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Schizophrenia is a serious psychiatric disorder that affects thinking, emotional life, and perception of reality. It belongs to the group of psychotic disorders and affects approximately 0.3–0.7% of the global population (equivalent to around 20–24 million people). In Sweden, about 35,000 people live with schizophrenia, and 1,500–2,000 new cases occur each year. The disease typically begins in late adolescence or early adulthood, somewhat earlier in men than in women.
It is characterized by episodes of psychosis – delusions, hallucinations, and disorganized thinking – as well as negative symptoms such as social withdrawal and emotional flattening. Schizophrenia causes significant functional impairment; according to the World Health Organization, it is among the most disabling conditions, comparable to terminal cancer or paralysis.
People with schizophrenia live on average 15–20 years shorter than the general population, partly due to an increased risk of suicide (5–10% die by suicide) and comorbid physical illnesses. Despite the seriousness of the condition, there are effective treatments and support systems today that can help many.
Schizophrenia is believed to arise from a complex interplay of biological and psychological factors. The disease has a multifactorial origin: a high degree of heritability in combination with neurobiological abnormalities and environmental stress increases the risk.
Heredity is the single greatest risk factor for schizophrenia. Twin and family studies show that the disease has a heritability of about 60–80%. People with a first-degree relative (parent or sibling) who has schizophrenia have about ten times higher risk of developing the disorder themselves.
However, there is no single “schizophrenia gene” – instead, the inheritance pattern is polygenic, with hundreds of genetic variants each contributing small risk increases. In the 2000s, large-scale genome studies identified many associated gene variants. An international study with over 300,000 participants (about 77,000 with schizophrenia) mapped 287 regions in the genome linked to schizophrenia and pointed out 120 specific genes likely involved.
Most of these genes are expressed in neurons, confirming that abnormal brain function underlies the condition. Rare genetic mutations also play a role – for example, some chromosomal anomalies (so-called copy number variations) and rare mutations have been observed in a small proportion of patients. Overall, research shows that the influence of genetic factors is complex and multifaceted. Genetic vulnerability is necessary but not sufficient; most people with risk genes do not develop schizophrenia, highlighting the importance of environmental and neurobiological processes.
Schizophrenia is often described as a brain disease because multiple neurobiological abnormalities have been linked to its onset. Brain imaging studies show that patients tend to have slightly smaller brain volume than healthy individuals, with moderately enlarged ventricles, reduced volume in the hippocampus (a key memory structure), and cortical thinning in the frontotemporal regions.
These changes suggest disrupted brain development and neuronal loss. Research indicates that people with schizophrenia have fewer synaptic connections between neurons, possibly due to excessive synaptic pruning during adolescence. A recently discovered mechanism involves immune-active brain cells (microglia) and the gene C4A: a specific variant of C4A increases production of a protein that activates synapse degradation, and patients with first-episode schizophrenia show elevated levels of this protein.
This discovery links genetic risk with inflammation and neuron loss.
Neurotransmitter systems in the brain are also central. The dopamine hypothesis has long been dominant: overactive dopamine signaling in certain brain regions (particularly the mesolimbic system) is thought to cause psychotic symptoms. Supporting evidence includes the fact that amphetamines, which release dopamine, can induce paranoid delusions and hallucinations in healthy individuals (or worsen psychosis in patients).
All currently approved antipsychotic drugs also suppress dopamine signaling by blocking Dâ‚‚ receptors. Meanwhile, findings have led to a complementary glutamate hypothesis: substances like phencyclidine (PCP) or ketamine – which block NMDA receptors for glutamate – can induce the full spectrum of schizophrenia-like symptoms, including hallucinations, disordered thinking, and apathy.
This suggests that impaired glutamate signaling (possibly due to excessive production of NMDA-blocking kynurenic acid in the brain) may underlie both positive and negative symptoms. Dopamine and glutamate systems likely interact in the pathophysiology of the disease.
In addition, dysfunction in several brain circuits is evident: for example, reduced activity in the prefrontal cortex during cognitive tasks and abnormal responses in the amygdala to emotional stimuli (which may contribute to misinterpretation of emotions). Neuropsychological studies often reveal impaired working memory, attention, and processing speed in patients.
These cognitive deficits are core symptoms that correlate with functioning and prognosis – for instance, poor attention and slow processing strongly predict difficulties managing work and daily life. In summary, neurological research suggests that schizophrenia is a neurodevelopmental disorder: brain development from fetal life to early adulthood deviates, and this, combined with genetic and environmental factors, leads to altered brain structure and function that give rise to symptoms.