Anatomic evaluation of the orbitofrontal cortex in major depressive disorder

Lacerda, Acioly L.T.; Keshavan, Matcheri S.; Hardan, Antonio Y.; Yorbık, Özgür; Brambilla, Paolo; Sassi, Roberto; Nicoletti, Mark; Mallinger, Alan G.; Frank, Ellen; Kupfer, David J.; Soares, Jair C.

doi:10.1016/j.biopsych.2003.08.021

Cited by 198 publications

(135 citation statements)

References 70 publications

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“…In addition, although only observed in white matter, these correlations are supported by a recent diffusion tensor imaging study that found reduced fractional anisotropy in white matter structures adjacent to the ventromedial prefrontal cortex in individuals with autism; alterations which could affect the neural pathways involved in social cognition (Barnea-Goraly et al, 2004). Further, our observation of alterations in only some subdivisions of the OFC is supported by fMRI studies (O'Doherty et al, 2001) and is consistent with findings of regional and asymmetric volumetric alterations of the OFC in several neuropsychiatric disorders with deficits in social cognition, such as schizophrenia (Hoptman et al, 2005), major depressive disorder (Lacerda et al, 2004), and obsessive-compulsive disorder (Kang et al, 2004), and could be related to the rich and diverse cytoarchitecture (Carmichael and Price, 1994) and connectivity (Carmichael and Price, 1995) of the OFC.…”

Section: Discussionsupporting

confidence: 87%

Volumetric alterations of the orbitofrontal cortex in autism

Girgis

Minshew

Melhem

et al. 2007

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Recent evidence has implicated the orbitofrontal cortex (OFC) in the pathophysiology of social deficits in autism. An MRI-based morphometric study of the OFC was conducted involving 11 children with autism (age range 8.1-12.7 years) and 18 healthy, age-matched controls (age range 8.9-12.8 years). Decreased grey matter volume in the right lateral OFC in the patient group was found, and correlations were observed between social deficits and white, but not grey, matter structures of the OFC. These findings support the role of OFC in autism and warrant further investigations of this structure using structural and functional methodologies.

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Section: Discussionsupporting

confidence: 87%

Volumetric alterations of the orbitofrontal cortex in autism

Girgis

Minshew

Melhem

et al. 2007

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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“…Patients with depression were found to have a loss of glia and/or neurons in the orbitofrontal cortex (Rajkowska et al 1999) and other related parts of the medial prefrontal cortex, including subgenual cortex (Ongur et al 1998). MRI brain imaging studies showed smaller volume of the orbitofrontal cortex in patients with depression Lacerda et al 2004;Lai et al 2000;Lee et al 2003) in addition to decreased orbitofrontal function with depressive relapse (Bremner et al 1997;Bremner et al 2003).…”

Section: Ra and The Frontal Cortexmentioning

confidence: 99%

The neurobiology of retinoic acid in affective disorders

Bremner

McCaffery

2008

Progress in Neuro-Psychopharmacology and Biological Psychiatry

144

154

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Current models of affective disorders implicate alterations in norepinephrine, serotonin, dopamine, and CRF/cortisol; however treatments targeted at these neurotransmitters or hormones have led to imperfect resolution of symptoms, suggesting that the neurobiology of affective disorders is incompletely understood. Until now retinoids have not been considered as possible contributors to affective disorders. Retinoids represent a family of compounds derived from Vitamin A that perform a large number of functions, many via the vitamin A product, retinoic acid. This signaling molecule binds to specific retinoic acid receptors in the brain which, like the glucocorticoid and thyroid hormone receptors, are part of the nuclear receptor superfamily and regulate gene transcription. Research in the field of retinoic acid in the CNS has focused on the developing brain, in part stimulated by the observation that isotretinoin (13-cis retinoic acid), an isomer of retinoic acid used in the treatment of acne, is highly teratogenic for the CNS. More recent work has suggested that retinoic acid may influence the adult brain; animal studies indicated that the administration of isotretinoin is associated with alterations in behavior as well as inhibition of neurogenesis in the hippocampus. Clinical evidence for an association between retinoids and depression includes case reports in the literature, studies of health care databases, and other sources. A preliminary PET study in human subjects showed that isotretinoin was associated with a decrease in orbitofrontal metabolism. Several studies have shown that the molecular components required for retinoic acid signaling are expressed in the adult brain ; the overlap of brain areas implicated in retinoic acid function and stress and depression suggest that retinoids could play a role in affective disorders. This report reviews the evidence in this area and describes several systems that may be targets of retinoic acid and which contribute to the pathophysiology of depression.

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“…18,70 However, morphometric magnetic resonance imaging studies report a decrease in the gray matter volume of specific key areas of the orbital cortex, MPFC, DLPFC, mesial temporal lobe, and basal ganglia [71][72][73][74][75] ( see FIG. 1).…”

Section: Volumetric Studies In Mood Disordersmentioning

confidence: 99%

Neural circuitry and neuroplasticity in mood disorders: Insights for novel therapeutic targets

Carlson¹,

Singh²,

Zarate³

et al. 2006

NeuroRX

135

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Summary:Major depressive disorder and bipolar disorder are severe mood disorders that affect the lives and functioning of millions each year. The majority of previous neurobiological research and standard pharmacotherapy regimens have approached these illnesses as purely neurochemical disorders, with particular focus on the monoaminergic neurotransmitter systems. Not altogether surprisingly, these treatments are inadequate for many individuals afflicted with these devastating illnesses. Recent advances in functional brain imaging have identified critical neural circuits involving the amygdala and other limbic structures, prefrontal cortical regions, thalamus, and basal ganglia that modulate emotional behavior and are disturbed in primary and secondary mood disorders. Growing evidence suggests that mechanisms of neural plasticity and cellular resilience, including impairments of neurotrophic signaling cascades as well as altered glutamatergic and glucocorticoid signaling, underlie the dysregulation in these circuits. The increasing ability to monitor and modulate activity in these circuits is beginning to yield greater insight into the neurobiological basis of mood disorders. Modulation of dysregulated activity in these affective circuits via pharmacological agents that enhance neuronal resilience and plasticity, and possibly via emerging nonpharmacologic, circuitry-based modalities (for example, deep brain stimulation, magnetic stimulation, or vagus nerve stimulation) offers promising targets for novel experimental therapeutics in the treatment of mood disorders.

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Anatomic evaluation of the orbitofrontal cortex in major depressive disorder

Cited by 198 publications

References 70 publications

Volumetric alterations of the orbitofrontal cortex in autism

Volumetric alterations of the orbitofrontal cortex in autism

The neurobiology of retinoic acid in affective disorders

Neural circuitry and neuroplasticity in mood disorders: Insights for novel therapeutic targets

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