INTRODUCTION:

Schizophrenia is defined as a psychiatric diagnosis that describes a neuropsychiatric abnormality and mental disorder characterized by abnormalities in the perception or expression of reality. It most commonly manifests as auditory hallucinations, paranoid or bizarre delusions, or disorganized speech and thinking with significant social or occupational dysfunction.[1]The individual with this disorder may also have hallucinations, disorganized speech, disorganized behavior, physically rigid or lax behavior, significantly decreased behaviors or feelings, as well as delusions, which are ideas about them or others that have no basis in reality.

The disorder is thought mainly to affect cognition but it also usually contributes to chronic problems with behavior and feeling.

People with schizophrenia are likely to have additional symptoms including major depression and anxiety disorders and the lifetime occurrence of substance abuse are almost

50%.[2] Social troubles like long-term unemployment, poverty and homelessness are common. People with the disorder may hear voices other people don't hear. They may believe that other people are reading their minds, controlling their thoughts or scheming to harm them. This can alarm people with the illness and make them withdrawn or extremely disturbed.

Schizophrenia is a chronic disease that afflicts approximately 1% of the population worldwide.[3] It usually afflicts people at a young age and, according to a report of the World Health Organization, it is among the seven most disabling diseases in the age group between 20 and 45, surpassing by far diabetes, HIV or cardiovascular diseases. Suicide rates of people with schizophrenia are high.[4] A number of reviews have shown that there is an excess mortality in people with schizophrenia, the overall mortality being twice as high as that in the general population, so that schizophrenia has been called a life-shortening disease.[5-7] Suicide and accidents account for only a part of this excess mortality; a substantial proportion is due to physical illness.[5]

There are so many mental disorders like Mood Disorders, Suicide, Anxiety Disorders, Panic Disorder, Obsessive-Compulsive Disorder (OCD), Post-Traumatic Stress Disorder (PTSD), Generalized Anxiety Disorder (GAD), Social Phobia, Eating Disorders, Attention Deficit Hyperactivity Disorder (ADHD), Autism, Alzheimer's disease and Schizophrenia are increase world-wide day by day.

Statistics of Schizophrenia:

· Approximately 2.4 million American adults or about 1.1% of the population age 18 and older in a given year have schizophrenia.

· Schizophrenia ranks among the top 10 causes of disability in developed countries worldwide.^[8]

· The risk of suicide is serious in people with schizophrenia.

· Schizophrenia affects about 24 million people worldwide.

· Schizophrenia is a treatable disorder, treatment being more effective in its initial stages.

· More than 50% of persons with schizophrenia are not receiving appropriate care.

· 90% of people with untreated schizophrenia are in developing countries.

· Care of persons with schizophrenia can be provided at community level, with active family and community involvement.

· The children of affected parents have approximately 10% risk of developing disease but this rises in 50% if both parents are affected

Aetiology:

Examination of patients brain in schizophrenia do not show any pathology but with the help of modern instruments of brain imaging identified minor structural abnormalities in like enlargement of lateral ventricles and reduction in brain size including reduction of temporal lobe volume. Schizophrenia is neurological developmental disorder caused by abnormalities of brain development associated with genetics tendency and early environmental influences and triggered by stress.

Types of Schizophrenia:

There are five types of schizophrenia each based on the kind of symptoms the person has at the time of assessment.

Paranoid schizophrenia:

The defining feature of the paranoid subtype also recognized as paranoid schizophrenia is the presence of auditory hallucinations or prominent delusional thoughts about persecution or conspiracy. The reasons are not entirely clear but may partly reflect that people suffering from this subtype often do not exhibit symptoms until later in life and have achieved a higher level of functioning before the onset of their illness.

Disorganized schizophrenia:

Prominent symptoms are disorganized speech and behavior, as well as flat or inappropriate affect. The person does not have enough symptoms to be characterized as suffering from catatonic schizophrenia.

Catatonic schizophrenia:

The person with this type of schizophrenia primarily has at least two of the following symptoms: difficulty moving, resistance to moving, excessive movement, abnormal movements, and/or repeating what others say or do.

Undifferentiated schizophrenia:

This is characterized by episodes of two or more of the following symptoms: delusions, hallucinations, disorganized speech or behavior, catatonic behavior or negative symptoms, but the individual does not qualify for a diagnosis of paranoid, disorganized, or catatonic type of schizophrenia.

