The DOI matches its Crossref record; 375 of the 379 references it cites were found in a registry or an index; 36 of the 262 sources its claims cite were checked for support.
Neurocircuitry of Mood Disorders
Open accessAbstract
This review begins with a brief historical overview of attempts in the first half of the 20th century to discern brain systems that underlie emotion and emotional behavior. These early studies identified the amygdala, hippocampus, and other parts of what was termed the 'limbic' system as central parts of the emotional brain. Detailed connectional data on this system began to be obtained in the 1970s and 1980s, as more effective neuroanatomical techniques based on axonal transport became available. In the last 15 years these methods have been applied extensively to the limbic system and prefrontal cortex of monkeys, and much more specific circuits have been defined. In particular, a system has been described that links the medial prefrontal cortex and a few related cortical areas to the amygdala, the ventral striatum and pallidum, the medial thalamus, the hypothalamus, and the periaqueductal gray and other parts of the brainstem. A large body of human data from functional and structural imaging, as well as analysis of lesions and histological material indicates that this system is centrally involved in mood disorders.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
This review synthesizes anatomical and clinical evidence that mood disorders arise from dysfunction in an extended medial prefrontal–limbic–striatal–pallidal–thalamic circuit. It argues that the medial prefrontal network and amygdala are central to emotional, autonomic, endocrine, and reward-related disturbances in major depression and bipolar disorder.
Key findings
- The paper describes two main prefrontal networks: an orbital network tied to sensory integration and value assessment, and a medial network tied to limbic structures, visceral control, and mood regulation. The medial network connects with the amygdala, ventral striatum, mediodorsal thalamus, hypothalamus, periaqueductal gray, and brainstem.
- In mood disorders, the most consistently reported structural abnormality is reduced gray matter in the left subgenual anterior cingulate cortex ventral to the corpus callosum genu. Reductions are also reported in orbitofrontal cortex, ventrolateral prefrontal cortex, frontal polar/dorsolateral prefrontal cortex, parahippocampal gyrus, and temporopolar cortex.
- Hippocampal volume reductions in major depression are reported at 8–19% in some studies, but other studies do not replicate this. Amygdala volume findings are mixed: smaller in unmedicated bipolar disorder in one high-resolution study, but larger in bipolar subjects receiving mood-stabilizing treatments.
- Postmortem and spectroscopy findings include reduced glia, especially oligodendrocytes, reduced synapses or synaptic proteins, reduced neuronal size, and reduced GABA and Glx levels in prefrontal regions. The review links these to stress-related dendritic atrophy and elevated glutamatergic/glucocorticoid activity.
Methods
- Narrative review, not a primary study. It integrates historical models of the limbic system with modern axonal tracing studies in macaque monkeys, human lesion and neuroimaging data, postmortem neuropathology, magnetic resonance spectroscopy, and rodent chronic stress models.
- The anatomical synthesis focuses on connectional networks of the orbital and medial prefrontal cortex, amygdala, striatum, pallidum, mediodorsal and midline thalamic nuclei, hypothalamus, and brainstem.
- Clinical synthesis reviews structural MRI, functional imaging, neuropathological, and treatment studies in major depressive disorder and bipolar disorder, then proposes a circuit-based model of depression.
Limitations
- The paper states that understanding remains at an early stage and that later generations may view current misconceptions with bemusement. It also states that translating monkey findings to humans is difficult, that the human cortex is not simply an enlarged monkey brain, and that new architectonic maps of human cortex are needed.
- The paper states that current DSM-based nosology is insufficient for discovering disease mechanisms and that a circuit-based nosology is needed.
- Evident from the text: as a narrative review, it does not use a systematic search or quantitative meta-analysis; it reports inconsistent findings across studies, including discrepant hippocampal and amygdala volumes and conflicting subgenual cingulate metabolism results, which the authors partly attribute to partial volume effects and clinical heterogeneity.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
36 of 262 cited sources checked · 11 supported · 1 flagged · accuracy not yet measured
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“Conversely, lesions of the mPFC enhance behavioral, sympathetic, and endocrine responses to stressors or fearconditioned stimuli in rats (Morgan and LeDoux, 1995;Sullivan and Gratton, 1999).”
§ Neurocircuitry of Mood Disorders > IMPLICATIONS FOR NEUROCIRCUITRY-BASED MODELS OF DEPRESSION
What the sources say
- Not checked — no full text of the sourcecites Morgan and LeDoux, 1995 source
- Disputedcites Sullivan and Gratton, 1999 sourceExperimental — accuracy not yet measured
The Discussion reports that right or bilateral mPFC lesions suppressed corticosterone responses and reduced stress-ulcer pathology, contrary to the claimed enhancement of endocrine and autonomic responses. Left-sided lesions increased restraint-induced defecation, but that isolated finding does not support the broad claim; this study did not test fear-conditioned stimuli. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In addition, lesions of the orbital cortex produce a deficit in the ability to use reward as a guide to behavior (Rudebeck and Murray, 2008)”
§ Neurocircuitry of Mood Disorders > Orbital Prefrontal Network
What the sources say
- Partly supportedcites Rudebeck and Murray, 2008 sourceExperimental — accuracy not yet measured
The Discussion reports that monkeys with orbitofrontal cortex lesions were impaired at using reward information to guide subsequent choices. The claim omits an important limit: this deficit was observed after a reversal, while initial discrimination learning was unaffected. (LLM, conf=0.88)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“and recent fMRI studies have shown that activity in the medial prefrontal cortex correlates with visceral activation in response to emotional (Critchley et al, 2000;Williams et al, 2000) or even non-emotional (Teves et al, 2004) stimuli.”
§ Neurocircuitry of Mood Disorders > CORTICAL PROJECTIONS TO HYPOTHALAMUS AND BRAINSTEM
What the sources say
- Not checked — no full text of the sourcecites Critchley et al, 2000 source
- Not checked — no full text of the sourcecites Williams et al, 2000 source
- Partly supportedcites Teves et al, 2004 sourceExperimental — accuracy not yet measured
The paper’s opening section reports medial prefrontal cortex activation during autonomic responses to hypoglycemia, without cognitive or emotional stress, supporting the non-emotional-stimulus portion attributed to Teves et al. But it explicitly says the study used positron emission tomography (PET), not fMRI. (LLM, conf=0.90)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Imaging studies show that a circuit including the medial prefrontal cortex and the periaqueductal gray area is activated by acute hypoglycemia (Teves et al, 2004)”
§ Neurocircuitry of Mood Disorders > Midline 'Intralaminar' Nuclei of Thalamus
What the sources say
- Partly supportedcites Teves et al, 2004 sourceExperimental — accuracy not yet measured
The Results report statistically significant activation of the medial prefrontal cortex during hypoglycemia. The Discussion reports evidence for periaqueductal gray activation, but says it did not meet the prespecified criteria for statistical significance. The claim omits that qualification for one component of the proposed circuit. (LLM, conf=0.90)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The striatal projection from the LPFC as a whole is directed to the central and dorsal part of the striatum (Calzavara et al, 2007).”
