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New Therapy Reverses Diabetic Neuropathy
New Therapy Reverses Diabetic Neuropathy -- Posted by Gumbo on 11-02-04 04:55
New Therapy Reverses Diabetic Neuropathy
With only 1 injection there was a complete reversal of established
peripheral neuropathy and restoration of lost nerve endings to their feet.
Researchers from the University of Pittsburgh School of Medicine have
demonstrated for the first time that gene therapy can reverse diabetic
neuropathy. While their studies have so far only involved mice, the results
are significant because they provide the earliest evidence that such an
approach might some day help people with diabetes, in whom neuropathy is a
common complication that causes irreversible nerve damage.
More than two thirds of patients with diabetes develop neuropathy, which
generally affects the sensory neurons within the peripheral nervous system
and is characterized by such symptoms as numbness, tingling, pins and
needles or loss of sensation, most often to the legs and feet. As a result,
patients may be unaware of the presence of ulcers or infections or that they
've experienced injury. No treatments exist that can stop progression of
neuropathy, let alone reverse any damage to nerves.
Five weeks after a one-time inoculation, diabetic animals receiving gene
therapy had complete reversal of established peripheral neuropathy and
restoration of lost nerve endings to their feet, reported James R. Goss,
Ph.D., research assistant professor of molecular genetics and biochemistry
at the University of Pittsburgh School of Medicine. He and colleagues had
previously found the same gene therapy approach could prevent the
development of neuropathy in diabetic animals.
While the exact cause of diabetic neuropathy is unknown, there is evidence
to suggest it is associated with a deficiency or dysfunction of certain
neurotrophic factors, which are proteins essential for the survival and
proper function of neurons. Therefore, the Pitt researchers sought to
develop a therapy that would shuttle the genes responsible for their
production directly into affected neurons. To gain entry into the cells, the
team designed vectors of inactivated herpes simplex virus (HSV), which
normally infects sensory neurons. The HSV vectors were encoded with genes
for one of two neurotrophin factors: nerve growth factor (NFG) and
neurotrophin-3 (NT-3).
"Herpes simplex virus appears to be an ideally suited gene therapy vector
for diabetic neuropathy, in part because very little of the virus is needed
to get inside the cell. But in addition, an important advantage with this
approach is that we can deliver the gene directly and solely to affected
neurons, without bombarding the entire the nervous system," explained Dr.
Goss.
In their study, the researchers induced diabetes in mice, which resulted in
the development of peripheral neuropathy within six weeks. Once neuropathy
was established, they treated two groups with gene therapy -- one received
the vector encoded for NGF and a second group received the vector encoded
with NT-3. To compare outcomes, another group of diabetic animals was
treated with the HSV vector encoded for a gene with no therapeutic value,
and a fourth group received no treatment. Five weeks after inoculation, the
neuropathy was reevaluated using measurements of heat sensitivity and the
ability of nerves in the feet to conduct electrical impulses. In diabetic
animals treated with either the NGF or NT-3 vectors, signs of neuropathy had
disappeared, whereas in the untreated diabetic animals and the diabetic
animals treated with the "empty" vector, neuropathy was still present.
Results of another Pitt study from the same group, found that genes
introduced by HSV vectors were still expressed six months after single
inoculation and could still protect against the development of neuropathy.
That study looked at gene expression for NT-3 and two other neurotrophic
factors.
Their research was supported by the National Institutes of Health, the
Veterans Affairs Administration and the Juvenile Diabetes Research
Foundation International. presented today at the 34th Annual Meeting of the
Society for Neuroscience, being held Oct. 23 - 27 in San Diego.
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