Schizophrenia is a group of common psychiatric disorders characterized by dissonance between thinking, emotion and behavior, and disconnection between mental activity and reality. The onset of the disease is usually in young adults, and the course of the disease is prolonged and slowly progresses, and can develop into decline. The disease has the highest prevalence rate among psychiatric disorders, with a lifetime prevalence rate of 5.69 per 1,000 in China in 1982. The hypothesis that the occurrence of schizophrenia may be related to metabolic abnormalities in patients has become one of the most active areas of theoretical research on this disease in the past two to three decades. Studies on the biochemical basis of schizophrenia include the following: (a) Dopamine hyperfunction hypothesis It is mainly believed that patients with schizophrenia have hyperfunction or abnormalities in central DA function, and the pharmacological evidence includes the psychogenic effect of amphetamines. Amphetamine has a central excitatory effect, mainly inhibiting DA reuptake, resulting in increased DA levels at the receptor sites and hyperfunction. Patients who take large amounts of amphetamines for a long time cause chronic amphetamine intoxication and develop paranoid psychosis with positive symptoms similar to schizophrenia, especially with abundant hallucinations, suggesting a central DA hyperfunction in schizophrenia. Psychotic symptoms occur in patients treated with levodopa for Parkinson’s disease, and levodopa is a precursor substance for DA, which increases DA synthesis. The antipsychotic drug haloperidol has a specific blocking effect on D2 receptors in the brain, and the therapeutic effect is achieved by blocking DA receptors to reduce their excessive DA function, and the clinical efficacy is proportional to the potency of blocking D2 receptors. The plasma DA metabolite HVA was reported to be elevated in untreated schizophrenic patients, and its HVA concentration was positively correlated with positive symptoms and treatment response of patients, while the reduced peripheral DβH and MAO activity in schizophrenic patients may be a genetic marker of susceptibility to psychiatric disorders. Crow et al. (1981) suggested that there are two types of schizophrenia: type I is dominated by positive symptoms of hallucinations and delusions, with hyperactive DA function, and responds well to treatment with neuroblocking agents that block DA receptors, probably with increased D2 receptor increase as the pathological basis; type II is dominated by negative symptoms (emotional indifference, lack of initiative), with insignificant changes in DA function, and poor response to neural blockers, often accompanied by organic brain changes. Regarding the causes of altered DA function, Waytt (1985) suggested that there may be a vulnerability of the central DA system in schizophrenic patients, which is genetically determined. When subjected to intense or prolonged stressful stimuli, their central DA endings are damaged, and early on they show an increased DA renewal rate and positive symptoms, and when progressive damage to DA endings occurs with neurological tissue loss, the DA renewal rate decreases and they show negative symptoms. The function of the central DA system has complex interactions with the NE and 5-HT systems, and is also closely related to neuropeptides. The mechanism of schizophrenia explained by altered DA function alone is inadequate. Therefore, the correlation between other neurotransmitters and schizophrenia has also received attention. For example, the 5-HT hypothesis suggests that lysergic acid diethylamide (LSD), an analog of 5-HT, has a significant hallucinogenic effect by blocking 5-HT receptors and inhibiting the function of 5-HT, which is similar to the positive symptoms of schizophrenia. system dysregulation and reduced pleasure and intentional activity, which may be associated with the negative symptoms of schizophrenia, and hyperactive NE, which is associated with paranoid symptoms. Elevated levels of NE have been reported in specific regions of the brain in schizophrenic patients, particularly in the NE-rich forebrain limbic system. In patients with paranoid schizophrenia, NE levels are approximately 3-fold higher in the nucleus ambiguus and papillae compared to controls. The functional imbalance between the dopaminergic and glutamatergic systems hypothesis suggests that schizophrenia is due to an imbalance between the subcortical DA functional system and the glutamatergic functional system.PCP (Phencyclidine) is a psychotomimetic agent and a noncompetitive antagonist of glutamate that produces symptoms mimicking schizophrenia, with the main site of action being through the ion pathway with N-methyl-D aspartate (NMDA) receptor, which is the primary receptor for