§ Neurocircuitry of Mood Disorders > Prefrontal Projections to the Striatum
What the sources say
- Supportedcites Calzavara et al, 2007 source
The Results (pages not provided) place the focal projections from areas 9 and 46 in central and dorsal regions of the caudate nucleus and describe their combined projections as occupying a large portion of the dorsocentral striatum at rostral levels. The paper also reports more widely distributed diffuse fibres, so the claim describes the main projection pattern rather than every terminal. (LLM, conf=0.86)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Many of the hypothalamic and brainstem inputs to the PVT utilize specific transmitters, including corticosteroid releasing hormone, orexin, serotonin, and norepinephrine (Hsu and Price, 2009).”
§ Neurocircuitry of Mood Disorders > Midline 'Intralaminar' Nuclei of Thalamus
What the sources say
- Supportedcites Hsu and Price, 2009 source
The Functional Considerations section says Pa receives inputs involving 5-HT, CRH, orexin, and norepinephrinergic fibers. The Discussion identifies hypothalamic orexin input and serotonin input from brainstem raphe nuclei. The paper calls CRH “corticotropin-releasing hormone,” rather than the citing sentence’s “corticosteroid releasing hormone.” (LLM, conf=0.92)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Moreover, oligodendrocytes express AMPA and kainate type glutamate receptors, and are sensitive to excitotoxic damage from excess glutamate (Dewar et al, 2003;Matute et al, 1997;McDonald et al, 1998).”
§ Neurocircuitry of Mood Disorders > NEUROPATHOLOGICAL CORRELATIONS WITH NEUROIMAGING ABNORMALITIES
What the sources say
- Supportedcites Dewar et al, 2003 source
The Excitotoxicity section states that glutamate is toxic to oligodendrocytes through AMPA and kainate receptor activation and describes glutamate receptor overactivation as an important mechanism of their injury. The supplied passages do not give a page number. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites Matute et al, 1997 source
- Not checked — no full text of the sourcecites McDonald et al, 1998 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Moreover, oligodendrocytes express AMPA and kainate type glutamate receptors, and are sensitive to excitotoxic damage from excess glutamate (Dewar et al, 2003;Matute et al, 1997;McDonald et al, 1998).”
§ Neurocircuitry of Mood Disorders > NEUROPATHOLOGICAL CORRELATIONS WITH NEUROIMAGING ABNORMALITIES
What the sources say
- Supportedcites Dewar et al, 2003 source
The Excitotoxicity section states that oligodendrocytes in adult rodent brain express AMPA/kainate receptor subunits. It also describes AMPA and kainate receptor expression in oligodendrocyte progenitor cells. Page numbers are not supplied in the excerpts. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites Matute et al, 1997 source
- Not checked — no full text of the sourcecites McDonald et al, 1998 source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Nevertheless, a longitudinal study also has shown progression of the abnormality in subjects with psychotic mood disorders (Koo et al, 2008).”
§ Neurocircuitry of Mood Disorders > Brain Structural Abnormalities in Mood Disorders
What the sources say
- Supportedcites Koo et al, 2008 source
The Comment’s Longitudinal Findings section states that gray matter volume deficits progressed in the subgenual cingulate in patients with first-episode affective psychosis compared with healthy controls. The Methods’ Participants section identifies this group as predominantly patients with bipolar disorder, supporting the reference to psychotic mood disorders. (LLM, conf=0.94)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Elevated glutamatergic transmission within discrete anatomical circuits also may explain the targeted nature of gray matter changes within mood disorders (eg, affecting left more than right sgACC) (McEwen and Magarinos, 2001;Drevets and Price, 2005a;Shansky et al, 2009).”
§ Neurocircuitry of Mood Disorders > Correlations with Rodent Models of Chronic and Repeated Stress
What the sources say
- Not checked — no full text of the sourcecites McEwen and Magarinos, 2001 source
- Not checked — no full text of the sourcecites Drevets and Price, 2005a source
- Partly supportedcites Shansky et al, 2009 sourceExperimental — accuracy not yet measured
The Abstract reports circuit-specific dendritic remodeling after stress in rats, and the Functional Implications section suggests that a spared pathway might receive increased input and become overstimulated (page numbers not supplied). The paper does not establish elevated glutamatergic transmission as the cause of targeted gray-matter changes in mood disorders, nor does it address left–right differences in the sgACC. (LLM, conf=0.84)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes
- It may state two separate claims as one. 46
- Probably not a substantial claim. 28
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“The perigenual prefrontal cortex is also connected to both the same ventromedial part of the striatum (Haber et al, 1995;Ferry et al, 2000b), and the same region of MD (Russchen et al, 1987;Ray and Price, 1992).”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
What the sources say
- Supportedcites Haber et al, 1995 source
Haber et al. is cited for the striatal connection, not the mediodorsal thalamic connection, which has separate citations. The Discussion reports that medial prefrontal areas 25 and 32 project to the medial ventral striatum, where orbitofrontal areas 13a and 13b also project. Page numbers are unavailable in our copy. (LLM, conf=0.92)
- Not checked — no full text of the sourcecites Ferry et al, 2000b source
- Not checked — no full text of the sourcecites Russchen et al, 1987 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In addition, many neurons appear to code for the presence or expectation of reward (Schultz et al, 1997), and for the relative value of stimuli (Padoa-Schioppa and Assad, 2006).”
§ Neurocircuitry of Mood Disorders > Orbital Prefrontal Network
What the sources say
- Partly supportedcites Schultz et al, 1997 sourceExperimental — accuracy not yet measured
The citation to Schultz et al. is attached to the presence-or-expectation-of-reward clause, not the relative-value clause. In “Information Encoded in Dopaminergic Activity” (p. 2), the paper reports responses to unpredicted rewards and reward-predicting cues, but identifies the neurons as dopaminergic neurons of the VTA and substantia nigra, not orbital neurons. It also characterizes their signal more specifically as a reward-prediction error, rather than a general code for reward presence or expectation. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites Padoa-Schioppa and Assad, 2006 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“In addition to its role in control of saccadic eye movements, the caudal system may be part of the dorsal attention system (Corbetta et al, 2002).”
§ Neurocircuitry of Mood Disorders > Caudal Prefrontal System
What the sources say
- Could not verifycites Corbetta et al, 2002 sourceExperimental — accuracy not yet measured
The Conclusions (page unavailable) identify the intraparietal and superior frontal cortex as a dorsal attention network. The section on the dorsal frontal-parietal network also discusses the frontal eye field, but our copy does not identify a ‘caudal system’ or place one in that network. Searches for ‘caudal system’ and ‘caudal’ did not resolve that link. (LLM, conf=0.72)
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The extant data suggest this volumetric reduction exists early in illness and in young adults at high familial risk for MDD (Botteron et al, 2002;Hirayasu et al, 1999;Drevets et al, 2004b;Boes et al, 2008).”
