Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A comparison of the cholinesterase blood activity with the clinical traits of the disease in 64 patients with paranoid schizophrenia treated by majeptile and haloperidol detected 2 variants in the reactivity of the enzyme link of the cholinergic system. A fluctuation of the cholinesterase activity of the sinusoid type (Ist variant) seen in patients with paranoial and hallucinatory-paranoid syndromes with a remission up to a year and more, speaks in favour of a relatively preserved compensatory-adaptive mechanisms in the neurohumoral regulation. The absence of fluctuation in the cholinesterase activity during the whole period of treatment (2nd variant) was characteristic of patients with negative results of treatment.
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PMID:[Dynamic study of blood cholinesterase activity of paranoid schizophrenic patients]. 1 5

More than a decade of scientific inquiry into the biochemistry of schizophrenia has been organized by the dopamine hypothesis. The evidence that neuroleptics reduce brain dopamine activity is compelling and derives from both human and animal studies. In addition, agents which enhance brain dopamine activity, such as amphetamine or cocaine, can cause a syndrome that can be indistinguishable from acute paranoid schizophrenia. However, a major problem with the dopamine hypothesis is the lack of strong direct evidence of altered dopamine concentrations or metabolism when measured in large groups of schizophrenic subjects. The idea that schizophrenia is more than one illness is an old concept, but it finds increasing support in new studies of the clinical phenomenology, genetics, and biochemistry of schizophrenic patients. The revival of the concept of multiple forms of schizophrenia, in turn, has fostered the development of new biochemical hypotheses of the disorder. These hypotheses propose that neurotransmitters, other than dopamine, may be involved in schizophrenic symptoms. Reports of elevated concentrations of norepinephrine is specific areas of the brain and in the spinal fluid have led to the hypothesis that norepinephrine may be involved in schizophrenia. At least two groups of investigators have suggested that phenylethylamine might be involved in schizophrenia. In part, this proposal is based on the structural and pharmacological similarities of phenylethylamine and amphetamine. gamma-Aminobutyric acid (GABA) is an important inhibitory neurotransmitter. Evidence for the inhibitory influence of GABA-ergic neurons on dopaminergic neurons has led to the hypothesis that decreased GABA-ergic activity may be involved in producing schizophrenic symptoms. Studies with the reversible acetylcholinesterase inhibitor physostigmine and the dopamine agonist methylphenidate have led to the suggestion that acetylcholine and dopamine imbalance may be involved in schizophrenia. This hypothesis is one example of the idea that altered balance between several neurotransmitters may underlie schizophrenia. The recent discovery of the endorphins has led to speculations about the possible role of these substances in schizophrenia. Both an excess and a deficiency of endorphin activity have been implicated in schizophrenia, and speculative evidence has been used to support both hypotheses. The ultimate aim of the search for biochemical defects in schizophrenia is the development of rational drug treatments which will correct these defects and in doing so, these drugs will provide effective treatments for patients with schizophrenic symptoms.
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PMID:Biochemistry and the schizophrenia. Old concepts and new hypothesis. 700 86