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Please quote Nature Neuroscience as the source of these items.

The January 2005 issue of Nature Neuroscience is available online.

 January 2005 Previous | Next

A new approach to ALS treatment

Nature Neuroscience pp 85 - 92

Amyotropic lateral sclerosis (ALS, often called Lou Gehrig's disease) is a paralyzing disorder caused by the death of motor neurons in the spinal cord and brainstem. It is currently incurable, and patients typically die within three to five years of disease onset. However, a new treatment approach delays the progression of the disease in an animal model, reports a paper in the January issue of Nature Neuroscience.

Unlike patients with other neurodegenerative disorders like Alzheimer's or Parkinson's disease, ALS patients have no cognitive impairment. The disease often strikes healthy individuals in their prime, and more than 90% of ALS patients have no family history of neurodegenerative disease. ALS patients usually notice muscle weakness first in their limbs (limb-onset) but in about 25%, the motor neurons in the brainstem degenerate first (bulbar-onset). Bulbar-onset ALS progresses faster and causes life-threatening respiratory problems sooner than limb-onset ALS; these patients typically survive only for 12 to 18 months after becoming ill.

Peter Carmeliet and colleagues delivered recombinant VEGF, a growth factor known to promote neuron growth and survival, directly into the brains of rats with ALS symptoms. This treatment caused the rats to survive 3.5 times longer than untreated animals and delayed the onset of paralysis. To date, this is among the greatest therapeutic effects reported with growth-factor treatment in ALS.

Direct delivery to the brain was particularly effective in rats suffering from forelimb-onset ALS (the equivalent of human bulbar-onset cases), stimulating motor neuron survival in the brainstem. The authors also report that the VEGF was transported from axons back to cell bodies elsewhere in the brain, and that it helped preserve synapses between motor neurons and muscles in these animals.

This work may help revive interest in clinical trials using growth factors as a potential treatment for ALS, and also establishes a new rat ALS model that could be used to evaluate novel treatments.


Treatment of motoneuron degeneration by intracerebroventricular delivery of VEGF in a rat model of ALS pp 85 - 92
Erik Storkebaum, Diether Lambrechts, Mieke Dewerchin, Maria-Paz Moreno-Murciano, Saskia Appelmans, Hideyasu Oh, Philip Van Damme, Bart Rutten, Wing Yan Man, Maria De Mol, Sabine Wyns, David Manka, Kristel Vermeulen, Ludo Van Den Bosch, Nico Mertens, Christoph Schmitz, Wim Robberecht, Edward M Conway, D�sir� Collen, Lieve Moons & Peter Carmeliet
Published online: 28 November 2004 | doi:10.1038/nn1360
Abstract | Full text | PDF | Supplementary Information

VEGF: multitasking in ALS pp 5 - 7
Christine Vande Velde & Don W Cleveland
doi:10.1038/nn0105-5
Abstract | Full text | PDF
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Reading emotions without seeing

Nature Neuroscience pp 24 - 25

Part of being a good diplomat - or poker player - is picking up on other people's emotions. We seem to automatically tell people's emotions from their facial expressions, and according to a report in the January issue of Nature Neuroscience we can do so even when we are not aware of what we're seeing.

Alan Pegna and colleagues examined a single patient who had suffered multiple strokes that damaged a part of the brain critical for normal vision. Although his eyes were unaffected, the patient was effectively blind, unable to tell apart the simplest of shapes such as circles and squares. When the researchers showed him pictures of faces, he could not tell whether the subject was a man or a woman, or whether if it was even a face or not. However, when they asked him to guess the subject's emotional state, he got it right more often than not. Scans of his brain activity indicated that the amygdala, a part of the brain that processes emotion, was active when he saw emotional faces although he was not aware of it. The authors conclude that facial expressions can be processed automatically, without conscious awareness.


Discriminating emotional faces without primary visual cortices involves the right amygdala pp 24 - 25
Alan J Pegna, Asaid Khateb, Francois Lazeyras & Mohamed L Seghier
Published online: 12 December 2004 | doi:10.1038/nn1364
Abstract | Full text | PDF | Supplementary Information
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Insulin regulates inebriation in flies

Nature Neuroscience pp 18 - 19

Do you enjoy a glass of wine with your dinner? After a meal, levels of the hormone insulin surge, telling cells in the body to take up sugar from the bloodstream. In the brain, insulin signaling regulates the intoxicating effects of alcohol, reports a new study in the January issue of Nature Neuroscience.

Ulrike Heberlein and colleagues impaired activity in a small group of cells in the fruit fly brain that make and release insulin-like molecules. The genetically modified flies were significantly more sensitive to alcohol than normal flies and rapidly became sedated. Blocking or reducing insulin signaling in the brains of normal flies also led to more rapid intoxication. In mammals, insulin targets neurons that regulate sensitivity to drugs as well as the rewarding properties of drugs and food. These results in flies suggest that insulin signaling may be an evolutionarily conserved mechanism important for the brain's response to addictive substances.


Insulin signaling in the nervous system regulates ethanol intoxication in Drosophila melanogaster pp 22 - 23
Ammon B Corl, Aylin R Rodan & Ulrike Heberlein
Published online: 12 December 2004 | doi:10.1038/nn1363
Abstract | Full text | PDF| Supplementary Information
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ISSN: 1097-6256
EISSN: 1546-1726
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