Therapeutic benefit of adjunctive dipyridamole in schizophrenia is probably due to adenosine-glutamate interactions.
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Adenosine↗
Biomedical subjects
P Belmonte-de-Abreu
Publications and source records attributed to P Belmonte-de-Abreu.
Allopurinol augmentation for poorly responsive schizophrenia.
Adenosine has been proposed to contribute to the pathophysiology of schizoprenia and as a target for therapeutic intervention. In the lack of direct adenosine agonists, allopurinol may indirectly elevate adenosine levels by inhibiting degradation of purines. We report two cases of poorly responsive schizophrenic patients who improved considerably with add-on allopurinol 300 mg/day. Their clear clinical improvement warrant further investigation of allopurinol, as well as other purinergic strategies, for the treatment of schizophrenia.
Adult↗
Neurodevelopmental risk factors in schizophrenia.
The authors review environmental and neurodevelopmental risk factors for schizophrenic disorders, with emphasis on minor physical anomalies, particularly craniofacial anomalies and dermatoglyphic variations. The high prevalence of these anomalies among schizophrenic subjects supports the neurodevelopmental theory of the etiology of schizophrenia, since they suggest either genetically or epigenetically controlled faulty embryonic development of structures of ectodermal origin like brain and skin. This may disturb neurodevelopment that in turn may cause these subjects to be at increased risk for the development of schizophrenia and related disorders. The precise confirmation of this theory, at least in some cases, will provide further understanding of these illnesses, allowing easy and inexpensive identification of subjects at risk and providing guidelines for the development of new pharmacological interventions for early treatment and even for primary prevention of the illness.
Brain Diseases↗
Allopurinol for refractory aggression and self-inflicted behaviour.
The impairment of the purinergic system, characterized by reduced adenosinergic activity, has been implicated in the neurobiology of aggressive behaviour. Since there are no direct adenosine agonists available for human use, inhibition of purine degradation by allopurinol was conceived as a possible strategy. We report two cases of adults with refractory aggressive behaviour due to a neurological condition (one mainly with self-inflicted behaviour) with dramatic response to therapy with allopurinol, 300 mg/day p.o. These preliminary results reinforce the involvement of the purinergic system in the neurobiology of aggression, warranting further testing of allopurinol as a new treatment for aggressive and self-inflicted behaviours.
Administration, Oral↗
Increased serum S100B protein in schizophrenia: a study in medication-free patients.
S100B protein, a calcium binding protein produced and released by glial cells, has been used as a sensitive marker of brain damage. Previous studies have found alterations in peripheral S100B levels in schizophrenic patients on medication. We compared serum S100B levels of 20 medication-free DSM-IV schizophrenic patients and 20 age-gender matched healthy controls. Schizophrenic patients presented higher serum S100B levels (mean 0.120 ng/ml+/-S.D. 0.140) compared to controls (mean 0.066 ng/ml+/-S.D. 0.067; P=0.014) and there was a negative correlation with illness duration (r=-0.496, P=0.031). The results of this study indicate that serum S100B levels may be a state marker of a limited neurodegenerative process, particularly in the early course of schizophrenia or, at least, in a subgroup of schizophrenic patients.
Adolescent↗