NT-3 genes strengthened mice with disease resembling CMT 1A

[Guest guest]

Gene Benefits Mice

Neurotrophin 3 genes strengthened mice with disease resembling CMT1A

http://www.mda.org/publications/Quest/extra/may09/benefits_mice.html

Zarife Sahenk at Nationwide Children's Hospital and Ohio State University in

Columbus, and colleagues, found mice with a disease resembling type 1A

Charcot-Marie-Tooth disease (CMT) benefited from a transfer of genes for the

neurotrophin 3 protein. CMT1A is caused by a duplication of the PMP22 gene.

Jerry Mendell, who has received many MDA research grants and co-directs the MDA

clinic at Nationwide Children's, was part of the study team, as was

Kaspar, who has MDA support at Nationwide.

The researchers injected the leg muscles of CMT1A mice with either neurotrophin

3 genes inside shells made from adeno-associated viruses, or with a sham

injection. The legs injected with the genes showed better grip strength and had

more normal-looking nerve fibers.

The investigators concluded that neutrophin 3 gene therapy is a promising avenue

for treatment development in human CMT 1A.

These findings were reported at the 2009 American Academy of Neurology meeting,

which was held recently in Seattle.

[Guest guest]

 great news...  sounds promissing

From: gfijig <gfijig@...>

Subject: NT-3 genes strengthened mice with disease resembling CMT 1A

Date: Wednesday, May 20, 2009, 1:19 PM

Gene Benefits Mice

Neurotrophin 3 genes strengthened mice with disease resembling CMT1A

http://www.mda. org/publications /Quest/extra/ may09/benefits_ mice.html

Zarife Sahenk at Nationwide Children's Hospital and Ohio State University in

Columbus, and colleagues, found mice with a disease resembling type 1A

Charcot-Marie- Tooth disease (CMT) benefited from a transfer of genes for the

neurotrophin 3 protein. CMT1A is caused by a duplication of the PMP22 gene.

Jerry Mendell, who has received many MDA research grants and co-directs the MDA

clinic at Nationwide Children's, was part of the study team, as was

Kaspar, who has MDA support at Nationwide.

The researchers injected the leg muscles of CMT1A mice with either neurotrophin

3 genes inside shells made from adeno-associated viruses, or with a sham

injection. The legs injected with the genes showed better grip strength and had

more normal-looking nerve fibers.

The investigators concluded that neutrophin 3 gene therapy is a promising avenue

for treatment development in human CMT 1A.

These findings were reported at the 2009 American Academy of Neurology meeting,

which was held recently in Seattle.