TABLE 3

Summary of neurobiological factors implicated in OCD, hypothesized mechanism by which they exert an effect on OCD, and the section number where the relevant research is discussed

Implicated FactorHypothesized MechanismSection
Serotonin neurotransmissionNeurotransmitter deficitIII.A.1
Low 5-HT transporter
Altered function of 5-HT1A receptors
Hypofunction of 5-HT2C receptors
Dopamine neurotransmissionD2 and/or D1 receptor activityIII.A.2
Interaction with serotonin
Glutamate and GABA neurotransmissionAltered glutamate concentrationIII.A.3
Faulty glutamate transporters
GABA-glutamate imbalance
Oxidative stressIncreased lipid peroxidationIII.B.1
Disturbances in cortical GSH
Phosphoinositide hyperactivityInsufficient MIIII.B.2
NO-cGMP pathwayIncreased levels of NOIII.B.2
cAMP-dependent pathwaySupersensitive AC activityIII.B.2
Increased PDE4 activity
Brain-gut-microbiota axisSpecific alterations in the gut microbiomeIII.B.3
Altered metabolism in the TRYCAT pathway
Neurosteroid dysregulationModified gene expression and neuronal excitabilityIII.B.4
OxytocinActivates threat detection circuitsIII.B.4
Neurotrophic factorsBDNF reduced, possibly due to geneticsIII.B.5
Regional neuroanatomical changesAlteration of a circuit composed of cortex-basal ganglia-thalamus-cortex pathwaysIII.C.
Specific genes or polymorphismsResult in alterations of serotonergic, dopaminergic, and glutamatergic signalingIII.D.1
Age of onsetChildhood onset may be distinctIII.D.2
Sex hormonesAlter serotonin neurotransmissionIII.D.3
Stressful life eventsInduction of HPA hyperactivityIII.D.3
Streptococcal infectionAltered immune functionIII.D.4.a
Other infections, autoimmune and inflammatory processesGlutamate neuro-excitotoxicityIII.D.4.a
Antibodies crossreact with brain antigens
Microglia activation
Change in TRYCAT metabolism
Disease-avoidance behavioral adjustments
NeuroinflammationCascade of cumulative responsesIII.D.4.b