Residual schizophrenia:

While the full-blown characteristic positive symptoms of schizophrenia those that involve an excess of normal behavior, such as delusions, paranoia, or heightened sensitivity are absent, the sufferer has a less severe form of the disorder or has only negative symptoms characterized by a decrease in function, such as withdrawal, disinterest and not speaking.

Figure 1: Depression

Early Warning Signs of Schizophrenia:

The most common early warning signs of schizophrenia include:

· Deterioration of personal hygiene

· Flat expressionless gaze

· Inability to cry or express joy

· Inappropriate laughter or crying

· Depression

· Oversleeping or insomnia

· Odd or irrational statements

· Extreme reaction to criticism Strange use of words or way of speaking

Figure 2: insomnia

Symptoms of Schizophrenia:

The symptoms of schizophrenia:

1. Positive symptoms

2. Negative symptoms

3. Cognitive symptoms

1. Positive symptoms:

Positive symptoms are psychotic behaviors not seen in healthy people. People with positive symptoms often "lose touch" with reality. These symptoms can come and go. Sometimes they are severe and at other times hardly noticeable, depending on whether the individual is receiving treatment.

Delusions:

Delusions are false beliefs that are not part of the person's culture and do not change. The person believes delusions even after other people prove that the beliefs are not true or logical. People with schizophrenia can have delusions that seem bizarre, such as believing that neighbors can control their behavior with magnetic waves.

Delusions of persecution:

Belief that others, often a vague “they,” are out to get him or her. These persecutory delusions often involve bizarre ideas and plots

Delusions of reference:

A neutral environmental event is believed to have a special and personal meaning. For example, a person with schizophrenia might believe a billboard or a person on TV is sending a message meant specifically for them.

Delusions of grandeur:

Belief that one is a famous or important personality like lord Krishna, Mahatma Gandhi, Jesus Christ or Napoleon. Alternately, delusions of grandeur may involve the belief that one has unusual powers and unlimited divine power that no one else has for example ability to see the future, the ability to fly, ability to go any where in at any time in all around the universe etc.

Delusions of control:

The patients of schizophrenia belief that his thoughts, mind and actions are being controlled by outside forces. Common delusions of control include thought broadcasting like his private thoughts are being transmitted to others, thought insertion, and thought withdrawal.

Hallucinations:

Schizophrenia is a mental disorder in which patients see the world differently from the rest of the population, unable "to tell the difference between real and unreal experiences, to think logically, to have normal emotional responses, and to behave normally in social situations," according to the National Institutes of Health (NIH).

Auditory Hallucinations:

The National Institute of Mental Health (NIMH) notes that auditory hallucinations are the most common type of hallucination in schizophrenia. A patient with auditory hallucinations hears voices that are not there, which can incite panic. Examples of auditory hallucinations are the patient hearing the voices talk about her behavior, warn her about impending danger or talk among themselves.

Visual Hallucinations:

The second type of schizophrenic hallucination is visual hallucination, which the NIMH defines as the patient seeing people or objects that do not exist. The images can appear to be distorted or strange to the patient, and can also be frightening.

Tactile Hallucinations:

Some schizophrenic patients can experience tactile hallucinations, where the patient feels something that is not there. The NIMH gives the example of feeling like invisible fingers are touching the patient, even if there is no one close to the patient. Another tactile hallucination is the feeling of electricity moving through the patient's body.

Olfactory Hallucinations:

The last type of hallucination in schizophrenia patients is olfactory hallucinations. During an olfactory hallucination, the NIMH notes that the patient will smell odors that no one else does. The perceived smell is usually an unpleasant odor.

Disorganized speech:

Fragmented thinking is characteristic of schizophrenia. Externally, it can be observed in the way a person speaks. People with schizophrenia tend to have trouble concentrating and maintaining a train of thought. They may respond to queries with an unrelated answer, start sentences with one topic and end somewhere completely different, speak incoherently, or say illogical things.

Common signs of disorganized speech in schizophrenia include

Disorganized behavior:

Schizophrenia disrupts goal-directed activity, causing impairments in a person’s ability to take care of him or herself, work, and interact with others. Disorganized behavior appears as:

A decline in overall daily functioning

Unpredictable or inappropriate emotional responses

Behaviors that appear bizarre and have no purpose

Lack of inhibition and impulse control

2. Negative Symptoms:

Negative symptoms are associated with disruptions to normal emotions and behaviors. These symptoms are harder to recognize as part of the disorder and can be mistaken for depression or other conditions.

