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HDAC2 as a new target to improve schizophrenia treatment

One of the main characteristics of treatment of psychiatric disorders, such as schizophrenia and depression, is the chronic administration (weeks, months or even years) of therapeutic compounds. A recent study suggests the existence of a compensatory mechanism through which neurons in the cerebral frontal cortex adjust the balance between two signaling pathways in response to chronic treatment with atypical antipsychotic drugs [1]. The ability of the system to maintain its dynamic equilibrium involves epigenetic changes in chromatin structure that may ultimately restrain the therapeutic efficacy of schizophrenia treatment. All life forms (microorganisms, plants and animals) function, reproduce and grow in an environment where conditions are often changing rapidly and unpredictably. However, to stay alive, the biological processes inside an organism need to remain mostly unchanged despite outside events. Survival depends on the ability of an organism to maintain a dynamic equilibrium (or homeostasis) between its internal and external environments [2]. Failure to respond adequately may result in disease, malfunction or death. There is growing evidence that epigenetics (the study of heritable modifications that regulate gene expression without alterations in the underlying DNA sequences) may play an essential role in the cellular events that facilitate the adaptation of an individual cell to its environment [3]. With this background, it is reasonable to speculate that some of the epigenetic changes induced by chronic administration of therapeutic drugs may be considered by the organism as external factors to reverse or compensate. Schizophrenia is a neuropsychiatric condition that affects more than one percent or the population worldwide [4]. The rates of schizophrenia are similar across populations and apparently uncorrelated with socioeconomic status or cultural background. Diagnostic features of schizophrenia include positive symptoms, such as hallucinations and delusions, as well as negative symptoms, such as inability to pay attention and social withdrawal. Treatment with either typical (e.g., chlorpromazine and haloperidol) or atypical (e.g., clozapine, olanzapine and risperidone) antipsychotics often results in substantial improvement or even remission of hallucinations and delusions. However, a fifth to a third of schizophrenic patients do not respond to antipsychotic medication, and will continue to experience psychosis and other positive symptoms in spite of the treatment [5]. Deficits in attention and memory function are also present in the majority of schizophrenic patients. Importantly, clinical studies suggest that these cognitive impairments show minimal improvement or exacerbations after treatment with atypical anti psychotic drugs [6], a conclusion that has been further supported by rodent models of memory formation [7]. Previous findings convincingly demonstrate that chronic treatment is involved in some of the mechanisms underlying the therapeutic HDAC2 as a new target to improve schizophrenia treatment