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Please quote Nature Neuroscience as the source of these items.

The April 2005 issue of Nature Neuroscience is available online.

 April 2005 Previous | Next

Visualizing Alzheimer disease in the living brain

Nature Neuroscience pp 527 - 533

A hallmark of Alzheimer disease is the build-up of amyloid plaques (toxic protein clumps) in the brain, but these have only been detectable by examining brains after death. In the April issue of Nature Neuroscience, Japanese scientists describe a new technique for seeing amyloid plaques in living brains using commonly available brain-scanning technology, an important step toward developing an early diagnostic test for this devastating disease.

Takaomi Saido and colleagues created a substance that would make amyloid plaques show up in brain scans by combining a form of fluorine, a common additive to drinking water, with a compound known to bind to amyloid. They injected this substance, called FSB, into the brains of mice genetically altered to express amyloid, which are often used as a model of Alzheimer disease. They scanned the mice using magnetic resonance imaging (MRI), a widely available technology in hospitals around the world, and were able to create images of their brains, with areas containing amyloid deposits highlighted. The authors confirmed that at the low doses they used, the compound did not cause toxic side effects.

Much work is still needed before such technology can be used to diagnose Alzheimer disease in human patients, but in the meantime, the authors say this is a valuable tool for experimental studies in mice. Because mice can be scanned repeatedly, the technology can be used to follow the progression of the disease across time, and to track the effectiveness of experimental drugs or treatments.


19F and 1H MRI detection of amyloid beta plaques in vivo pp 527 - 533
Makoto Higuchi, Nobuhisa Iwata, Yukio Matsuba, Kumi Sato, Kazumi Sasamoto & Takaomi C Saido
Published online: 13 March 2005 | doi:10.1038/nn1422
Abstract | Full text | PDF | Supplementary Information

Alzheimer disease, in living color pp 404 - 405
Scott A Small
doi:10.1038/nn0405-404
Abstract | Full text | PDF
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Lose the addiction, keep the reward

Nature Neuroscience pp 484 - 489

Drug addiction is a hard habit to break, partly because it taps into brain mechanisms that normally promote attraction to healthier rewards. New research reported in the April issue of Nature Neuroscience suggests a potential way to decrease the appeal of drugs without affecting motivation for normal rewarding activities, such as eating.

Damage to the subthalamic nucleus - a structure buried deep inside the brain - reduces rats´┐Ż motivation for cocaine, but increases their motivation for food. Christelle Baunez and colleagues trained a group of rats to press a lever to obtain either a food pellet or a dose of cocaine. They then lesioned the subthalamic nucleus in some of the rats, and found that these animals were less motivated to get a dose of a cocaine than a group without such damage. In contrast, animals with subthalamic lesions worked harder for food pellets than did normal controls.

These results suggest that the subthalamic nucleus may represent a new target for drug addiction treatment. Curiously, modulation of the same area has previously been shown to improve Parkinson disease symptoms as well.


The subthalamic nucleus exerts opposite control on cocaine and 'natural' rewards pp 484 - 489
Christelle Baunez, Carine Dias, Martine Cador & Marianne Amalric
Published online: 27 March 2005 | doi:10.1038/nn1329
Abstract | Full text | PDF
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Nature Neuroscience
ISSN: 1097-6256
EISSN: 1546-1726
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