The Human Brain:
The Structural Basis for Understanding Human Brain Function and Dysfunction

+++ INTERNATIONAL CONFERENCE +++ ROME +++ IRCCS SANTA LUCIA +++ Oct. 5-10, 2002 +++

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Novel Brain Mapping Reveals How Schizophrenia Engulfs Teen Brains: Dramatic Images Hold Hope for Early Diagnosis, Treatment of Devastating Disease:

 

Background:  To date, there is a lack of adequate information about how abnormal brain development changes during pre- and post-birth and adolescent years, or how polygenetic and environmental risks, might contribute to the pathology of neurological and psychological diseases during adolescent onset.  In response to this challenge, an international team of scientists designed a brain mapping strategy to uncover deficit patterns as they emerged in populations imaged longitudinally through adolescence for 5 years.  They employed magnetic resonance imaging (MRI) technology to scan a group of teenagers repeatedly as they developed schizophrenia.

 

Advance:  Using a novel imaging approach, these investigators detected a wildfire of tissue loss spreading across the brains of individuals as they developed schizophrenia.  Teenagers, including patients and healthy controls, were scanned repeatedly with MRI.  In patients, a pattern of gray matter loss began in a small region of the parietal cortex, where gray matter is lost normally in healthy teens.  A dynamic wave of deficits then flooded across the cortex over a period of 5 years in the schizophrenia patients.  The severity of these structural changes mirrored the severity and time-course of patients’ symptoms, including hallucinations and depression.

 

Implications: This is the first study to visualize how schizophrenia develops in the brain. Scientists have been perplexed about how schizophrenia progresses, and whether there are any physical changes in the brain. This finding provides a new model of schizophrenia, in which gray matter deficits first appear in a small region of the brain. The dynamic profile observed suggests that schizophrenia might involve an exaggeration of normal teenager gray matter loss, and has a dynamic pattern, that might be blocked using drug therapy. Second, the detection sensitivity of the imaging approach will allow the effective testing of novel drugs to oppose this wildfire of loss. Third, relatives of patients can be screened to evaluate whether their genetic risk for the disease is leading to detectable deficits in the brain.  In those affected, their DNA markers can be minded for risk genes. Their expression can be related to the topography and dynamics of loss, to better understand what triggers the disease and how best to treat it. Hence, this advance provides a new model of schizophrenia, providing insight into what might trigger the disease, its dynamics, and a new strategy to test novel antipsychotic drugs.

 

(A.W.. Toga)

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