curcumin and Schizophrenia

Schizophrenia is a mental disorder characterized by episodes of psychosis; major symptoms include hallucinations, delusions, and disorganized thinking. More recent theories focus on particular disorders of interneurons, dysfunctions in the immune system, abnormalities in the formation of myelin, and augmented oxidative stress that lead to alterations in brain structure. Decreased dopaminergic activity and increased phospholipid metabolism in the prefrontal cortex might be involved in schizophrenia. Antipsychotic drugs used to treat schizophrenia have many side effects. Alternative therapy such as curcumin (CUR) can reduce the severity of symptoms without significant side effects. CUR has important therapeutic properties such as antioxidant, anti-mutagenic, anti-inflammatory, and antimicrobial functions and protection of the nervous system. Also, the ability of CUR to pass the blood-brain barrier raises new hopes for neuroprotection. CUR can improve and prevent further probable neurological and behavioral disorders in patients with schizophrenia. It decreases the side effects of neuroleptics and retains lipid homeostasis. CUR increases the level of brain-derived neurotrophic factor and improves hyperkinetic movement disorders. CUR may act as an added counteraction mechanism to retain cell integrity and defense against free radical injury. Thus it appears to have therapeutic potential for improvement of schizophrenia. In this study, we review several properties of CUR and its ability to improve schizophrenia and minimize the side effects of antipsychotic drugs, and we explore the underlying mechanisms by which CUR affects schizophrenia and its symptoms.

Topics: Antipsychotic Agents; Blood-Brain Barrier; Brain; Curcumin; Humans; Schizophrenia

Curcumin is a natural polyphenol, which has a variety of pharmacological activities, including, antineoplastic, antioxidative and neuroprotective effects. Recent studies provided evidence for the bioactive role of curcumin in the prevention and treatment of various central nervous system (CNS)-related diseases including Parkinson's, Alzheimer's, Schizophrenia disease and glioma neoplasia. Schizophrenia is a disabling psychiatric disorder related with an aberrant functional coupling between hippocampus and prefrontal cortex that might be crucial for cognitive dysfunction. Animal studies have lent support to the hypothesis that curcumin could improve cognitive functioning and enhance cell proliferation of dentate gyrus. In relation to brain tumors, specifically gliomas, the antineoplastic action of curcumin is based on the inhibition of cell growth promoting apoptosis or autophagy and preventing angiogenesis. However, one of the main impediments for the application of curcumin to patients is its low bioavailability. In intracranial lesions, curcumin has problems to cross the blood-brain barrier (BBB). Currently nano-based drug delivery systems are opening a new horizon to tackle this problem. The bioavailability and effective release of curcumin can be made possible in the form of nanocurcumin. This nanoformulation preserves the properties of curcumin and makes it reach tissues with pathology. This review try to study the beneficial effects of the curcumin nanodelivery in central nervous pathologies such us schizophrenia and glioma disease.

Topics: Animals; Antineoplastic Agents; Blood-Brain Barrier; Curcumin; Glioblastoma; Humans; Schizophrenia

Topics: Brain-Derived Neurotrophic Factor; Cognition Disorders; Curcumin; Double-Blind Method; Enzyme Inhibitors; Female; Humans; Male; Schizophrenia; Time Factors

Curcumin as an antioxidant natural herb has shown numerous pharmacological effects. However, the poor bioavailability of curcumin is a significant pharmacological barrier for its antioxidant activities. The present study was conducted to develop curcumin-loaded nanophytosome (CNP) and explore their therapeutic potential in a ketamine (KET)-induced schizophrenia (SCZ) model. The mice in our experiment were treated orally with curcumin and CNP (20 mg/kg) for 30 consecutive days. In addition, the animals received intraperitoneal injection of KET (30 mg/kg/day) from the 16th to the 30th day. SCZ-like behaviors were evaluated employing forced swimming test (FST), open field test (OFT), and novel object recognition test (NORT), and oxidative stress markers in the brain were estimated. Our results revealed that CNP has a greater neuroprotective effect compared to free curcumin. CNP pretreatment significantly ameliorated KET-induced brain injury evidenced by a marked reduction in the depressive and anxiety-like behaviors, memory deficits, and oxidative stress markers in cortical and subcortical tissues. Therefore, CNP, as a suitable drug delivery system, may improve curcumin bioavailability and confer stronger neuroprotective effects against KET-induced behavioral deficits and oxidative damages.

Topics: Administration, Oral; Animals; Biological Availability; Curcumin; Disease Models, Animal; Humans; Ketamine; Male; Mice; Nanoparticle Drug Delivery System; Neuroprotective Agents; Oxidative Stress; Schizophrenia

The aim of this study was to investigate the neurotoxic effects of Fe. We designed CMN loaded superparamagnetic iron oxide nanoparticles (SPIONs) (Fe. We showed that effective treatment with CMN reduced or prevented Fe. Taken together, Fe

Topics: Adenosine Triphosphate; Animals; Behavior Rating Scale; Cerebellum; Curcumin; Cytochromes c; Disease Models, Animal; Magnetite Nanoparticles; Male; Membrane Potential, Mitochondrial; Mitochondria; Neuroprotection; Neuroprotective Agents; Random Allocation; Rats; Rats, Wistar; Reactive Oxygen Species; Schizophrenia