§ Neurocircuitry of Mood Disorders > Brain Structural Abnormalities in Mood Disorders
What the sources say
- Not checked — no full text of the sourcecites Botteron et al, 2002 source
- Partly supportedcites Hirayasu et al, 1999 sourceExperimental — accuracy not yet measured
The Discussion reports reduced left subgenual cingulate volume at first hospitalization, supporting the early-illness part of the claim. The Method describes a young first-episode affective-disorder group, predominantly with bipolar disorder, and the comparison is based on family history of affective disorder—not specifically young adults at high familial risk for MDD. (LLM, conf=0.88)
- Not matchedcites Drevets et al, 2004b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“One study showed that the mean sgACC gray matter volume was reduced significantly vs controls in subjects with psychotic affective illness who also had mood-disordered first-degree relatives but not in subjects without mood-disordered first-degree relatives (Hirayasu et al, 1999).”
§ Neurocircuitry of Mood Disorders > Brain Structural Abnormalities in Mood Disorders
What the sources say
- Partly supportedcites Hirayasu et al, 1999 sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“It has also been reported that the left perigenulate ACC volume was smaller in boys with subclinical depressive symptoms, and that the negative correlation between left sgACC volume and depression symptoms was particularly robust in boys with a family history of depression (Boes et al, 2008).”
§ Neurocircuitry of Mood Disorders > Brain Structural Abnormalities in Mood Disorders
What the sources say
- Partly supportedcites Boes et al, 2008 sourceExperimental — accuracy not yet measured
The Results (Tables 2 and 3; page unavailable) show smaller left rostral ACC (rACC) volume in boys with depressive symptoms and a stronger negative correlation in boys with a positive nuclear family history of depression. The study measured rACC, which includes the subgenual region, but did not establish these findings specifically for left subgenual ACC or an isolated perigenual region. (LLM, conf=0.88)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“The volumetric deficit applies to males (Hastings et al, 2004;Boes et al, 2008) and females (Botteron et al, 2002), to psychotic unipolar and bipolar depression (Hirayasu et al, 1999;Coryell et al, 2005;Adler et al, 2007), and to bipolar-spectrum illness (Haznedar et al, 2005).”
§ Neurocircuitry of Mood Disorders > Brain Structural Abnormalities in Mood Disorders
What the sources say
- Not checked — no full text of the sourcecites Hastings et al, 2004 source
- Supportedcites Boes et al, 2008 source
Boes et al. is cited for the male portion of the sentence, not for females or the specified diagnoses. The Results report significantly smaller rACC volume in boys with depressive symptoms than in boys without them. These were healthy children without a psychiatric diagnosis, so the finding should not be read as evidence about diagnosed depression. (LLM, conf=0.91)
- Not checked — no full text of the sourcecites Botteron et al, 2002 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The burst-firing patterns increase DA release in the accumbens, which may encode information about reward prediction in monkeys (Schultz et al, 1997).”
§ Neurocircuitry of Mood Disorders > Effects of Altered Medial Prefrontal Network-Limbic Interactions
What the sources say
- Partly supportedcites Schultz et al, 1997 sourceExperimental — accuracy not yet measured
The ‘Information Encoded in Dopaminergic Activity’ section (p. 2) says dopamine-neuron output in monkeys appears to encode errors in reward prediction. It identifies the nucleus accumbens as a target of these neurons, but does not establish that burst-firing increases dopamine release there or that release there carries the prediction signal. (LLM, conf=0.84)
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In spite of this the initial framework was adequate to indicate that the system included the hippocampus and amygdala, the anterior and medial thalamus, the cingulate gyrus, and related visceral control areas in the hypothalamus and brainstem.”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Remarkably, although recording studies have indeed indicated that neurons in the orbital network areas respond to multi-modal stimuli (eg, the sight, flavor, and texture of food stimuli) the responses reflect affective as well as sensory qualities of the stimuli.”
§ Neurocircuitry of Mood Disorders > Orbital Prefrontal Network
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Recently a projection from the amygdala has been identified to the posterior cingulate cortex (Buckwalter et al, 2008).”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
What the sources say
- Not checked — no full text of the sourcecites Buckwalter et al, 2008 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Subsequently, the hippocampus has been shown to be more involved in memory processing, and the amygdala to be more related to emotion (Zola- Morgan et al, 1991)”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
What the sources say
- Not checked — no full text of the sourcecites Zola- Morgan et al, 1991 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“These early studies identified the amygdala, hippocampus, and other parts of what was termed the 'limbic' system as central parts of the emotional brain.”
§ Neurocircuitry of Mood Disorders > Abstract
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Emotions are obviously linked to visceral function, and visceral reactions provide the means of emotional expression and possibly even the basis for the emotions themselves, as James W (1884) argued.”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
What the sources say
- Not matchedcites James W (1884)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“As discussed in later parts of this chapter, these circuits form the core of the neural system that has been implicated in mood disorders.”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
- Rests on an assumption: The anatomical and functional organization of the emotion-related circuits described in monkeys and other animals is sufficiently similar to that in humans to inform conclusions about human mood disorders.
None of the sources cited for this claim have been checked yet.
In the paper
“Work by Gaskell, Langley, Cannon and others in the late nineteenth and early twentieth century established that many visceral functions are controlled by the autonomic nervous system, which is itself controlled and coordinated by the hypothalamus, the so-called 'head ganglion of the autonomic nervous system'.”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
Strength:boosted· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“These striatal areas in turn project to the ventral and rostral pallidum, which itself sends GABAergic axons to the mediodorsal thalamic nucleus (MD, Russchen et al, 1987).”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
What the sources say
- Not checked — no full text of the sourcecites Russchen et al, 1987 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Papez and MacLean proposed that the 'Limbic System,' including the hippocampal formation, cingulate gyrus, and anterior thalamus, elaborates emotion and, through its interaction with the hypothalamus, is involved in emotional expression (Figure 1).”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
What the sources say
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The orbital network therefore appears to function both as a system for integration of multi-modal stimuli, and as a system for assessment of the value of those stimuli.”
§ Neurocircuitry of Mood Disorders > Orbital Prefrontal Network
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Observations on decorticate cats by Bard (1928) and others suggested that the hypothalamus was involved in the production of sham rage, and was responsible for the experience as well as the expression of emotion.”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
What the sources say
- Not checked — no full text of the sourcecites Bard (1928) source
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Subsequently, however, many observations indicated that the structures in the cerebral hemispheres are responsible for the generation and experience of emotion, although the hypothalamus and other visceral control structures are responsible for many aspects of emotional expression.”
§ Neurocircuitry of Mood Disorders > HISTORICAL INTRODUCTION
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“As with the medial network, there are outputs from dorsal areas to the hypothalamus and PAG, so this system can also modulate visceral functions.”
