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Please quote Nature Neuroscience as the source of these items.

The November 2004 issue of Nature Neuroscience is available online.

 November 2004 Previous | Next

Switching senses

Nature Neuroscience pp 1266 - 1270

In blind people, areas of the brain that would normally process visual information do not simply pack up and disappear. Instead, they find new work processing language-related information, reveal new findings to be published in the November issue of Nature Neuroscience.

Previous brain imaging studies had shown that in blind people, visual brain areas are active during language-related tasks. However, it was not known whether this activity was actually necessary for language processing. Leonardo Cohen and colleagues asked blind and sighted subjects to respond to a noun with an appropriate matching verb as quickly as possible (e.g., say 'eat' when they hear 'apple'). While the subjects were performing this simple task, the researchers used a technique called transcranial magnetic stimulation to disrupt brain activity in visual cortex. In sighted individuals, this manipulation had no effect. Blocking visual cortex activity in blind subjects, however, caused them to be less accurate in generating an appropriate verb. This was not due to an impairment in the ability to say words, but rather was due to an inability to think of the correct verb (a semantic error).

In the current study, all of the blind individuals had lost their sight early in life; it remains unclear whether a similar reorganization of the brain occurs in people who lose their sight at later ages.


Transcranial magnetic stimulation of the occipital pole interferes with verbal processing in blind subjects pp 1266 - 1270
Amir Amedi, Agnes Floel, Stefan Knecht, Ehud Zohary & Leonardo G Cohen
Published online: 03 October 2004 | doi:10.1038/nn1328
Abstract | Full text | PDF | Supplementary Information
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Imaging neuronal damage in Alzheimer's disease

Nature Neuroscience pp 1181 - 1183

Alzheimer's disease (AD) is among the most common cause of dementia in elderly people. Although the causes of AD are not fully understood, abnormal production of the protein beta-amyloid are thought to cause the formation of clumps (called amyloid plaques) in the brain, which kill neurons. In the November issue of Nature Neuroscience, Wen-Biao Gan and colleagues use state-of-the-art imaging techniques to visualize the neuronal damage caused by these amyloid plaques.

The authors use transcranial two-photon imaging to study the degree of neuronal abnormalities near fibrillar amyloid deposits in a transgenic mouse model of AD. They report that dendrites passing through or in the vicinity of these fibrillar amyloid deposits show a loss of spines, along with a general atrophy of the dendritic shaft. Axons are also affected, with axons close to the plaques develop large swellings. These local abnormalities eventually lead to a gradual elimination of many neuronal branches, and a general shortening of neuronal projections. The study shows that amyloid deposition can lead to permanent and global disruption of synaptic connections, which could in turn be partly responsible for causing the dementia seen in Alzheimer's patients.


Fibrillar amyloid deposition leads to local synaptic abnormalities and breakage of neuronal branches pp 1181 - 1183
Julia Tsai, Jaime Grutzendler, Karen Duff & Wen-Biao Gan
Published online: 10 October 2004 | doi:10.1038/nn1335
Abstract | Full text | PDF | Supplementary Information
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Different neural strategies for problem solving

Nature Neuroscience pp 1193 - 1194

Mathemetical problems presented in words are logically equivalent to those presented as numbers, but as many students may have suspected, the brain does not approach the two formats in the same way. A brain imaging study in the November issue of Nature Neuroscience confirms this intuition, showing that word problems engage the anterior prefrontal cortex, while the same problems presented numerically engage the posterior parietal cortex.

The authors asked whether students presented with mathematical problems in different formats would convert them to a common abstract representation, or whether the format of the problem would influence how the brain processed the information. Although the two groups got a similar number of correct answers, brain imaging indicated that they took different routes to get there. The authors conclude that the brain is able to choose between alternative neural representations to achieve the same efficiency of problem solving, and that equivalent behavioral performance does not imply equivalent neural strategies.


Behavioral equivalence, but not neural equivalence—neural evidence of alternative strategies in mathematical thinking pp 1193 - 1194
Myeong-Ho Sohn, Adam Goode, Kenneth R Koedinger, V Andrew Stenger, Kate Fissell, Cameron S Carter & John R Anderson
Published online: 10 October 2004 | doi:10.1038/nn1337
Abstract | Full text | PDF
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A new obesity gene

Nature Neuroscience pp 1187 - 1189

Much research is devoted to uncovering why some people chronically overeat and how medicine might be able to help them. Severe childhood obesity may be caused by partial loss of a growth factor receptor, reports a study in the November issue of Nature Neuroscience.

Stephen O'Rahilly and colleagues from Addenbrooke's Hospital in Cambridge, UK, found in a severely obese and mildly retarded child that one of the two copies of the gene for the receptor TrkB was mutated and thereby rendered inactive. TrkB is present on the surface of nerve cells, where it binds the nervous system growth factor BDNF and transmits its signal to the cell interior. The BDNF/TrkB system is well known for its role in supporting the survival of nerve cells, and it was quite a surprise when a few years ago an American group of researchers showed that lack of BDNF or TrkB could cause severe obesity in mice.

The current paper's authors now report the first human in whom obesity may be caused by insufficient BDNF/TrkB signaling; their patient does not carry any mutations in other genes linked to obesity. The authors screened another 288 people with severe childhood-onset obesity for defects in the TrkB gene, and found five different mutations in five patients. These results do not yet prove that TrkB mutations are a significant cause of morbid obesity, but they do suggest that TrkB signaling is involved in body weight regulation, and that it could be a target for drug development.


A de novo mutation affecting human TrkB associated with severe obesity and developmental delay pp 1187 - 1189
Giles S H Yeo, Chiao-Chien Connie Hung, Justin Rochford, Julia Keogh, Juliette Gray, Shoba Sivaramakrishnan, Stephen O'Rahilly & I Sadaf Farooqi
Published online: 24 October 2004 | doi:10.1038/1336
Abstract | Full text | PDF
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ISSN: 1097-6256
EISSN: 1546-1726
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