BBC Science – Scientists believe they have worked out exactly how we recognise a face when we see it. Experts have known for some time that there is something special about faces that draws us to look at them, even after the first few hours of birth. A brain region called the fusiform face area (FFA) has been pinpointed as key. Now a team at Massachusetts Institute of Technology say in the journal Neuron that they have figured out how the FFA processes this visual information.  To find out what was going on in the brain, the researchers asked volunteers to take part in an experiment. The volunteers were asked to look at pictures of different faces and also pictures of an inanimate object - a house. At the same time, the volunteers’ brains were scanned using functional magnetic resonance imaging (fMRI), which shows up which areas of the brain are active at any given time. Some of the faces that the volunteers looked at were completely normal, while others had features that were spaced differently or had features that were replaced by those of different faces, such as a different nose or mouth. Similarly, the pictures of the houses were manipulated in the same way - differently spaced windows or different doors.  From these experiments, Galit Yovel and Nancy Kanwisher were able to confirm that it was the FFA that processed the visual information. The FFA was not activated when the volunteers looked at the pictures of houses, suggesting that it is indeed specific for faces. They also worked out that it was the face as a whole that was recognised, rather than the individual features or the relative spacing of these features. (12/06/04)
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BBC Health – An antibiotic used to treat leprosy and tuberculosis is showing promise as a therapy for Parkinson’s disease. In laboratory tests, rifampicin was found to prevent the formation of protein fibrils associated with the death of brain cells in Parkinson’s. Researchers from the University of California, Santa Cruz, also found the drug dissolved existing fibrils. The research, which is still at an early stage, is published in the journal Chemistry and Biology. The researchers studied the effects of rifampicin in test-tube experiments and are currently doing studies with cell cultures and mice to see if the same effects occur in living cells. Researcher Professor Anthony Fink said: “Clearly more work is needed to determine if this would work therapeutically, but if it does it would probably be most useful as a prophylactic therapy used in the early stages of the disease, before there is general neurological damage. “The disaggregation of existing fibrils is probably the most interesting and novel finding in this study. “If it works in people, that would really open up the possibility of stopping the progression of Parkinson’s disease when it is first diagnosed.” Parkinson’s is a progressive movement disorder resulting from the death of nerve cells in the brain which produce a key chemical called dopamine. It is thought a critical step in the development of the condition is the collection of a protein, known as alpha-synuclein, into insoluble fibrils. Certainly, deposits called Lewy bodies, composed mostly of alpha-synuclein fibrils, appear in affected nerve cells. Some people believe the fibrils themselves are toxic and cause brain cells to die, others that the toxic agents are smaller component parts formed earlier in the process. Previous research has found that rifampicin may also prevent the formation of the protein deposits associated with Alzheimer’s disease. (12/06/04)
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