Irritable or tense feeling, Trouble concentrating, Trouble sleeping, Childlike behavior, Problems thinking and explaining your ideas clearly, Showing little emotion, Lack of activity not responding much to other people, Lack of pleasure in everyday life, Lack of ability to begin and sustain planned activities, Speaking little even when forced to interact

3. Cognitive Symptoms:

Cognitive symptoms are subtle. Like negative symptoms, cognitive symptoms may be difficult to recognize as part of the disorder. Often, they are detected only when other tests are performed.

Treatment:

Because the causes of schizophrenia are still unknown, treatments focus on eliminating the symptoms of the disease. Treatments include antipsychotic medications and various psychosocial treatments.

Antipsychotic medications:

Commonly used antipsychotic medications are listed below by drug group. Trade names appear in parentheses.

First generation antipsychotics:

1. Butyrophenones:

Haloperidol, Droperidol

Haloperidol

Droperidol

2. Phenothiazines

Chlorpromazine: It acts as an antagonist (blocking agent) on different postsynaptic receptors on dopaminergic-receptors on serotonergic-receptors on histaminergic-receptors, alpha1/alpha2-receptors and finally on Muscarinic (cholinergic) M1/M2-receptors.

Fluphenazine: It blocks postsynaptic mesolimbic dopaminergic D1 and D2 receptors in the brain; depresses the release of hypothalamic and hypophyseal hormones and is believed to depress the reticular activating system thus affecting basal metabolism, body temperature, wakefulness, vasomotor tone and emesis.

Chlorpromazine (Thorazine, Largactil)

Fluphenazine (Prolixin)

Perphenazine and Trifluoperazine Binds to the dopamine D1 and dopamine D2 receptors and inhibits their activity. The mechanism of the anti-emetic effect is due predominantly to blockage of the dopamine D2 neurotransmitter receptors in the chemoreceptor trigger zone and vomiting centre.

Perphenazine (Trilafon)

Trifluoperazine (Stelazine)

Mesoridazine: Like other phenothiazines, acts indirectly on reticular formation, whereby neuronal activity into reticular formation is reduced without affecting its intrinsic ability to activate the cerebral cortex. In addition, the phenothiazines exhibit at least part of their activities through depression of hypothalamic centers. Neurochemically the phenothiazines are thought to exert their effects by a central adrenergic blocking action.

Pericyazine act like other phenothiazine, is presumed to act principally in the subcortical areas, by producing what has been described as a central adrenergic blockade of the alpha adrenergic receptors as well as antagonism of the D (1) dopamine receptor.

Mesoridazine (Serentil)

Periciazine

Promazine's antipsychotic effect is due to antagonism at dopamine and serotonin type 2 receptors, with greater activity at serotonin 5-HT2 receptors than at dopamine type-2 receptors. This may explain the lack of extrapyramidal effects. Antagonism at muscarinic receptors, H1-receptors, and alpha(1)-receptors also occurs with promazine. Promethazine Like other H1-antagonists, promethazine competes with free histamine for binding at H1-receptor sites in the GI tract, uterus, large blood vessels, and bronchial muscle.

Promazine

Promethazine

Thioxanthenes

Chlorprothixene and Flupenthixol blocks postsynaptic mesolimbic dopaminergic D1 and D2 receptors in the brain.

Chlorprothixene

Flupenthixol

Second generation antipsychotics

Structurally and pharmacologically similar to clozapine, olanzapine binds to alpha (1), dopamine, histamine H1, Muscarinic, and serotonin type 2 (5-HT2) receptors.

Clozapine

Olanzapine

Risperidone gives it action like other 5-HT2 antagonists; risperidone also binds at alpha (1)-adrenergic receptors and, to a lesser extent, at histamine H1 and alpha (2)-adrenergic receptors.

Quetiapine's antipsychotic activity is likely due to a combination of antagonism at D2 receptors in the mesolimbic pathway and 5HT2A receptors in the frontal cortex. Antagonism at D2 receptors relieves positive symptoms while antagonism at 5HT2A receptors relieves negative symptoms of schizophrenia.