§ Neurocircuitry of Mood Disorders > Dorsal Prefrontal System
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“To account for such deficits, Damasio and his colleagues have proposed the 'somatic marker hypothesis,' which supposes that the visceral or bodily reaction that normally accompanies emotion (the somatic marker) serves as a subconscious warning or guide, indicating some behaviors are disadvantageous and should be avoided (Damasio, 1994).”
§ Neurocircuitry of Mood Disorders > CORTICAL PROJECTIONS TO HYPOTHALAMUS AND BRAINSTEM
What the sources say
- Not checked — no full text of the sourcecites Damasio, 1994 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In this case, however, the brainstem areas do not project directly to the cortex, so lateral MD serves as a relay of information to cortex, possibly as well as modulating thalamo-corticothalamic interactions.”
§ Neurocircuitry of Mood Disorders > Lateral Segment of Mediodorsal Thalamic Nucleus
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Although the organization of the thalamocortical interconnections are complex, the OMPFC is generally related to medial MD (MDm), whereas the LPFC is related to more lateral parts of MD (Ray and Price, 1993).”
§ Neurocircuitry of Mood Disorders > CORTICO-STRIATAL-THALAMIC CIRCUITS RELATED TO OMPFC
What the sources say
- Not checked — no full text of the sourcecites Ray and Price, 1993 source
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It is possible that this region represents a multi-modal cortex that also connected to circuits responsible for emotion.”
§ Neurocircuitry of Mood Disorders > Area 45a
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A similar deficit in subjects with mood disorders might be the difficulty of 'letting go' of a negative mood or mind-set long after the resolution of any traumatic events that might have justified it.”
§ Neurocircuitry of Mood Disorders > Medial Segment of Mediodorsal Thalamic Nucleus
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Rests on an assumption: The anatomical and functional organization of the emotion-related circuits described in monkeys and other animals is sufficiently similar to that in humans to inform conclusions about human mood disorders.
None of the sources cited for this claim have been checked yet.
In the paper
“Indeed, in most cases the projection to the cortex involves more neurons than that to MD, suggesting that the non-thalamic input to cortex carries more detailed information (Russchen et al, 1987;Carmichael et al, 1994;Price, 2003).”
§ Neurocircuitry of Mood Disorders > Medial Segment of Mediodorsal Thalamic Nucleus
What the sources say
- Not checked — no full text of the sourcecites Russchen et al, 1987 source
- Not matchedcites Carmichael et al, 1994
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites Price, 2003
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The prefrontal cortex as a whole is reciprocally connected to the mediodorsal thalamic nucleus (MD), with different prefrontal regions related to different portions of MD (Figure 6).”
§ Neurocircuitry of Mood Disorders > CORTICO-STRIATAL-THALAMIC CIRCUITS RELATED TO OMPFC
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The major difference with the orbital network is that there do not appear to be olfactory or taste inputs to the ventral system; it is possible that it functions in the assessment of non-food sensory objects.”
§ Neurocircuitry of Mood Disorders > Ventral Prefrontal System
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It can be suggested that these convergent but antagonistic inputs would interact to modulate the reciprocal thalamocortical interactions between the OMPFC and MDm.”
§ Neurocircuitry of Mood Disorders > Medial Segment of Mediodorsal Thalamic Nucleus
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
In the paper
“For example, the medial network is primarily connected with the anterior and posterior parts of the cingulate cortex, whereas the orbital network connects primarily to the middle portion of the cingulate (Miller et al, 2008).”
§ Neurocircuitry of Mood Disorders > Medial Prefrontal Network
What the sources say
- Not matchedcites Miller et al, 2008
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although the limbic inputs are dominant, ongoing patterns of thalamo-cortical and cortico-thalamic activity would be maintained, allowing for consistent behavior.When pallidal inputs become more prominent, ongoing patterns would be interrupted, allowing a switch from one behavior to another.”
§ Neurocircuitry of Mood Disorders > Medial Segment of Mediodorsal Thalamic Nucleus
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“It consists of areas on the ventromedial surface of the frontal cortex, rostral and ventral to the genu, areas along the medial edge of the orbital cortex, and a small caudolateral orbital region at the rostral end of the insula (Carmichael and Price, 1996; Figure 3).”
§ Neurocircuitry of Mood Disorders > Medial Prefrontal Network
What the sources say
- Not checked — no full text of the sourcecites Carmichael and Price, 1996 source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The ventral system of the LPFC consists of areas ventral to the principal sulcus, including area 46v, 12r, and 45b (area 45a is a special case, section 45a see below) (Figure 3).”
§ Neurocircuitry of Mood Disorders > Ventral Prefrontal System
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“There is some degree of organization within this system, such that the subgenual cortex provides the heaviest projection, which terminates in both the medial and lateral hypothalamus, and in both dorsolateral and ventrolateral columns of the PAG, while the fibers from the lateral part of the medical network (areas Iai, and 47/12s) are restricted to the lateral hypothalamus, and the ventrolateral P”
§ Neurocircuitry of Mood Disorders > CORTICAL PROJECTIONS TO HYPOTHALAMUS AND BRAINSTEM
What the sources say
- Not matchedcites O ¨ngu ¨r et al, 1998a, b
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites An et al, 1998
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This analysis has indicated that large parts of the LPFC are closely related to the medial and orbital prefrontal networks, and may have similar functional roles.”
§ Neurocircuitry of Mood Disorders > LATERAL PREFRONTAL CORTEX (LPFC)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“As with the orbital network, the areas of the medial network are preferentially interconnected with each other, and the network is also characterized by outputs to visceral control areas in the hypothalamus and periaqueductal gray.”
§ Neurocircuitry of Mood Disorders > Medial Prefrontal Network
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The specific projections from the dorsal, ventral, and caudal parts of the LPFC that were described above have not been clearly defined.”
§ Neurocircuitry of Mood Disorders > Prefrontal Projections to the Striatum
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“They are specifically and reciprocally connected to the medial prefrontal network areas, with little connection to the orbital network.”
§ Neurocircuitry of Mood Disorders > Midline 'Intralaminar' Nuclei of Thalamus
What the sources say
- Not matchedcites Hsu andPrice, 2007, 2009
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Not matched
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The dorsal system is interconnected with the medial prefrontal network, and shares most of its other connections (Figure 5).”
§ Neurocircuitry of Mood Disorders > Dorsal Prefrontal System
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These studies have implicated subgenual PFC regions of the infralimbic cortex (BA 25) (eg, Coryell et al, 2005) and the adjacent sgACC corresponding to BA 24sg (eg, O ¨ngu ¨r et al, 1998a, b, 2003;Drevets et al, 1997a) (Figure 9).”
§ Neurocircuitry of Mood Disorders > Brain Structural Abnormalities in Mood Disorders
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Because the amount of GFAP varies with the functional state of astrocytes, and GFAP staining often does not demonstrate all astrocytes, it is unclear whether these results indicate changes in astrocyte number or function.”
