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Neuroscience 2008- News Tips - 11/17/2008

Neuroscience 2008- News Tips

Release Date: November 17, 2008

November 14, 2008

The following news tips are based on abstracts or posters to be presented at NEUROSCIENCE 2008, Nov. 15-19, Washington, D.C.

Histaminergic clinical and autopsy abnormalities in restless legs syndrome
Program #143.13, Poster #U7; Washington Convention Center: Hall A-C 

People with restless leg syndrome often have found that sleep-inducing allergy drugs worsen their symptoms. Now, researchers at the Johns Hopkins University School of Medicine have discovered a possible reason for that and help explain why RLS in general interferes with sleep but doesn’t seem to result in daytime drowsiness. The common thread, the researchers say, is that histamine receptors — proteins found on the surface of some cells that are triggered by histamine — in the brain work to modulate nerve responses. When activated, histamine receptors stimulate alertness or wakefulness.

To sort out the relationship they suspected, the researchers first gave 12 RLS patients either a true sedative or diphenhydramine, the active ingredient in many allergy medications that tames histamine and induces sleepiness. They found that while sedatives had little to no effect on RLS, diphenhydramine made the RLS as much as three to four times worse. The team then looked at autopsied brains from RLS patients for possible differences in histamine receptor location and found that the substantia nigra, the part of the brain implicated in RLS, contained a higher number of histamine-3 receptor proteins, suggesting that this molecular pathway is more active in people with RLS.

“Five out of six patients in our study showed this elevated number of histamine receptor proteins,” says Richard Allen, Ph.D., a research associate in neurology at Hopkins. “The histamine system appears to alter the balance of the nervous system so that one is not sleepy in the daytime, even with sleep loss, which might explain why RLS patients can get by on so little sleep. This also suggests that histamine receptors might be a new target for study and therapy of RLS.”

Constituents in grapes have antihyperalgesic effects in a rat model of joint inflammation
Program #468.4, Poster #LL20; Washington Convention Center: Hall A-C

Table grapes are high in flavonoids, which are thought to have strong antioxidant and anti-inflammatory properties. Now, researchers at the Johns Hopkins University School of Medicine have shown that powdered grapes appear to reduce pain and inflammation in a rat model of arthritis, where rats knees are inflamed using a chemical injection.

Some rats were fed the powdered equivalent of 10 cups of grapes once a day after the arthritis-inducing injection, while others got only sugar water. Over the course of four days after the chemical injection, the researchers tested the rats’ inflammation levels and pain responses by measuring their sensitivity to mechanical stimulation such as prodding their paws and measuring the amount of knee swelling. Rats fed grape powder could withstand stronger prodding than their sugar-fed counterparts.

The researchers also compared the grape powder treatment with a common nonsteroidal anti-inflammatory drug, meloxicam, and found that while the dose of meloxicam alone was not sufficient to reduce pain, animals fed a combination of grape powder and meloxicam experienced even less pain from their arthritis than animals that received either substance alone. The combination treatment also reduced the knee swelling associated with inflammation.

“I think there are two important messages here,” says Jasenka Borzan, Ph.D., a research associate in anesthesiology at Hopkins. “That consuming flavonoids through natural products like grapes can be beneficial to health in general and also specifically for reducing inflammatory pain; and that consuming natural products like grapes may also be beneficial in reducing the amount of medication necessary to reduce inflammation.”

Curcumin protects against A53T alpha-synuclein-induced toxicity
Program #48.7, Poster #W5; Washington Convention Center: Hall A-C

Curcumin, derived from the curry spice turmeric, has strong antioxidant and anti-inflammatory properties. Both oxidative damage — damage caused by oxygen — and inflammation have been implicated in nerve cell death associated with Parkinson's disease. Now, researchers at the Johns Hopkins University School of Medicine have shown in a laboratory model of Parkinson's disease that curcumin does protect cells from dying.

To test the protective effects of curcumin, the research team used a Parkinson's disease cell model system. They tested curcumin on nerve-like cells that make a mutant form of the protein alpha-synuclein, called A53T, that clumps together inside of cells to cause harmful biochemical and cellular changes that eventually kill the cells. A53T alpha-synuclein causes 50 percent of untreated cells to die, whereas only 19 percent of A53T cells treated with curcumin died. Further research showed that curcumin itself reduces oxidative damage.

"These results suggest that curcumin is a potential candidate for inhibiting the oxidative damage that leads to Parkinson's disease," says Wanli Smith, Ph.D., an assistant professor of psychiatry and behavioral sciences at Hopkins. "This common curry spice could be a weapon to protect the brain."

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