2-[2-(4-{2-thia-9-azatricyclo[9.4.0.0^{3,8}]pentadeca-1(11),3(8),4,6,9, 12,14-heptaen-10-yl}piperazin-1-yl)ethoxy]ethan-1-ol

Ziprasidone (Geodon) - Approved in 2004 to treat bipolar disorder. Side-effects include a prolonged QT interval in the heart, which can be dangerous for patients with heart disease or those taking other drugs that prolong the QT interval.

Ziprasidone

Amisulpride

Paliperidone (Invega) - Derivative of risperidone that was approved in 2006. Paliperidone is the major active metabolite of risperidone. The mechanism of action of paliperidone, as with other drugs having efficacy in schizophrenia, is unknown, but it has been proposed that the drug's therapeutic activity in schizophrenia is mediated through a combination of central dopamine Type 2 (D2) and serotonin Type 2 (5HT2A) receptor antagonism.

Iloperidone Approved by the FDA on 6 May 2009 which is a monoamine directed towards acting upon and antagonizing specific neurotransmitters, particularly multiple dopamine and serotonin receptor subtypes. It is considered an ‘atypical’ antipsychotic because it displays serotonin receptor antagonism, similar to other atypical antipsychotics. The older typical antipsychotics are primarily dopamine antagonists. Iloperidone has been shown to act as an antagonist at all tested receptors. It was found to block the sites of noradrenaline (α2C), dopamine (D2A and D3), and serotonin (5-HT1A and 5-HT6) receptors.

Zotepine (Nipolept, Losizopilon, Lodopin, Setous)- An atypical antipsychotic indicated for acute and chronic schizophrenia. It was approved in Japan circa 1982 and Germany in 1990. The antipsychotic effect of zotepine is thought to be mediated through antagonist activity at dopamine and serotonin receptors. Zotepine has a high affinity for the D1 and D2 receptors. It also affects the 5-HT2A, 5-HT2C, 5-HT6, and 5-HT7 receptors. In addition, it acts as a norepinephrine reuptake inhibitor, likely contributing to its efficacy against the negative symptoms of schizophrenia.

Third generation antipsychotics

Aripiprazole Mechanism of action is thought to reduce susceptibility to metabolic symptoms seen in some other atypical antipsychotics. The extent to which these effects differ from other atypical antipsychotics is debated. Aripiprazole's antipsychotic activity is likely due to a combination of antagonism at D2 receptors in the mesolimbic pathway and 5HT2A receptors in the frontal cortex. Antagonism at D2 receptors relieves positive symptoms while antagonism at 5HT2A receptors relieves negative symptoms of schizophrenia.

Cannabidiol is one of the main components of Cannabis sativa. One study has suggested that cannabidiol may be as effective as atypical antipsychotics in treating schizophrenia.^[9] Some further research has supported these results, and found fewer side effects with cannabidiol than with amisulpride.^[10]

Figure 3: Cannabis sativa

RG1678 has been shown in phase 2 clinical trials to be selectively effective for the negative symptoms of schizophrenia.^[11]

A placebo-controlled trial has suggested that adding L-theanine, an amino acid found in green tea and available as supplement, to ongoing antipsychotic medication may be helpful in reducing some symptoms of schizophrenia.^[12]

New Treatment Strategies for Schizophrenia:

The NMDA receptor hypofunction hypothesis for schizophrenia arises from observations that the NMDA receptor antagonist phencyclidine can produce a psychotic condition similar to the positive, negative, and cognitive symptoms of schizophrenia. [13-17] These observations, coupled with genetic studies in schizophrenia that also implicate dysfunctional NMDA receptors, have led to a new strategy for the treatment of schizophrenia, namely targeting mechanisms that enhance deficient NMDA receptor functioning.[16, 18-29]

Pharmacologic approaches that involve direct enhancement of glutamate risk excitotoxicity from excessive glutamate action.[16, 17, 19] Thus, a potentially safer way to enhance glutamate is to exploit the fact that NMDA glutamate receptors also require glycine actions at a co-transmitter site.[19-29] NMDA receptors are an interesting type of “coincidence detector” that can open to allow calcium into the neuron to trigger postsynaptic actions from glutamate neurotransmission only when three things occur at the same time: glutamate occupies its binding site on the NMDA receptor, glycine or D-serine binds to its site on the NMDA receptor, and depolarization occurs.[16, 19, 30, 31]

In order to understand the actions of new drugs directed at the glycine co-transmitter site on NMDA receptors, it is useful to review the synthesis of endogenous agonists for this site, including glycine and D-serine.