§ Neurocircuitry of Mood Disorders > NEUROPATHOLOGICAL CORRELATIONS WITH NEUROIMAGING ABNORMALITIES
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The neuroimaging abnormalities found in MDD and BD generally have corroborated hypotheses regarding the neural circuitry underlying depression that initially were based on observations from the behavioral effects of lesions experimentally placed in experimental animals (see 'Cortico-Striatal-Thalamic Circuits Related to the OMPFC' above)”
§ Neurocircuitry of Mood Disorders > Neuroimaging Abnormalities in Mood Disorders
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“elevated glucocorticoid concentrations and repeated stress decrease the proliferation of oligoden-drocyte precursors (Alonso, 2000;Banasr and Duman, 2007).”
§ Neurocircuitry of Mood Disorders > NEUROPATHOLOGICAL CORRELATIONS WITH NEUROIMAGING ABNORMALITIES
What the sources say
- Not checked yetcites Alonso, 2000
- Not checked — no full text of the sourcecites Banasr and Duman, 2007 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Notably, the short allele of the serotonin transporter promoter region length polymorphism (5HTT-PRL) has been identified as a genetic factor that is associated with both an increased vulnerability for developing MDD within the context of stress (Caspi et al, 2003) and a reduction in sgACC gray matter volume (Pezawas et al, 2005).”
§ Neurocircuitry of Mood Disorders > Brain Structural Abnormalities in Mood Disorders
What the sources say
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, the same domains are implicated in depression and mania, although the characteristic disturbance in emotional behavior within these syndromes appears opposite with respect to emotional valence.”
§ Neurocircuitry of Mood Disorders > Neuroimaging Abnormalities in Mood Disorders
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In BD, episodes of depression occur alternately with manic or hypomanic episodes during which the mood becomes euphoric and labile, the capacity for deriving pleasure increases, behaviors aimed at deriving pleasure increase, and energy psychomotor activity, libido, and self esteem become elevated.”
§ Neurocircuitry of Mood Disorders > Neuroimaging Abnormalities in Mood Disorders
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Extant neural models of depression posit that dysfunction within the medial network and related limbic structures underlie the disturbances in emotional behavior and other cognitive aspects of the major depressive syndrome.”
§ Neurocircuitry of Mood Disorders > RECENT OBSERVATIONS IN HUMANS WITH MOOD DISORDERS
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The neuropathological changes evident in the mPFC and amygdala in mood disorders may impair their roles in modulating visceral responses to stressors and emotional stimuli.”
§ Neurocircuitry of Mood Disorders > IMPLICATIONS FOR NEUROCIRCUITRY-BASED MODELS OF DEPRESSION
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
In the paper
“Rats exposed to fear-conditioned stimuli show reduced mPFC neuronal firing activity, the magnitude of which correlates inversely with the corresponding increase in amygdala neuron activity and fear behavior (Garcia et al, 1999).”
§ Neurocircuitry of Mood Disorders > IMPLICATIONS FOR NEUROCIRCUITRY-BASED MODELS OF DEPRESSION
What the sources say
- Not checked — no full text of the sourcecites Garcia et al, 1999 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Such reciprocal relationships between the medial prefrontal network and amygdala may be related to the observations that in MDD depression severity correlates positively with amygdala and sgACC activity, but negatively with activity in the left VLPFC/lateral OFC (approximately BA 45a and 47s) (Drevets et al, 2004a).”
§ Neurocircuitry of Mood Disorders > IMPLICATIONS FOR NEUROCIRCUITRY-BASED MODELS OF DEPRESSION
What the sources say
- Not matchedcites Drevets et al, 2004a
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Not matched
None of the sources cited for this claim have been checked yet.
In the paper
“The results from MRS studies of MDD show reductions in cerebral GABA levels and in the 'Glx' peak, which reflects the combined concentrations of glutamate plus glutamine, that appear compatible with the postmortem findings of cellular reductions.”
§ Neurocircuitry of Mood Disorders > Magnetic Resonance Spectroscopy (MRS) Imaging of Glutamate and GABA
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Dendritic atrophy presumably would be reflected by a decrease in the volume of the neuropil, which occupies most of the gray matter volume.”
§ Neurocircuitry of Mood Disorders > Correlations with Rodent Models of Chronic and Repeated Stress
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
- Rests on an assumption: Neuropil occupies most of the gray matter volume.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“One neural model that could account for the neuroendocrine autonomic neurotransmitter attention and rewardseeking abnormalities associated with MDE suggests that impairment of medial prefrontal network and BLA function disinhibits the efferent transmission from the ACe and BNST to the hypothalamus and brainstem (Figure 10).”
§ Neurocircuitry of Mood Disorders > Effects of Altered Medial Prefrontal Network-Limbic Interactions
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“Severe depression is associated with hypersecretion of cortisol during the circadian nadir, pituitary and adrenal gland enlargement, and CSF-CRF levels that are increased to an extent that is inappropriate to the plasma cortisol concentrations”
§ Neurocircuitry of Mood Disorders > Effects of Altered Medial Prefrontal Network-Limbic Interactions
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“If the neuropathological changes extant within the ACC in mood disorders interfere with the cortical drive on VTA-DA neuronal burst-firing activity, they may impair perception or learning of reward, and potentially interfere with behavioral engagement in pleasurable or positively reinforcing activities.”
§ Neurocircuitry of Mood Disorders > Effects of Altered Medial Prefrontal Network-Limbic Interactions
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes? Based: unclearIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The autonomic imbalance associated with depression also could reflect medial network dysfunction coupled with excessive amygdala activity.”
§ Neurocircuitry of Mood Disorders > Effects of Altered Medial Prefrontal Network-Limbic Interactions
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“although this has not been found in primates (An et al, 1998;Freedman et al, 2000), it may be expected that multisynaptic pathways would serve a similar function.”
§ Neurocircuitry of Mood Disorders > Effects of Altered Medial Prefrontal Network-Limbic Interactions
What the sources say
- Not matchedcites An et al, 1998
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked yetcites Freedman et al, 2000
Tests✓ Asserted: passes✗ Checkable: fails✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. It may be too vague to check against evidence. The paper may give no reason why it holds.
- Not matched
None of the sources cited for this claim have been checked yet.
In the paper
“In addition, depressed subjects showed abnormal reductions in the CSF and jugular vein plasma levels of the DA metabolite homovanillic acid (Willner, 1995;Lambert et al, 2000), striatal DA transporter binding (Meyer et al, 2001), [ 11 C]L-DOPA uptake across the blood-brain barrier (A ˚gren et al, 1993), and striatal dopamine D 1 receptor binding (Cannon et al, 2009).”
