Schizophrenia deficits

Lieberman JA, Sheitman BB, Kinon BJ (1997) Neurochemical sensitization in the pathophysiology of schizophrenia Deficits and dysfunction in neuronal regulation and plasticity. Neuropsychopharmacology 17 205-229. 

Cognitive Effiects. Along with the overt psychotic symptoms that characterize schizophrenia, deficits in cognitive function are commonly manifested by impairments in attention, information processing, and memory (14, 701-703). While antipsychotic drugs can ameliorate impaired attention and information processing, their effects on memory... 

Geyer, MA, Swerdlow, NR, Mansbach, RS and Braff, DL (1990) Startle response models of sensorimotor gating and habituation deficits in schizophrenia. Brain Res. Bull. 25 485-498. 

Histamine produces its pharmacological actions by three subtypes of receptors the postsynaptic Hi and H2 receptors and the presynaptic H3 receptor. The H3 receptor is mainly located in the central nervous system (CNS), where it acts as an inhibitory autoreceptor in the central histaminergic neuronal pathways [176]. A number of therapeutic applications have been proposed for selective H3 receptor antagonists, including several CNS disorders such as Alzheimer s disease. Attention Deficit Hyperactivity Disorder, Schizophrenia, or for enhancing memory or obesity control. 

Amphetamine Clinically used for narcolepsy (sudden day-time onset sleep) and Attention Deficit Hyperactivity Disorder (ADHD) formerly used as a short-term slimming agent, as an antidepressant and to boost athletic performance recreational use widespread tolerance develops readily highly addictive regular users suffer many health problems and a reduced life expectancy amphetamine psychosis may develop, with similar symptoms to acute paranoid schizophrenia. 

Leonard, S., Gault, J., Hopkins, J. et al. Association of promoter variants in the alpha7 nicotinic acetylcholine receptor subunit gene with an inhibitory deficit found in schizophrenia. Arch. Gen. Psychiatry 59 1085-1096,2002. 

Schizophrenia is a chronic heterogeneous syndrome of disorganized and bizarre thoughts, delusions, hallucinations, inappropriate affect, cognitive deficits, and impaired psychosocial functioning. 

A PDE10A inhibitor may also have the potential to treat the cognitive symptoms of schizophrenia. The principal evidence for this claim is papaverine reversal of a PCP-induced deficit in the EDID-set shifting assay in rats [35]. This assay translates into human behavior in the form of the Wisconsin Card Sorting Test (WCST). EDID-set shifting is a test of executive function, a measure in which schizophrenics have a robust deficit. It has also been shown recently that papaverine is efficacious in the Novel Object Recognition cognition assay [36]. 

Tourette s syndrome, schizophrenia, attention deficit disorder, anxiety, pain and for the mai r other diseases [1]. 

The term psychotomimetic was coined to compare the effects of hallucinogens to the symptoms of schizophrenia and other psychotic conditions. However, the effects produced by hallucinogens and mental illness are qualitatively different. While drug-induced hallucinations tend to be more visual, auditory hallucinations are most common in schizophrenia. The hallucinogenic drugs discussed here may induce positive symptoms (e.g., hallucinations), but do not induce the negative symptoms (e.g., cognitive deficits, social withdrawal) of schizophrenia. 

Parkinsonism, or Parkinson s disease, is named for James Parkinson who first described the disease back in 1817. It is nsnally a disease of the elderly characterized by a spectrnm of movement disorders involnntary movements, rigidity, slowness, and loss of balance. It may progress to mental impairment, including depression. This is basically the same spectrum of movement disorders sometimes seen in schizophrenia patients taking dopamine antagonists. This snggests that parkinsonism may reflect, in some manner, a deficit in dopamine activity. 

The characteristic symptoms of schizophrenia have historically been conceptually divided into positive and negative symptoms. At least two of these symptoms must be present for a month during the so-called active phase of illness. One can conceptualize the positive symptoms as the presence of abnormal beliefs or behaviors, whereas, in contrast, negative symptoms are a deficit or absence of normal behaviors. 

In view of these factors, it has been suggested that a deficiency of omega-3 fatty acid in the diet will decrease the concentration of these fatty acids available for synthesis of the required phospholipids in the body, including the brain. If this was a chronic deficiency it could increase the risk of development of some disorders, including depression, schizophrenia and attention deficit syndrome. There is some evidence that this is the case. 

Much attention has been paid to the catecholamines noradrenaline and dopamine following the discovery that their depletion in the brain leads to profound mood changes and locomotor deficits. Thus noradrenaline has been implicated in the mood changes associated with mania and depression, while an excess of dopamine has been implicated in schizophrenia and a deficit in Parkinson s disease. 

The 1960 s and 1970 s saw several other hypotheses proposed and dis-proven. The monoamine oxidase (MAO) deficiency hypothesis was based on the observation of diminished activity of platelet MAO-B in schizophrenia, although this was likely to be an artifact of drug treatment and the small deficits could not, in any case, account for changes in monoamine transmitters. Other hypotheses relating to, among other transmitter molecules, noradrenaline and enkephalin/endorphin have also been proposed. Each of these have had propo-... 

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