Synthesis of Glutamate Co-transmitter Glycine:

Glycine is not known to be synthesized by glutamate

neurons, so glutamate neurons must acquire the glycine they need for their NMDA receptors from glycine neurons or from glial cells.[16, 19, 30, 31]

However, they contribute only a small amount of glycine to glutamate synapses, since glycine is unable to diffuse far from neighboring glycine neurons because the glycine they release is taken back up into those neurons by a type of glycine reuptake pump known as the type-2 glycine transporter.

Thus, neighboring glial cells are thought to be the source of most of the glycine available for glutamate synapses. Glycine itself can be taken up into glial cells either by a type-1 glycine transporter (GLY-T1) or by a glial specific neutral amino acid transporter.[19, 22-27] Glycine is released into glutamate synapses from glial cells by riding on a reversed GLY-T1 transporter.[19] Once outside, glycine can re-enter the glial cell by riding on an inwardly directed GLY-T1, which functions as a reuptake pump and is the main mechanism responsible for terminating the action of synaptic glycine.[19]

Glycine can also be synthesized from the amino acid L-serine, which is transported into the glial cell by an L-serine transporter, and then converted from L-serine into glycine by the glial enzyme serine hydroxy methyl transferase.^[19] This enzyme functions in both directions, either converting L-serine into glycine or glycine into L-serine.^[19]

Synthesis of Glutamate Co-transmitter D-serine:

D-serine is unusual in that it is a D-amino acid, whereas the 20 known essential amino acids are all L-amino acids, including D-serine’s mirror image amino acid L-serine.[19, 30, 31]

It just so happens that D-serine has a high affinity for the glycine site on NMDA receptors, and that glial cells are equipped with an enzyme that can convert regular L-serine into the neurotransmitting amino acid D-serine by means of an enzyme that can go back and forth between D- and L-serine (D-serine racemase). Thus, D-serine can be derived from glycine or from L-serine, both of which can be transported into glial cells by their own transporters, and then glycine converted to L-serine by serine hydroxy methyl transferase, and finally L-serine converted into D-serine by the enzyme D-serine racemase. D-serine’s actions are not only terminated by synaptic reuptake via the inwardly acting glial serine transporter but also by an enzyme D-amino acid oxidase that converts D-serine into hydroxy-pyruvate.

Targeting Glycine Modulation of NMDA Receptors:

Glycine Agonists:

Agonists at the glycine site of NMDA receptors include the naturally occurring amino acids glycine and D-serine an analogue of D-serine, called D-cycloserine is also active at the glycine co-agonist site of NMDA receptors. All of these agents have been tested in schizophrenia with evidence that they can reduce negative and/or cognitive symptoms.[18, 19-28, 30, 31] Further testing of these naturally occurring agents is in progress and synthetic agonists with greater potency are in discovery.

GLY-T1 Inhibitors:

The GLY-T1 reuptake pump is the major route of inactivation of synaptic glycine, so it is logical to explore the ability of GLY-T1 inhibitors to enhance synaptic actions of glycine and, thus, of NMDA receptors.[18, 19-26, 28-31] Several GLY-T1 inhibitors are now in testing, including the natural agent N-methyl-glycine, also known as Sarcosine, as well as drugs in preclinical testing, such as SSR 504734, SSR 241586, JNJ17305600, and Org 25935. GLY-T1 inhibitors are analogous to drugs that inhibit reuptake of other neurotransmitters, such as the serotonin selective reuptake inhibitors and their actions at the serotonin transporter. When GLY-T1 pumps are blocked by a GLY-T1 inhibitor, this increases the synaptic availablility of glycine, and thus enhances NMDA neurotransmission. Sarcosine has been shown to improve negative, cognitive, and depressive symptoms, including symptoms such as alogia and blunted affect in schizophrenia.[43, 44]The hope is that GLY-T1 inhibitors with greater potency, such as those in preclinical testing mentioned above, will be even more effective.

An outgrowth of the NMDA receptor hypofunction hypothesis of schizophrenia is the novel therapeutic strategy of enhancing the glycine modulatory component of neurotransmission at these receptors. Already, early testing with direct-acting agonists at the glycine modulatory site, such as D-serine and D-cycloserine, as well as indirect enhancers of synaptic glycine that act by blocking the glycine reuptake transporter or GLY-T1, such as sarcosine, is yielding encouraging results.

