Biological hypotheses, risk factors, and biomarkers of schizophrenia

Fišar, Zdeněk

doi:10.1016/j.pnpbp.2022.110626

Cited by 49 publications

(37 citation statements)

References 335 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Atopsis-induced neuropil loss, retention, and degeneration without cell death cause synaptic degeneration and neuron size reduction [14]. Neurodegeneration causes negative symptoms and hypofrontality [15]. Rotenberg (1984) [9] found many similarities between right hemisphere damaged patients (due to accident) and schizophrenia patients, including apathy, indifference, inability to show emotions, poor appraisal of negative emotions, impaired fear and anger perception, affect process deficits, and general cognitive deficits [9].…”

Section: Negative Symptomatologymentioning

confidence: 99%

Genesis of Schizophrenia: An Introspective Review

Dudi¹

2023

OJMP

View full text Add to dashboard Cite

Research and Results: Schizophrenia begins with nasal obstruction, disrupting supraschalemic nucleus output and lateralized ultradian body rhythms. If one nostril is blocked, vaso-choking occurs in the ipsilateral brain hemisphere cortex, which has vesicles connected to the nose. This disturbs the ultradian balance of the body and brain hemispheres causing abnormal behavior and bizarre thinking. The brain has a bidirectional connection and communication with the body via the nervous system. The Hypothalamic-Pituitary-Adrenal (HPA) axis, Autonomic Nervous System (ANS), and vagus nerve are linked. ANS lateralization can switch from parasympathetic to sympathetic due to vagus nerve changes. Schizophrenia is characterized by Basic Rest Activity Cycle (BRAC) energy balance disruption. Let's examine how a disruption in the lateralization of the nasal cycle can lead to pathology in the mind. Purpose and Method: A literary search is conducted in comparison with authors' introspective insights to summarize schizophrenia's genesis after curing this disease to fill the knowledge gap between a few relevant theories to build a percept of the disease through this (mini) narrative review. Conclusion: Nasal cycle and vagus nerve toning can play roles in mental health.

show abstract

Section: Negative Symptomatologymentioning

confidence: 99%

Genesis of Schizophrenia: An Introspective Review

Dudi¹

2023

OJMP

View full text Add to dashboard Cite

show abstract

“…Methamphetamine‐induced psychotic disorder occurs as a result of methamphetamine use. In contrast, schizophrenia is a primary psychiatric disorder with complex aetiology involving genetic, environmental and neurobiological factors 12 . The psychotic symptoms and behavioural manifestations of methamphetamine‐induced psychotic disorder are often indistinguishable from schizophrenia, 13 notably in terms of positive and cognitive symptomatology; however, negative symptoms appear to be more severe in schizophrenia.…”

Section: Introductionmentioning

confidence: 99%

Lymphocyte‐related ratios in methamphetamine‐induced psychotic disorder in Taiwan, comparing with patients with schizophrenia

Ng,

Lu,

Chen

et al. 2024

Addiction Biology

View full text Add to dashboard Cite

The lymphocyte‐related ratios, neutrophil‐to‐lymphocyte ratio (NLR), monocyte‐to‐lymphocyte ratio (MLR) and platelet‐to‐lymphocyte ratio (PLR) are new measures of inflammation within the body. Few studies have investigated the inflammatory response of patients with methamphetamine‐induced psychotic disorder. Clinically, the psychotic symptoms and behavioural manifestation of methamphetamine‐induced psychotic disorder are often indistinguishable from paranoid schizophrenia. We aimed to determine the differences in these inflammatory markers between patients with methamphetamine‐induced psychotic disorder, patients with schizophrenia and healthy individuals. A total of 905 individuals were recruited. The NLR and MLR were found to be higher in both patients with methamphetamine‐induced psychotic disorders and patients with schizophrenia compared with healthy controls. There was no significant difference between the three groups in PLR. When compared with the control group, the methamphetamine‐induced psychotic disorder group was significantly higher in NLR 27% (95%CI = 11 to 46%, p = 0.001), MLR 16% (95%CI = 3% to 31%, p = 0.013) and PLR 16% (95%CI = 5% to 28%, p = 0.005). NLR of the group with methamphetamine‐induced psychotic disorder was 17% (95%CI = 73% to 94%, p = 0.004) less than the group with schizophrenia, while MLR and PLR did not differ significantly between the two groups. This is the first study that investigated the lymphocyte‐related ratios in methamphetamine‐induced psychotic disorder when compared with patients with schizophrenia and healthy individuals. The results showed that both patients with methamphetamine‐induced psychotic disorder and patients with schizophrenia had stronger inflammatory responses than the healthy control. Our finding also indicated that the inflammatory response of methamphetamine‐induced psychotic disorder was between those of patients with schizophrenia and healthy individuals.

