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Quetiapine for ADHD


Quetiapine for ADHD

Quetiapine is an atypical antipsychotic.1
It has an antidepressant effect at the same time.2

In lower doses, it is used as a sleep aid. The relatively short plasma half-life of 2.5 to 5 hours3 is favorable for this.

1. Quetiapine is an antagonist of

  • Serotonin receptor 5-HT2A2
    • Thereby increasing the dopamine level in the PFC
  • Serotonin receptor 5-HT2C via the metabolite norquetiapine2
    • Receptor binding in the PFC of 72% after 2 hours at 450 mg3
    • Receptor binding of 50% after 26 hours at 450 mg3
  • Dopamine receptor D2
    • Leads to antipsychotic effect
    • Receptor binding in the striatum of 44% after 2 hours at 450 mg3
    • Receptor binding after 26 hours as in untreated healthy subjects at 450 mg3
    • The D2 antagonism of quetiapine is thus weaker than the 5HT antagonism.4
    • Relatively low affinity for dopamine D2 receptors, with an occupancy half-life of 10 hours, thus about twice as long as that of plasma3
  • Σ-Adrenergic receptor (especially A2)2
    • Thereby increasing the dopamine level in the PFC
  • Noradrenaline transporter NAT via the metabolite norquetiapine2
    • Thereby increased norepinephrine level
  • Histamine receptor H1
  • Glutamate NMDA
    • Quetiapine reduces mRNA levels for some subunits of the glutamate NMDA receptor NR-1 and NR-2.2
    • Reduction in the density of NMDA receptors in the caudate nucleus (putamen) (but not in the cortex or limbic system), as well as clozapine or haloperidol2

2. Quetiapine is an agonist of

  • Serotonin receptor 5-HT1A (partial)2
    • Thereby increasing the dopamine level in the PFC
  • Glutamate AMPA
    • Increase in the density of glutamate AMPA receptors in the caudate nucleus (putamen) (but not in the cortex or limbic system), as well as clozapine or haloperidol 2
    • Quetiapine caused a significant increase in the GluR-B and GluR-C subunits of the AMPA receptor in rat hippocampus.2
  • Sigma-1 receptors
    • Mediates antidepressant effect5
      • Can be additionally increased by σ1-agonist (+)-pentazocine
      • Can be reduced by σ1-antagonist BD1063

Indirect inhibition of 5-HT2C receptors causes inhibition of GABA release in the brainstem, which in turn causes release of norepinephrine and dopamine in the PFC.2

According to this understanding, GABA is underrepresented in ADHD-I and overrepresented in ADHD-HI. Given this background, quetiapine would hypothetically be more useful in ADHD-HI and less recommended in ADHD-I,

3. Use of quetiapine

Quetiapine is used primarily for schizophrenia and bipolar disorder (manic-depressive).
Primary use to date tends to be in relation to (massive) comorbidities, not ADHD itself.

A study of the treatment of ODD by concomitant quetiapine administration (= augmentation) to SSRI administration found no significant improvement in effect.6

In ADHD, quetiapine is used off-label in low doses in relation to the frequent sleep problems. Because of its short half-life, it is said to be applicable for this purpose despite its (albeit relatively weak) D2 antagonism.7 Nevertheless, at 450 mg, qetiapine showed a receptor occupancy of dopamine D2 receptors in the striatum of 44% within 2 h, which only returned to the level of untreated healthy subjects after 26 h. The study found that the drug was effective as a sleep aid.3 As a sleep aid, however, the dosage is much lower at between 12.5 and 100 mg.

Diese Seite wurde am 13.03.2023 zuletzt aktualisiert.