§ Neurocircuitry of Mood Disorders > Effects of Altered Medial Prefrontal Network-Limbic Interactions
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“Preliminary reports indicate that chronic SSRI treatment or deep brain stimulation of the anterior capsule also reduces the abnormally elevated metabolism in the accumbens area in depression (Drevets et al, 2006) or in depression associated with obsessive-compulsive disorder (Van Laere et al, 2006)”
§ Neurocircuitry of Mood Disorders > Antidepressant Treatment Effects
What the sources say
- Not matchedcites Drevets et al, 2006
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites Van Laere et al, 2006
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Not matched
In the paper
“The mesolimbic DA projections from the VTA to the nucleus accumbens shell and the mPFC thus have major roles in learning associations between operant behaviors, or sensory stimuli and reward, and in mediating the reinforcing properties of natural rewards such as food and sex (Nestler and Carlezon, 2006).”
§ Neurocircuitry of Mood Disorders > Effects of Altered Medial Prefrontal Network-Limbic Interactions
What the sources say
- Not checked — no full text of the sourcecites Nestler and Carlezon, 2006 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“both deficits in negative feedback systems and excessive central stimulation of the secretion of CRF and/or other ACTH secretagogues are implicated in mood disorders (Gold and Chrousos, 2002;Drevets et al, 2004a;Swaab et al, 2005;Carroll et al, 2007).”
§ Neurocircuitry of Mood Disorders > Effects of Altered Medial Prefrontal Network-Limbic Interactions
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Antidepressant therapies may compensate for this dysfunction by modulating the pathological limbic activity that putatively mediates depressive symptoms (Drevets et al, 2002a), or by enhancing the expression of neurotrophic factors that protect medial network function from the effects of repeated stress (Manji et al, 2001).”
§ Neurocircuitry of Mood Disorders > FUTURE DIRECTIONS
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
The paper relies on this without support.
The anatomical and functional organization of the emotion-related circuits described in monkeys and other animals is sufficiently similar to that in humans to inform conclusions about human mood disorders.
“In the last 15 years these methods have been applied extensively to the limbic system and prefrontal cortex of monkeys, and much more specific circuits have been defined.”
“A large body of human data from functional and structural imaging, as well as analysis of lesions and histological material indicates that this system is centrally involved in mood disorders.”
The paper relies on this without support.
MDD and BD are not associated with gross brain pathology or with clear animal models for spontaneous recurrent mood episodes.
“As these conditions are not associated with gross brain pathology, or with clear animal models for spontaneous recurrent mood episodes, the development of tools that allowed noninvasive assessment of human brain structure and function has proven critical to elucidating their neurobiology.”
The paper relies on this without support.
Findings from animal models of stress and lesions can be generalized to humans to understand mood disorders.
“It is likely that the role of the PVT is general across many types of stressors.”
The paper relies on this without support.
Neuroimaging abnormalities in mood disorders reflect the underlying neural circuitry rather than epiphenomenal changes.
“The neuroimaging abnormalities found in MDD and BD generally have corroborated hypotheses regarding the neural circuitry underlying depression that initially were based on observations from the behavioral effects of lesions experimentally placed in experimental animals (see 'Cortico-Striatal-Thalamic Circuits Related to the OMPFC' above)”
The paper relies on this without support.
MRS spectra reflect combined intracellular and extracellular pools of glutamate-glutamine and GABA but are dominated overwhelmingly by the intracellular pools.
“Although these spectra reflect the combined intracellular and extracellular pools of glutamate-glutamine and GABA, they are dominated overwhelmingly by the intracellular pools.”
The paper relies on this without support.
The majority of the GABA pool exists within GABAergic neurons.
“The majority of the GABA pool exists within GABAergic neurons, so the reduction in GABA in the dorsal anterolateral PFC is compatible with the report of reduced GABAergic neurons in this region (BA9) in MDD (Rajkowska et al, 2007).”
The paper relies on this without support.
The Glx measure reflects the intracellular glutamate and glutamine pools.
“As the Glx measure reflects the intracellular glutamate and glutamine pools this abnormality appears compatible with the reductions in glial cells found postmortem in the same regions in MDD.”
The paper relies on this without support.
Perineuronal oligodendroglia and astroglia play roles in glutamate-glutamine cycling.
“Both perineuronal oligodendroglia and astroglia play roles in glutamate-glutamine cycling.”
The paper relies on this without support.
Neuropil occupies most of the gray matter volume.
“Dendritic atrophy presumably would be reflected by a decrease in the volume of the neuropil, which occupies most of the gray matter volume.”
The paper relies on this without support.
The ACC receives extensive dopaminergic innervation from the VTA and sends projections to the VTA that regulate phasic dopamine release.
“The ACC receives extensive dopaminergic innervation from the VTA and sends projections to the VTA that regulate phasic dopamine (DA) release.”
The paper relies on this without support.
Stimulation of projections from the amygdala to the ventral striatum interrupts the maintenance of cortically driven response patterns.
“Stimulation of projections from the amygdala to the ventral striatum interrupts the maintenance of these cortically driven response patterns, providing an adaptive over-ride that interrupts goal-directed thought or behavior in response to threat or novelty.”
The paper relies on this without support.
Antidepressant drugs impact serotonergic, dopaminergic, noradrenergic, cholinergic, glutamatergic, GABAergic, glucocorticoid, and peptidergic systems through either primary or secondary pharmacological actions.
“Antidepressant drugs (AD) impact these systems through either primary or secondary pharmacological actions.”
The paper relies on this without support.
The medial and orbital prefrontal networks connect to separate but parallel cortico-striato-pallido-thalamic loops that use adjacent cortical, mediodorsal thalamic, striatal, and pallidal regions.
“Note that the two networks are related to parallel but distinct loops that involve adjacent parts of the cortex MD thalamus striatum and pallidum.”
The paper relies on this without support.
The amygdala and hippocampus, as limbic structures, are mainly associated with the medial network.
“Limbic structures such as the amygdala and hippocampus are primarily related to the medial network.”
The paper relies on this without support.
The dorsal midline paraventricular nucleus of the thalamus connects with frontal cortex, striatum, hypothalamus, amygdala, and dorsal midbrain regions.
“Diagram of connections between the dorsal midline paraventricular nucleus of the thalamus (PVT) with areas of the frontal cortex striatum hypothalamus amygdala and dorsal midbrain.”
The paper relies on this without support.
Within the amygdala, connections link the basal and lateral nuclei to the central and medial nuclei and to the bed nucleus of the stria terminalis.
“Intra-amygdaloid connections link the basal and lateral amygdaloid nuclei to the central and medial nuclei of the amygdala and the bed nucleus of the stria terminalis (BNST).”
The paper relies on this without support.
The amygdala and medial prefrontal network interact with a shared cortico-striatal-pallidal-thalamic loop via strong connections to the accumbens nucleus, medial caudate, and mediodorsal and paraventricular thalamic nuclei; this interaction may control and limit stress responses.
