ABSTRACT
Molecular genetics and Biochemistry have been devoted to establish the genetic contribution to aetiology of schizophrenia. The biochemical changes in brain neurotransmitters may contribute to the patho genesis of schizophrenia. The human platelets contain monoamine oxidase [MAO] which is similar in many physiochemical properties to that of the brain, the similarity was also established between brain catechol-O-methytransferase [COMT] and acetyicholinesterase [AChE] and that of RBCs. So, this study was directed towards monitoring the platelet MAO and RBCs, COMT and AchE as possible indices for the CNS cellular events. The present study was carried out on 144 subjects classified into normal control group free of any psychiatric manifestation and schizophrenic patients group. Assessment of the changes in neurotransmitters metabolism, was tested e.g. that of catecholamine and acetylcholine by determination of the activity of the enzymes involved in its catabolism e.g. MAO, COMT and AChE either by fluorimetric method or colorimetric method. Our results indicated a highly significant reduction in platelets MAO activity among schizophrenic patients than control group [P<0.001]. Concerning the COMT activity, there was no statistical significant difference between control and patients group. Assessment of AChE activity indicated a significant reduction in patients group [P<0.02]. So, the changes in cholinergic activity in relation of that catecholamine may play a role in the explanations of schizophrenic dysfunction. The genetic contribution was conducted by phenotyping of group specific component [Gc] and phosphoglucomutase I [PGMI] as genetic makers of schizophrenia using isoelectro focusing techniques. In the present study analyzing the distribution of different Gc genotypes among control and schizophrenic groups demonstrated the increase of Gc 2-1 genotype frequency among schizophrenics [P<0.001] with a relative risk factor of RR=2.56. There was significant difference in distribution of PGM1 1+1+ between normal control group and schizophrenic group [P<0.001]. No correlation could be detected between MAO, COMT, AChE enzyme activity and Gc genotypes or PGM1 phenotypes