Future prospects:

Because of the current limitations in treatment responsiveness, it can be expected that the pharmaceutical industry will in the future develop innovative adjunctive treatments targeting negative symptoms to be used in conjunction with antipsychotics. There are indications that new approaches to understanding and treating negative symptoms are emerging. Already, research is underway identifying linkages between temperament traits and gene polymorphisms. The D4 dopamine receptor and the 5 HTTLPR transporter gene have been linked with abnormalities in novelty seeking and harm avoidance, respectively, although more recent research has not replicated these findings.[32-34] Simultaneously, autism

researchers have begun investigating the roles of the pituitary hormones Oxytocin and Vasopressin on affiliative

behaviors, based on their apparent role in pair-bonding behaviors among prairie voles.[35]

For clinicians, meaningful interpretation of any forthcoming data on new adjunctive treatment will depend on a clarification of negative symptoms. The current understanding, that negative symptoms are restricted to schizophrenia and form a single domain, appears less certain than previously.

A definitive conceptualization would need to address whether negative symptoms should be considered homogeneous or heterogeneous, categorical or dimensional, and whether and how they are distributed beyond patients with schizophrenia, as suggested by some studies.[36, 37] Simultaneously, to evaluate patient responsiveness to proposed co-medications, consideration should be given to refining the existing rating instruments. Although the instruments used to measure negative symptoms were designed for research application, they are already used by clinicians, and their use in this context is likely to become more common. Common difficulties experienced in the use of SANS and the SDS relate to the inherent difficulty of rating patients' subjective experience, the vagueness of the anchor points, and the possible influence of secondary causes, including psychosocial and cultural factors. Possible options include refining the anchor points to incorporate more concrete data and the possible inclusion of performance measures.

In its MATRICS initiative supporting the development of pharmacological agents to improve cognition in schizophrenia, NIMH attempted to foster greater collaboration between industry, academia, and regulators. The recent NIMH initiative to address barriers to improved treatment for schizophrenia negative symptoms is encouraging. If progress is to be made in the treatment of negative symptoms, increased collaboration between the basic sciences and clinical research over potential sources of heterogeneity should also be encouraged.

The outlook for people with schizophrenia continues to improve. Although there is no cure, treatments that work well are available. Many people with schizophrenia improve enough to lead independent, satisfying lives. Continued research and understanding in genetics, neuroscience, and behavioral science will help scientists and health professionals understand the causes of the disorder and how it may be predicted and prevented. This work will help experts develop better treatments to help people with schizophrenia achieve their full potential. Families and individuals who are living with schizophrenia are encouraged to participate in clinical research.

CONCLUSION:

Psychological disorders like schizophrenia its treatment with the help of various typical and atypical antipsychotic medications are available in current scenario. Butyrophenone, Thioxanthenes, phenothiazine are use right now. All antipsychotic drugs tend to block D2 receptors in the dopamine pathways of the brain. This means that dopamine released in these pathways has less effect. Excess release of dopamine in the mesolimbic pathway has been linked to psychotic experiences. It is the blockade of dopamine receptors in this pathway that is thought to control psychotic experiences. New Treatment Strategies for Schizophrenia is NMDA receptor hypofunction hypothesis for schizophreniaarises from observations that the NMDA receptor antagonist phencyclidine can produce a psychotic condition similar to the positive, negative, and cognitive symptoms of schizophrenia. These observations, coupled with genetic studies in schizophrenia that also implicate dysfunctional NMDA receptors,have led to a new strategy for the treatment of schizophrenia, namely targeting mechanisms that enhance deficient NMDA receptor functioning. Agonists at the glycine site of NMDA receptors include the naturally occurring amino acids glycine and D-serine. An analogue of D-serine, called D-cycloserine is also active at the glycine co-agonist site of NMDA receptors. All of these agents have been tested in schizophrenia with evidence that they can reduce negative and/or cognitive symptoms. Further testing of these naturally occurring agents is in progress and synthetic agonists with greater potency are in discovery.

Courtesy: The book chapter has been published in Lambert Academic Publisher (LAP, Germany):Ishan I. Panchal, Dhrubo Jyoti Sen and Samir K. Shah; Schizophrenia a psychological disorder treatment and future aspects: Lambert Academic Publishing GmbH & Co. KG, Germany: 1-65, 2012. (ISBN: 978-3-659-10447-3)

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Received on 18.11.2012 Modified on 28.11.2012

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