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Can EPO prevent loss of brain function in schizophrenia?

The causes and mechanisms of most brain diseases still evade scientists. A causal treatment exists for only few conditions. Therapeutic approaches at present aim predominantly at harm reduction. Harm reducing, brain function protecting measures are addressed with the term "neuroprotection". Neuroprotection is best defined as the effort to maintain / restore the highest possible integrity of cellular interactions in the brain, resulting in an overall undisturbed neural function.

Neuroprotection is a novel approach for the treatment of schizophrenia. Over the last decade it has become clear that in addition to disturbed brain development, continuous neurodegenerative processes are involved in the progression of this brain disease. Nevertheless, molecular and cellular mechanisms accounting for the various dysfunctions of schizophrenic psychosis are far from clear. Existing animal models of schizophrenia only reflect certain aspects of the human disease. Therefore, novel concepts to treating schizophrenia should be immediately translated into clinical pilot trials. This is particularly appropriate if the beneficial compounds that are suggested are safe. During early episodes of schizophrenic psychosis, a dramatic worsening of cognitive performance is often observed. More than 100 years ago, the famous psychiatrist Emil Kraepelin described these phenomena and called the disease "Dementia praecox" (premature dementia). Neuroleptic therapy, one of the major achievements of psychiatry over the last century, has prepared the ground for any further therapy aiming at influencing the course of disease: Reduction in psychotic symptoms (paranoia, delusions) through neuroleptic treatment is a prerequisite for creating a stable therapeutic interaction between patients and therapists. Neuroleptic treatment by itself, however, is unlikely to influence the neurodegenerative course of schizophrenia. Therefore, a neuroprotective add-on therapy using well-tolerated and safe comp
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Contact: Aimee Midei
molecularpsychiatry@mednet.ucla.edu
310-206-6739
Molecular Psychiatry
3-Dec-2003


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