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Molecular Imaging for Depressive Disorders

T.-S. Lee, S.Y. Quek and K.R.R. Krishnan
American Journal of Neuroradiology June 2014, 35 (6 suppl) S44-S54; DOI: https://doi.org/10.3174/ajnr.A3965
T.-S. Lee
aFrom the Duke-National University of Singapore Graduate Medical School, Singapore.
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S.Y. Quek
aFrom the Duke-National University of Singapore Graduate Medical School, Singapore.
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K.R.R. Krishnan
aFrom the Duke-National University of Singapore Graduate Medical School, Singapore.
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    Fig 1.

    2D chemical shift imaging of N-acetylaspartate. Courtesy of Cecil Charles, Duke University.

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    Fig 2.

    Proton MR spectroscopy identification of assignments of compounds. Courtesy of Cecil Charles, Duke University.

Tables

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    Table 1:

    Summary of metabolites/compounds detected by each type of MRS and findings

    Type of MRSMetabolites/Compounds DetectedSummary of Findings
    19F MRSFluorine 19 nucleus
    Fluorinated drugs (including SSRIs)
    Used to study pharmacokinetics of fluoxetine and fluvoxamine31
    31P MRSPhosphomonoesters
    Phosphodiesters
    Inorganic phosphate
    Phosphocreatine
    α-, β-, and γ-nucleoside triphosphate
    Membrane phospholipid and energy metabolism abnormalities in frontal and temporal lobes of patients with bipolar disorder36
    Lower phosphomonoester levels for patients with euthymic bipolar disorder37
    Increased phosphomonoester and decreased ATP levels in frontal lobes of unipolar depressed patients38
    Proton MRSGlx
    GABA
    NAA
    Cr+PCr
    Cho
    mIns
    See Table 2
    • Note:—APT indicates adenosine triphosphate; SSRI, selective serotonin reuptake inhibitor.

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    Table 2:

    Summary of metabolites detected by proton MRS and findings

    Metabolite of InterestKey PropertiesFindings for Patients with Depression Relative to Controls
    Glu/GlutamineComplex signal
    Requires difference technique at intermediate field strengths
    Decreased Glu/Gln in anterior cingulate19,56,57
    Decreased Glu/Gln in amygdala-hippocampus58
    Decreased Glu/Gln in prefrontal cortex62
    Elevated Glu in occipital cortex59
    Reduction of Glx (mainly Glu and Gln) in depressive disorder but elevation in bipolar disorder60
    Response to treatment: increased levels with ECT19
    GABAComplex signal
    Requires different technique at intermediate field strengths
    Decreased in occipital cortex59,61
    Decreased in occipital and anterior cingulate cortex63
    Decreased in prefrontal cortex62
    Response to treatment: patients who were most severely depressed and who had lowest GABA concentrations showed largest increase after SSRI treatment59
    NAA or NAA/CrOnly present in neurons
    Change reflects loss or decreased function of neurons
    Decreased NAA/Cr in thalamus64
    Decreased NAA in caudate65
    Meta-analysis: no significant differences in NAA between depressed and healthy subjects in basal ganglia and frontal lobe structures50
    Cr+PCrReflects tissue energetics
    ∼7.8 μmol/g117
    No significant differences in Cr levels in frontal lobe structures between depressed and healthy subjects50
    ChoConcentration of pool: ∼2 μmol/g117
    Reflects mobile Cho (TMA) moieties
    Cho concentration rate limiting step in acetylcholine synthesis
    Dynamic equilibrium with acetylcholine and phospholipid pathways
    Mixed findings
    Meta-analysis: elevated in basal ganglia50
    Response to treatment: choline elevation reverses with antidepressant treatment50
    mInsDiverse role in central nervous system (gliosis, cytoskeleton, cellular signaling)Generally negative findings in anterior cingulate cortex, basal ganglia
    Mixed results for prefrontal cortex54
    • Note:—ECT indicates electroconvulsive therapy; SSRI, selective serotonin reuptake inhibitor; TMA, trimethylamine.

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    Table 3:

    Common neurotransmitter systems studied in PET imaging and radioligands used for each component or pathway involved

    Neurotransmitter SystemComponent/Pathway InvolvedRadioligands Used
    SerotoninSynthesisα-[11C]MTrp
    Transport[11C]McNeil 5652
    [11C]DASB
    Type 1A receptor[11C]WAY-100635
    [18F]FCWAY
    [18F]MPPF
    Type 1B receptor[11C]P943
    Type 2 receptor[18F]setoperone
    [18F]altanserin
    [11C]MDL 100907
    [18F]FESP
    DopamineSynthesis[18F]fluoro-L-DOPA
    D1 receptor[11C]SCH 23,390
    [11C]NNC 112
    D2/3 receptor[11C]raclopride
    [11C]FLB 457
    Transporter[11C]RTI-32
    [11C]CFT
    Monoamine oxidaseMonoamine oxidase type A[11C]harmine
    Non-monoaminergic mechanismsMuscarinic type 2 receptor[18F]FP-TZTP
    Nicotinic receptor[18F]FA-85380
    GABA type A receptor[11C]flumazenil
    Phosphodiesterase type 4[11C]-(R)-rolipram
    Amyloid and τ proteins[18F]DDNP
    p-glycoprotein[11C]verapamil
    Histamine H1 receptor[11C]doxepin
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Cite this article
T.-S. Lee, S.Y. Quek, K.R.R. Krishnan
Molecular Imaging for Depressive Disorders
American Journal of Neuroradiology Jun 2014, 35 (6 suppl) S44-S54; DOI: 10.3174/ajnr.A3965

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Molecular Imaging for Depressive Disorders
T.-S. Lee, S.Y. Quek, K.R.R. Krishnan
American Journal of Neuroradiology Jun 2014, 35 (6 suppl) S44-S54; DOI: 10.3174/ajnr.A3965
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