“In addition, the amygdala and medial prefrontal network interact with the same cortico-striatal-pallidal-thalamic loop, through prominent connections both with the accumbens nucleus and medial caudate, and with the mediodorsal and paraventricular thalamic nuclei, which may function to control and limit responses to stress.”
The paper relies on this without support.
The medial prefrontal network serves as a central node in the cortical default system, which seems to support self-referential functions like mood.
“Finally, the medial prefrontal network is a central node in the cortical 'default system' that appears to support self-referential functions such as mood.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Brain-imaging studies of depressed patients provide strong and consistent evidence of decreased volume of cortical and limbic brain regions— such as the prefrontal cortex (PFC) and the hippocampus—that control emotion, mood, and cognition, suggestive of neuronal atrophy that is related to length of illness and time of treatment (8, 9).”
From Synaptic Dysfunction in Depression: Potential Therapeutic Targets (2012) · cites this paper as [9]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Two independent seed ROIs placed in the pregenual anterior cingulate cortex (pgACC) and the dorsal anterior cingulated cortex (dACC) were chosen based on previous reports on their involvement in meditation and affective disorders such as depression [55].”
From State and training effects of mindfulness meditation on brain networks reflect neuronal mechanisms of its antidepressant effect (2016) · cites this paper as [55]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Both these accounts of depression are supported by the involvement of agranular visceromotor cortices in the pathophysiology of depression (e.g. [89]).”
From Active interoceptive inference and the emotional brain (2016) · cites this paper as [89]
The cited source says what the claim attributes to it.
In the citing paper
“Basic and clinical studies demonstrate that depression is associated with reduced size of brain regions that regulate mood and cognition, including the prefrontal cortex and the hippocampus, and decreased neuronal synapses in these areas.”
From Synaptic Dysfunction in Depression: Potential Therapeutic Targets (2012) · cites this paper as [9]
The cited source says what the claim attributes to it.
In the citing paper
“Research on mood disorder pathophysiology has implicated abnormalities in glutamatergic transmission, along with disrupted function and structure in neural circuits involved in mood regulation (4), findings that led to further investigation of glutamatergic N-methyl-D-aspartate (NMDA) receptor modulators in treating depression (5,6).”
In the citing paper
“Similar reductions have been found in proteins such as CREB and its upstream effectors ERK and PKC172-174.”
From Dysregulation of adult hippocampal neuroplasticity in major depression: Pathogenesis and therapeutic implications (2022) · cites this paper as [174]
In the citing paper
“It has been proposed that major depressive symptoms are associated with the dysregulation of a distributed neuronal network encompassing cortical and limbic regions rather than with the (functional) breakdown of a single discrete brain region (Mayberg, 1997(Mayberg, , 2003;;Davidson et al., 2002;Drevets, 2003;Phillips et al., 2003;Seminowicz et al., 2004;Drevets et al., 2008;Price and Drevets, 201”
From Identifying major depression using whole-brain functional connectivity: a multivariate pattern analysis (2012) · cites this paper as Price and Drevets, 2010
In the citing paper
“These vmPFC-subcortical pathways are thought to constitute a ‘visceromotor’ system whose functions are to coordinate several aspects of autonomic activity [11].”
From Ventromedial prefrontal–subcortical systems and the generation of affective meaning (2012) · cites this paper as [11]
In the citing paper
“However, the major subdivisions of the vmPFC are interconnected with each other and with subcortical nuclei in several interlocked functional systems [11], prompting a number of researchers to characterize the region’s broad functional roles with terms such as ‘affect’ [14], ‘regulation’ [3], ‘valuation’ [7,15], ‘self-projection’ [5], ‘self-reference’ [8], ‘mentalizing’ [9], ‘somatic markers’ [16]”
From Ventromedial prefrontal–subcortical systems and the generation of affective meaning (2012) · cites this paper as [11]
In the citing paper
“Conversely, dysfunction of the vmPFC is thought to be critical in a number of brain disorders, most notably post-traumatic stress disorder (PTSD) [10], depression [11] and dysregulation related to chronic stress [12] and pain [13].”
From Ventromedial prefrontal–subcortical systems and the generation of affective meaning (2012) · cites this paper as [11]
In the citing paper
“The vmPFC is also directly connected with memory-related circuits in hippocampus and medial temporal lobe [11] that can subserve both memory and future projection[5].”
From Ventromedial prefrontal–subcortical systems and the generation of affective meaning (2012) · cites this paper as [11]
In the citing paper
“What is suggested is that a potential mechanism of action of rTMS to dmPFC is increased influence of cognitive control networks over thalamic and striatal regions, possibly linked with improved facilitation of goal-directed behavior (Corbetta and Shulman, 2002; Price and Drevets, 2010; Sheline et al, 2010).”
From Resting-state cortico-thalamic-striatal connectivity predicts response to dorsomedial prefrontal rTMS in major depressive disorder (2014) · cites this paper as Price and Drevets, 2010
In the citing paper
“an area that also has strong projections to medial prefrontal cortical regions associated with the regulation of emotions and visceral reactions (Price and Drevets, 2010).”
From Phasic and sustained fear in humans elicits distinct patterns of brain activity (2011) · cites this paper as Price and Drevets, 2010
In the citing paper
“Subgenual anterior cingulate cortex (sACC) is central to the medial prefrontal network that has been associated with mood and anxiety dysregulation, and has been implicated in the regulation of visceral responses during stress and anxiety (Price and Drevets, 2010).”
From Phasic and sustained fear in humans elicits distinct patterns of brain activity (2011) · cites this paper as Price and Drevets, 2010
In the citing paper
“Numerous studies suggest that depression and anxiety in humans result in part from hypo–activation and reduced volume of frontal cortical and hipppocampal regions that control subcortical structures such as nucleus accumbens (NAc) and amygdala, although hyper–activation of certain PFC regions (e.g., subgenual area of anterior cingulate cortex) is also involved58–61.”
From Neurobiology of resilience (2012) · cites this paper as [58]
In the citing paper
“The amygdala has strong, bidirectional connections to medial prefrontal regions along the anterior cingulate cortex surrounding the corpus callosum, extending from ventral regions (subgenual cingulate cortex) to rostral (pregenual cingulate) and dorsal (supragenual cingulate) regions (Fig. 2).”
From Neural Substrates of Childhood Anxiety Disorders (2012) · cites this paper as [36]
In the citing paper
“Among these findings, abnormal activity in the ventromedial prefrontal cortex (vmPFC) is probably the most widely reported (1–4).”
From Functional anatomy of ventromedial prefrontal cortex: implications for mood and anxiety disorders (2012) · cites this paper as [4]
In the citing paper
“IL/25 projects directly to a number of autonomic regions which have been found to enhance sympathetic activity, including the perifornical area, dorsomedial hypothalamus, dorsolateral periaqueductal gray, lateral parabrachial nucleus, cuneiform nucleus, and lateral septum, among other regions (4, 33, 35–37, 39, 47, 82, 97, 98).”
