Comparison of clinical, biochemical, and genetic characteristics between ASD and schizophrenia
| ASD | |
|---|---|
| Clinical | Behavioral flexibility, delay of language, social cognitive deficits.a Worse performance than schizophrenia children in the theory of mind task.b Manifests in early childhood.a |
| Biochemical | Disturbances in glutamate, GABA, and dopamine neurotransmission.c Increases in proinflammatory cytokine (IL-1β, IL-6, TNF-α, IFN-γ) levels in the brain, CSF, and blood.d No alterations in anti-inflammatory cytokine (IL-4, IL-10) levels in the blood.e |
| Genetic | CNTNAP2, NLGN, NRXN, SHANK3, CADM1, etc.f |
| Schizophrenia | |
| Clinical | Positive, negative, cognitive symptoms (social cognitive deficits).g Develops in late adolescence most frequently.g |
| Biochemical | Disturbances in glutamate, GABA, and dopamine neurotransmission.g Increases in proinflammatory cytokine (IL-1β, IL-6, TNF-α) levels in the brain, CSF, and blood.h Reduction of anti-inflammatory cytokine (IL-10, IL-13) levels in the CSF and blood.h |
| Genetic | DISC1, DTNBP1, NRG1, DRD2, HTR2A, COMT, etc.i |
CADM1, cell adhesion molecule 1; COMT, catechol-O-methyltransferase; DISC1, disrupted in schizophrenia 1; DRD2, dopamine receptor D2; DTNBP1, dystrobrevin-binding protein 1; GABA, γ-aminobutyric acid; HTR2A, 5-hydroxytryptamine (serotonin) receptor 2A; NLGN, neuroligin; NRG1, neuregulin 1; NRXN, neurexin; SHANK3, Src homology 3 and multiple ankyrin repeat domain 3; TNF-α, tumor necrosis factor-α.
↵a Volkmar et al., 2014.
↵b Pilowsky et al., 2000.
↵c Money and Stanwood, 2013.
↵d Onore et al., 2012.
↵e Ashwood et al., 2011b.
↵f Bourgeron, 2009.
↵g Stahl, 2013.
↵h Meyer et al., 2011b.
↵i Gejman et al., 2010.