glutamate.PCP induces the release of catecholamines (CA), which is inhibited by cortical striatal glutamatergic channels. The schizophrenia-like symptoms caused by a functional defect in the glutamatergic system or by a glutamate antagonist such as PCP that induces CA release can be viewed as a syndrome caused by a central neurotransmitter balance in the dopamine-glutamate feedback regulatory system. (B) Neuropeptides and schizophrenia The endorphin content in the cerebrospinal fluid of schizophrenic patients is increased and decreases as their condition improves. Although there are a lot of studies on the mechanism of neuropeptides in schizophrenia, there are two different views: one believes that neuropeptides (including endorphins, enkephalins and prednisolone) are overfunctioning in schizophrenic patients, and the antagonist naloxone can improve their symptoms; the other believes that the disease has insufficient opioid peptide function, and supplementation of such peptides may be beneficial, and a large number of clinical studies have not achieved agreement. In recent years, more attention has been paid to the role of CCK in schizophrenia. CCK specifically exists in common neurons with DA in the brain and has a role in regulating the function of the DA system. When CCK is deficient in the brain, DA function appears to be excessive. ferrier et al. (1983) studied changes in six neuropeptides and found that schizophrenia type II patients had significantly lower CCK levels in the hippocampus, amygdala and frontal lobe. Some data reported decreased levels of CCK in the cerebrospinal fluid of schizophrenic patients. These results suggest that the dysfunction of CCK and the altered DA function regulated by it can lead to schizophrenia. (iii) Molecular genetic studies of schizophrenia Systematic genealogical surveys over more than half a century have demonstrated that genetic factors play a role in the occurrence of schizophrenia, and that the prevalence of schizophrenia among relatives of patients with schizophrenia is much higher than that of the general population, and the closer the blood relationship with the patient, the higher the prevalence. Available data from genetic studies hypothesize that there are two main modes of inheritance, monogenic and polygenic. Slater proposed the hypothesis that schizophrenia is inherited as a single gene dominant with a low epistasis rate, arguing that only a minority of schizophrenics are pure congeners, 97% are heterozygous, and the epistasis rate of heterozygotes is low at 26%, with only 1/4 of those carrying the dominant gene exhibiting the disease. Gottesman and Schield concluded that the occurrence of schizophrenia is the result of a combination of genetic susceptibility and environmental factors, and that polygenic inheritance has no specific genes. The degree of influence of genetic factors on the production of inherited traits and inherited disorders is called heritability. The heritability of schizophrenia was calculated to be 75.7% in Daqing, Northeast China, and 70%-80% in Tieling, Liaoning. The association of polymorphic loci with the transmission of schizophrenia in family lines has been reported, with Basset suggesting that trisomies on chromosome 5, fragment 5q11.2-13.3, are associated with the development of schizophrenia.Sherrington noted Basset’s report of the use of two gene probes, D5s76 and D5s39, located on chromosome 5, for five Icelandic The chronic maximum dominance count (Lod Score) of 2.45 was obtained using restriction fragment length polypeptide (RFLP) analysis on five Icelandic families with schizophrenia and two British families, confirming the presence of a linkage. This study by Sherrington became the first positive result in the field of molecular genetics of schizophrenia, and has generated a wide range of reactions.Crow (UK) based on: 1. Different clinical manifestations of the onset of the disease in the two sexes, with early onset and severe symptoms in males. 2. The rate of same-gender patients is higher in relatives of pre-documented individuals than in those of the opposite gender. 3.Sex chromosome abnormalities were much higher in schizophrenics than in controls. 4, Inheritance in schizophrenic families has a considerable degree of autosomal inheritance characteristics and other four aspects to propose the hypothesis that the quality genes of schizophrenia are located in the sex chromosome pseudo-autosomal region. He used gene probes from the Dxys14 region (a pseudo-autosomal region of the X and Y chromosomes) for diseased sibling pairwise analysis, and his results supported the presence of a linkage between schizophrenia and gene probes from the sex chromosome pseudo-autosomal region. The genetic localization of schizophrenia is currently inconclusive. Further studies are needed.