Schizophrenia and the brain

Article Abstract:

Schizophrenia is a devastating disease that affects about one percent of people worldwide with, as yet, no reliably effective treatment. Two major advances are improved diagnostic criteria, as outlined in the Diagnostic and Statistical Manual of Mental Disorders, and the introduction of drugs that produce relief of many of the symptoms of schizophrenia. Searches for the causes of the disease have been hindered by failure to identify whether they lie in the brain structure itself, or in the early experience or environment of the affected individual. Most investigators now believe there is some biologic component. Although discoveries about substances such as dopamine, a chemical important for electrical transmission between certain neurons (nerve cells), made the possibility of a biological basis for schizophrenia seem all the more real, no neurotransmitter or neurotoxin (substance that kills neurons) has yet been shown to play a primary role. Focus has shifted recently to neuroanatomical or neurophysiological abnormalities. Schizophrenic patients seem to have a reduced metabolic rate in regions of the brain associated with motivation and emotion and an increased rate in some of the same regions that are active in epileptic patients experiencing hallucinations. It is not known, however, to what extent these changes cause schizophrenia or are the result of it. Modern imaging techniques are in agreement about an enlargement, in schizophrenics, of the cerebral ventricles, fluid-filled spaces in the brain through which cerebrospinal fluid circulates, and a reduction in the amount of brain tissue. Such findings, however, do not reveal whether the disorder is genetic or acquired, or whether the results are due to medication or prolonged suffering. Neuropathology, the study of brain cells, has also failed to discover any change in the brains of schizophrenics that can reliably be attributed to the disease. Given its complex nature and varied symptoms, schizophrenia seems unlikely to arise from disruption to just one region or transmitter system. Rather, the abnormality may lie at a higher level of neural organization. Collaborative resources from both the psychiatric and neurological domains will offer the best opportunity for successful treatment of this debilitating disorder. (Consumer Summary produced by Reliance Medical Information, Inc.)

Abnormalities, Brain, Schizophrenia, Brain abnormalities, editorial

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Beta-amyloid and the pathogenesis of Alzheimer's disease

Article Abstract:

Alzheimer's disease (AD) is by far the most important cause of dementia among elderly patients; from 60 to 80 percent of cases of dementia among people over 65 are the result of this brain disorder. Between two and four million Americans are currently suffering from AD. For more than 80 years, the pathological hallmarks of AD have been recognized as neurofibrillary tangles, twisted fibers visible with special staining techniques, and senile plaques. In recent years, the new techniques of molecular biology have been brought to bear on the pathology of Alzheimer's disease, and an explosion of new knowledge has been the result. The authors provide a review of the current state of knowledge about the brain pathology found in Alzheimer's disease and discuss the implications of these findings for understanding the development and progression of the disease. Senile plaques in AD contain amyloid, but it should be remembered that the term amyloid refers to different substances in different diseases. The amyloid found in AD senile plaques has been found to be abnormal fragments, dubbed beta-amyloid protein, which have been cleaved from a larger normal protein called amyloid precursor protein. One theory of the pathogenesis of Alzheimer's disease suggests the following sequence of events. Abnormal cleavage of amyloid precursor protein results in the accumulation of beta-amyloid protein. The beta-amyloid protein binds to receptors for the serpin-enzyme complex. It is believed that the function of these receptors is to remove, from the extracellular fluid, enzymes that break down proteins (proteases). The inhibition of serpin-enzyme complex binding would, by this hypothesis, leave the cell surface proteins of brain cells open to damage by protease attack. The chronic damage resulting from these proteases may then lead to the degeneration of the neuron. Unfortunately, the pathological process may even feed on itself; the very proteases that damage the neurons may also lead to the formation of more beta-amyloid protein, resulting in almost explosive multiplication of the pathological effects. (Consumer Summary produced by Reliance Medical Information, Inc.)

Development and progression, Alzheimer's disease

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Primary progressive aphasia -- a language-based dementia

Article Abstract:

The physiology and diagnosis of primary progressive aphasia are reviewed. Aphasia means a person stops talking. Patients with this type of dementia may still have a good memory and may still recognize friends and family members. For this reason, they should not be diagnosed as having Alzheimer's disease.

Diagnosis, Physiological aspects, Aphasia

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