From Functional anatomy of ventromedial prefrontal cortex: implications for mood and anxiety disorders (2012) · cites this paper as [4]
In the citing paper
“of the mPFC as a modulatory region interconnected with limbic structures8 and involved in emotion regulation.9”
From Altered resting-state amygdala functional connectivity in men with posttraumatic stress disorder (2012) · cites this paper as [8]
In the citing paper
“Studies utilizing brain-imaging methods have shown that cortical and limbic region atrophy, including decreased volumes in the prefrontal cortex (PFC) and hippocampus, is associated with the duration of illness and treatment.”
From Epigenetic mechanisms of major depression: Targeting neuronal plasticity (2018) · cites this paper as [9]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Two 1978 references start on the same journal page
MinorThe two differently titled papers are both listed as beginning on page 225 of volume 178 of the same journal, although their stated ending pages differ.
“142. Krettek JE, Price JL (1978a). Amygdaloid projections to subcortical structures within the basal forebrain and brainstem in the rat and cat. J Comp Neurol 178: 225-254.”
“143. Krettek JE, Price JL (1978b). A description of the amygdaloid complex in the rat and cat with observations on intra-amygdaloid axonal connections. J Comp Neurol 178: 225-280.”
Two 1977 references have identical journal pages
MinorThe bibliography assigns the same journal, volume, and complete page range to two differently titled papers by the same authors.
“145. Krettek JE, Price JL (1977b). An autoradiographic study of projections from the amygdaloid complex to the thalamus and cerebral cortex. J Comp Neurol 172: 723-752.”
“146. Krettek JE, Price JL (1977c). The connections of the amygdaloid complex and related olfactory cortical areas with the entorhinal cortex and the hippocampus. J Comp Neurol 172: 723-752.”
Citations
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Flagged first, then by citations
4 of the 379 references couldn’t be matched to a known paper.
Research works printed but not linked: 7
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Determinants of adverse health outcomes in late-life depression
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Structural brain abnormalities in bipolar disorder
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Neurotrophic Mechanisms of Depression
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Bartlett, E. A., Zanderigo, F., Shieh, D., et al. (2021) · doi:10.31234/osf.io/e9wbm
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Passingham, R. E., & Lau, H. C. (2022) · doi:10.31234/osf.io/zjf6x
New Developments in the Treatment of Depression with tDCS
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The anatomy of obsessive-compulsive disorderPreprint
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VASCULAR DEPRESSION AND CARDIOVASCULAR COMPLICATIONS OF TYPE 2 DIABETES
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Nöropsikoloji ve Nöropsikolojik Psikoterapi
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“Por lo tanto, el aumento de la activación de mpfc en respuesta a la rumia da origen a la tendencia de las personas con depre-sión a interpretar los estímulos y problemas como autorreferenciales, dicho de otro modo, el evento estresante perturba la autoimagen y la autoestima (42, 46, 47).”
BackgroundNeuroanatomical Systems Relevant to Neuropsychiatric Disorders
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Brain Structures Involved in Major Depressive Disorder
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Endocannabinoids in pain modulation
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Additional file 4 of Taste receptor type 1 member 3 enables western diet-induced anxiety in mice
Song, J. W., Lee, K.-H., Seong, H., Shin, D.-M., & Shon, W.-J. (2024) · Figshare · doi:10.6084/m9.figshare.26636019
Yang, H. G., Liu, W. V., Wen, Z., et al. (2022) · Figshare · doi:10.6084/m9.figshare.19625553
Additional file 1 of Taste receptor type 1 member 3 enables western diet-induced anxiety in mice
Song, J. W., Lee, K.-H., Seong, H., Shin, D.-M., & Shon, W.-J. (2024) · Figshare · doi:10.6084/m9.figshare.26636010
Additional file 1 of Whole-brain morphological alterations associated with trigeminal neuralgia
Mo, J., Zhang, J., Hu, W., Luo, F., & Zhang, K. (2021) · Figshare · doi:10.6084/m9.figshare.15178518
Additional file 3 of Whole-brain morphological alterations associated with trigeminal neuralgia
Mo, J., Zhang, J., Hu, W., Luo, F., & Zhang, K. (2021) · Figshare · doi:10.6084/m9.figshare.15178524
Additional file 3 of Taste receptor type 1 member 3 enables western diet-induced anxiety in mice
Song, J. W., Lee, K.-H., Seong, H., Shin, D.-M., & Shon, W.-J. (2024) · Figshare · doi:10.6084/m9.figshare.26636016
Yang, H. G., Liu, W. V., Wen, Z., et al. (2022) · Figshare · doi:10.6084/m9.figshare.19625550
Additional file 2 of Whole-brain morphological alterations associated with trigeminal neuralgia
Mo, J., Zhang, J., Hu, W., Luo, F., & Zhang, K. (2021) · Figshare · doi:10.6084/m9.figshare.15178521
Keller, M., Mendoza-Quiñones, R., Cabrera Muñoz, A., et al. (2022) · Figshare · doi:10.6084/m9.figshare.19327025
Additional file 2 of Taste receptor type 1 member 3 enables western diet-induced anxiety in mice
Song, J. W., Lee, K.-H., Seong, H., Shin, D.-M., & Shon, W.-J. (2024) · Figshare · doi:10.6084/m9.figshare.26636013
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“In anxiety and depressive disorders, neuroimaging evidence related to negative emotional processing biases and regulatory network abnormalities is also frequently observed (Etkin and Wager, 2007; Price and Drevets, 2010).”
Cognitive performance modulates regional brain age differences in clinical anxiety and depression
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Metadata
- Authors
- Price, J. L., & Drevets, W. C.
- Affiliations
- Washington University in St. Louis (US)
- National Institutes of Health (US)
- Corresponding author
- Price, Joseph L
- ORCID
- Drevets, Wayne C
- Venue
- Neuropsychopharmacology
- Published
- 2009-08-19
- Volume
- 35
- Issue
- 1
- Pages
- 192-216
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC3055427
- OpenAlex
- W2122384242
- Cited by
- 1,606
- References
- 379
- Citations by year
- 2026: 50 · 2025: 75 · 2024: 71 · 2023: 57 · 2022: 89 · 2021: 122 · 2020: 102 · 2019: 110 · 2018: 83 · 2017: 101 · 2016: 105 · 2015: 119 · 2014: 127 · 2013: 124 · 2012: 113
- FWCI
- 6.57
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Neuropsychopharmacology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Public Health Service
- National Institute of Mental Health (R01MH070941)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- mood disorders, neurocircuitry, limbic system, amygdala, medial prefrontal cortex, ventral striatum, globus pallidus, medial thalamus, hypothalamus, periaqueductal gray, brainstem, emotional behavior, history of emotion research, monkeys, human brain imaging
- MeSH terms
- Animals, Brain, Humans, Models, Neurological, Neural Pathways, Mood Disorders
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