Low Arylsulphatase A Activity in the Development of Psychiatric Disorders

• Published in: Neuropsychobiology Vol. 43; no. 2; pp. 75 - 78
• Main Authors: Mihaljevic-Peles, A, Jakovljevic, M, Milicevic, Z, Kracun, I
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland Karger 01.01.2001; S. Karger AG
• Subjects: Adult; Adult and adolescent clinical studies; Aged; Biological and medical sciences; Biological Psychiatry. Main Editor: J. Mendlewicz (Brussels) / Original Paper; Case-Control Studies; Cerebroside-Sulfatase - deficiency; Dementia - enzymology; Depressive Disorder, Major - enzymology; Female; Humans; Male; Medical sciences; Mental Disorders - enzymology; Middle Aged; Psychology. Psychoanalysis. Psychiatry; Psychopathology. Psychiatry; Psychoses; Schizophrenia; Schizophrenia - enzymology; Schizophrenia; Major depression; Arylsulphatase A deficiency; Dementia; Mood disorder; Human; Metachromatic leukodystrophy; Enzyme; Pathogenesis; Depression; Esterases; Personality disorder; Psychosis; Enzymatic activity; Arylsulfatase; Hydrolases; Degenerative disease; Sulfuric ester hydrolases
• ISSN: 0302-282X; 1423-0224
• DOI: 10.1159/000054870

Previous studies have suggested that arylsulphatase A (ASA) deficiency may be present in psychiatric patients. A number of patients with low ASA activity and various neuropsychiatric symptoms have been observed. Metachromatic leucodystrophy (MLD) is a disease caused by deficiency of the enzyme ASA. Clinically, adult MLD may present as a schizophrenia-like psychosis, deterioration of cognitive functions, personality changes, depression and dementia. However, there are individuals with low ASA activity without clinical symptoms of MLD. This state is described as ASA pseudodeficiency. It remains controversial whether low ASA activity predisposes to or influences the development of psychiatric symptoms. Relatively little attention has been paid to the role of neurodegenerative processes in the pathophysiology of psychiatric disorders. The hypothesis underlying this work is that there is a subclass of mentally ill patients whose psychiatric problems are at least partly caused by an abnormal ASA. The purpose of this particular study was to determine whether an abnormal ASA could be detected in schizoprenic, major depressed and demented patients and control subjects. There were 66 schizophrenic, 59 major depressed and 61 demented patients. The control group consisted of 102 healthy volunteers. Leucocyte ASA activity was determined from blood samples, using p-nitrocatechol sulphate as substrate. Our results show that low ASA activity is more frequently found in psychiatric patients than in control subjects. Our findings indicate that clinical types of major depression and schizophrenia could be connected with low ASA activity. The presence of a decreased ASA activity points to the conclusion that an enzyme deficit entails vulnerability to psychiatric disorders.