this data helps identify the behavioral and neural mechanisms motivating costly altruism, while demonstrating that individual differences in empathic concern-related brain responses can predict real prosocial choice.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 25462694 · DOI · PMC4275572
Atypical intrinsic neural timescale in autism [3]
Abstract reading summary — source excerpts
- Opening excerpt
- How long neural information is stored in a local brain area reflects functions of that region and is often estimated by the magnitude of the autocorrelation of intrinsic neural signals in the area.
- Closing excerpt
- This study shows that functional and structural atypicality in local brain areas is linked to higher-order cognitive symptoms in autism.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (151 words)
How long neural information is stored in a local brain area reflects functions of that region and is often estimated by the magnitude of the autocorrelation of intrinsic neural signals in the area. Here, we investigated such intrinsic neural timescales in high-functioning adults with autism and examined whether local brain dynamics reflected their atypical behaviours. By analysing resting-state fMRI data, we identified shorter neural timescales in the sensory/visual cortices and a longer timescale in the right caudate in autism. The shorter intrinsic timescales in the sensory/visual areas were correlated with the severity of autism, whereas the longer timescale in the caudate was associated with cognitive rigidity. These observations were confirmed from neurodevelopmental perspectives and replicated in two independent cross-sectional datasets. Moreover, the intrinsic timescale was correlated with local grey matter volume. This study shows that functional and structural atypicality in local brain areas is linked to higher-order cognitive symptoms in autism.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30717827 · DOI · PMC6363380
Cell type-specific multi-omics analysis of cocaine use disorder in the human caudate nucleus [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Structural and functional alterations in the brain's reward circuitry are present in cocaine use disorder (CocUD), but their molecular underpinnings remain unclear.
- Closing excerpt
- This study highlights cell type-specific molecular alterations in CocUD and provides targets for further investigation, demonstrating the value of multi-omics approaches in addiction research.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (148 words)
Structural and functional alterations in the brain's reward circuitry are present in cocaine use disorder (CocUD), but their molecular underpinnings remain unclear. To investigate these mechanisms, we performed single-nuclei multiome profiling on postmortem caudate nucleus tissue from six individuals with CocUD and eight controls. We profiled 30,030 nuclei, identifying 13 cell types including D1- and D2-medium spiny neurons (MSNs) and glial cells. We observed 1485 differentially regulated genes and 10,342 differentially accessible peaks, with alterations in MSNs and astrocytes related to neurotransmitter activity and synapse organization. Gene regulatory network analysis identified transcription factors including ZEB1 as exhibiting distinct CocUD-specific subclusters, activating downstream expression of ion- and calcium-channels in MSNs. Further, PDE10A emerged as a potential drug target, showing conserved effects in a rat model. This study highlights cell type-specific molecular alterations in CocUD and provides targets for further investigation, demonstrating the value of multi-omics approaches in addiction research.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40204703 · DOI · PMC11982542
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article A meta-analysis of functional neuroimaging in obsessive-compulsive disorder [5]
- Research article The extended amygdala: are the central nucleus of the amygdala and the bed nucleus of the stria terminalis differentially involved in fear versus anxiety? [6]
- Research article Amygdala modulation of multiple memory systems: hippocampus and caudate-putamen [7]
- Research article Increased anterior cingulate and caudate activity in bipolar mania [8]
- Research article Caudate infarcts [9]
- Research article The role of the basal ganglia in learning and memory: neuropsychological studies [10]
References
- Yao JK, Leonard S, Reddy R. Altered glutathione redox state in schizophrenia. . 2006. PMID 16410648 · DOI · PMC3850558
- FeldmanHall O, Dalgleish T, Evans D, Mobbs D. Empathic concern drives costly altruism. . 2015. PMID 25462694 · DOI · PMC4275572
- Watanabe T, Rees G, Masuda N. Atypical intrinsic neural timescale in autism. . 2019. PMID 30717827 · DOI · PMC6363380
- Zillich L, Artioli A, Pohořalá V, Zillich E, Stertz L, Belschner H, et al.. Cell type-specific multi-omics analysis of cocaine use disorder in the human caudate nucleus. . 2025. PMID 40204703 · DOI · PMC11982542
- Whiteside SP, Port JD, Abramowitz JS. A meta-analysis of functional neuroimaging in obsessive-compulsive disorder. Psychiatry Res. 2004. PMID 15546704 · DOI
- Davis M, Shi C. The extended amygdala: are the central nucleus of the amygdala and the bed nucleus of the stria terminalis differentially involved in fear versus anxiety?. Ann N Y Acad Sci. 1999. PMID 10415655 · DOI
- Packard MG, Teather LA. Amygdala modulation of multiple memory systems: hippocampus and caudate-putamen. Neurobiol Learn Mem. 1998. PMID 9619995 · DOI
- Blumberg HP, Stern E, Martinez D, Ricketts S, de Asis J, White T, et al.. Increased anterior cingulate and caudate activity in bipolar mania. Biol Psychiatry. 2000. PMID 11094137 · DOI
- Caplan LR, Schmahmann JD, Kase CS, Feldmann E, Baquis G, Greenberg JP, et al.. Caudate infarcts. Arch Neurol. 1990. PMID 2405818 · DOI
- Grahn JA, Parkinson JA, Owen AM. The role of the basal ganglia in learning and memory: neuropsychological studies. Behav Brain Res. 2009. PMID 19059285 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.