Table 1.

Summary of symptoms and core abnormalities in schizophrenia

Property	Abnormalities in schizophrenia
Risk factors	Obstetric complications (e.g. bleeding during pregnancy, abnormal fetal growth, premature labor and neonatal asphyxia) [56, 57] Maternal infection, premature labor and delivery [55] Familial disease [306]
Prodromal/high-risk state/psychosis risk syndrome	Poor prenatal care (e.g. low socioeconomic status, inadequate prenatal nutrition, maternal obesity and substance abuse) [307, 308] Attenuated psychotic symptoms, e.g. unusual thoughts, perceptual abnormalities, suspiciousness Brief and self-limiting psychotic symptoms, e.g. delusions Disturbances in cognitive processing, impaired speech fluency and self-perception Negative symptoms, e.g. awkwardness, anxiety, decreased expression of emotion, decreased engagement and role functioning [9, 309] Reduction in WM volume prior to onset of psychosis [42]
Behavioral symptoms	Positive: hallucinations, delusions, confused thought and speech process Negative: apathy, disinterest, social withdrawal and isolation, mood symptoms [310, 311] Endophenotypes: deficient prepulse inhibition or suppression of EMG response to auditory stimulus after prepulse stimulus. Impaired gain in eye movements when following object. Low performance IQ, reduced verbal memory, working memory, attention span, reduced processing speed [16]
Brain structure	Low cerebral volume, higher lateral ventricle volume, reduced WM volume [20, 312] Altered WM connectivity and ultrastructure [2] Reduced FA and increased radial diffusivity in WM regions, including corpus callosum, measured by DTI indicating compromised WM integrity even in early stages of schizophrenia [312]
Cellular and biochemical changes	Lack of normal developmental increase in mature oligodendrocytes in high-risk individuals, resulting in loss of myelin-producing cells [23, 67, 312] Stem cells from schizophrenia patients generate a larger pool of proliferating progenitor cells with reduced cell cycle period [53] Impaired monocyte activation, reducing pathogen clearance that can cause low-grade inflammation [111] Neuroinflammation and increased microglia activation, dysregulation of chemokine and cytokine production [109, 110, 313]
Gene expression changes	Reduction in expression of multiple myelin genes – e.g. myelin and lymphocyte protein, 2′,3′-cyclic nucleotide 3′-phosphodiesterase, myelin-associated glycoprotein [33] Abnormalities in genes involved in neuronal communication involving glutamatergic, GABAergic, dopaminergic, and cholinergic synapses, synaptic plasticity and neuronal development [24, 314, 315] Changes in markers of GABA signaling, e.g. decreased glutamic acid decarboxylase 65 and 67 expression [316, 317]