show abstract

“…These observations together with epidemiologic evidence in humans showing an association of maternal infection and immune activation, with the pathogenesis of neuropsychiatric disorders such as schizophrenia, raise the question of the mechanisms involved in triggering brain and behavioral alterations in the offspring. In this line, the neurodevelopmental theory of schizophrenia suggests that an event during the gestational period or early life negatively affects brain development by inducing changes in the brain structure, function, and activity, which later can lead to cognitive and psychosocial dysfunction [ 2 , 3 ]. Normally, the neurodevelopment process includes brain cell proliferation and migration, myelinization as well as the formation of neural circuits [ 4 ], so when some of these processes are disrupted it may result in long-term alterations in the adulthood.…”

Section: Introductionmentioning

confidence: 99%

Pregestational Exposure to T. gondii Produces Maternal Antibodies That Recognize Fetal Brain Mimotopes and Induces Neurochemical and Behavioral Dysfunction in the Offspring

Núñez

Ayala

Cervantes

et al. 2022

Cells

View full text Add to dashboard Cite

The activation of the maternal immune system by a prenatal infection is considered a risk factor for developing psychiatric disorders in the offspring. Toxoplasma gondii is one of the pathogenic infections associated with schizophrenia. Recent studies have shown an association between high levels of IgG anti-T. gondii from mothers and their neonates, with a higher risk of developing schizophrenia. The absence of the parasite and the levels of IgGs found in the early stages of life suggest a transplacental transfer of the anti-T. gondii IgG antibodies, which could bind fetal brain structures by molecular mimicry and induce alterations in neurodevelopment. This study aimed to determine the maternal pathogenic antibodies formation that led to behavioral impairment on the progeny of rats immunized with T. gondii. Female rats were immunized prior to gestation with T. gondii lysate (3 times/once per week). The anti-T. gondii IgG levels were determined in the serum of pregestational exposed females’ previous mating. After this, locomotor activity, cognitive and social tests were performed. Cortical neurotransmitter levels for dopamine and glutamate were evaluated at 60 PND in the progeny of rats immunized before gestation (Pregestational group). The maternal pathogenic antibodies were evidenced by their binding to fetal brain mimotopes in the Pregestational group and the reactivity of the serum containing anti-T. gondii IgG was tested in control fetal brains (non-immunized). These results showed that the Pregestational group presented impairment in short and long-term memory, hypoactivity and alteration in social behavior, which was also associated with a decrease in cortical glutamate and dopamine levels. We also found the IgG antibodies bound to brain mimotopes in fetuses from females immunized with T. gondii, as well as observing a strong reactivity of the serum females immunized for fetal brain structures of fetuses from unimmunized mothers. Our results suggest that the exposure to T. gondii before gestation produced maternal pathogenic antibodies that can recognize fetal brain mimotopes and lead to neurochemical and behavioral alterations in the offspring.

show abstract

Biological hypotheses, risk factors, and biomarkers of schizophrenia

Cited by 49 publications

References 335 publications

Genesis of Schizophrenia: An Introspective Review

Genesis of Schizophrenia: An Introspective Review

Lymphocyte‐related ratios in methamphetamine‐induced psychotic disorder in Taiwan, comparing with patients with schizophrenia

Pregestational Exposure to T. gondii Produces Maternal Antibodies That Recognize Fetal Brain Mimotopes and Induces Neurochemical and Behavioral Dysfunction in the Offspring

Contact Info

Product

Resources

About