You are currently browsing the monthly archive for April 2010.
And at a very low dose, too! I take gabapentin for nerve pain, also an anti-epilepsy drug. Zonisamide is a newer version.
The discovery of an antiparkinsonian drug, zonisamide; Murata M; Clinical Neurology (Rinsho Shinkeigaku) 50 (2), 67-73 (Feb 2010)
We serendipitously found that zonisamide (ZNS), an antiepileptic agent, has beneficial effects on Parkinson disease. A 25 mg once a day of ZNS (200-600 mg/day for epilepsy), significantly improves motor function of advanced patients with Parkinson disease. Its effects maintained at least one year even in patients with advanced stage.
It was finally approved as an anti parkinsonian agent in Japan on January 2009. As the mechanism of antiparkinsonian effects of ZNS, we showed that ZNS increases dopamine contents in the striatum by activating dopamine synthesis through increasing the levels of tyrosine hydroxylase (TH) mRNA and TH protein. It moderately inhibits monoamine oxydase (MAO) activity.
ZNS shows significant inhibition on T-type Ca++ channel. It may also affect the beneficial effects of ZNS on Parkinson disease. ZNS also showed neuroprotective effects on several parkinsonian models. It markedly inhibited quinoprotein formation and increased the level of glutathione by enhancing the astroglial cystine transport system and/or astroglial proliferation through S100beta.
Decoded genome of the zebra finch will will help scientists understand how humans learn language and may someday provide insights into diseases like autism that can inhibit speech, team members say.
“Now we can look deep into the genome, not just at the genes involved in vocal learning, but at the complex ways in which they are regulated,” said Richard K. Wilson, the research’s senior author and director of Washington University’s Genome Center. “This information provides clues to how vocal learning occurs at the most basic molecular level in birds and people.”
Past research has shown that hundreds of genes light up in the finch’s brain as the bird learns a new song.
The new research show that significantly more genes about 800 total are activated by the act of singing….
The FDA says it is evaluating clinical trial data that suggests that patients taking Stalevo, Novartis and Orion’s Parkinson’s disease treatment, may be at an increased risk for developing prostate cancer. The agency emphasizes its review of Stalevo is ongoing and no new conclusions or recommendations about the use of this drug have been made.
Although Orion shares went 10.9 percent lower on the news to €14.58, analysts downplayed the announcement. “The study results were already communicated a year ago, and now the FDA is looking further into it,” says analyst Sami Sarkamies at Nordea Markets, as quoted by Reuters. “If it was a new drug with a ten-year patent, possibly the impact would be bigger, but this is a drug living the last moments of its life cycle,” he adds.
The data under review are from a long-term clinical trial called Stalevo Reduction in Dyskinesia Evaluation-Parkinson’s Disease (STRIDE-PD). The trial evaluated the time to onset of dyskinesia in patients with Parkinson’s disease taking Stalevo compared with those taking Sinemet (carbidopa/levodopa). An unexpected finding in the trial was that a greater number of patients taking Stalevo were observed to have prostate cancer compared with those taking Sinemet.
GDNF (glial cell-line derived neurotrophic factor) is a natural brain substance involved in the embryonic establishment of the nigrostriatal dopaminergic system and maintenance of adult nigrostriatal dopaminergic neuron health. With degeneration of these dopaminergic neurons critical to the neuropathology of PD, investigators have postulated that addition of exogenous GDNF to the nigrostriatal system may improve motor function by stimulating residual dopaminergic neuron function and preventing further degeneration.
…..Researchers at the University of Florida have been successful in controlling expression of a modified gene construct that includes GDNF, delivered to the brain of rodents by a single AAV vector (adeno-associated viral vectors). The AAV vector was able to package not only the GDNF gene but also additional regulatory sequences which respond to dietary doxycycline in regulating gene expression. Control of GDNF expression may be important in avoiding clinical morbidity in Parkinson’s disease (PD) patients.
MRI can characterize neural stem cell implantation by assessing the migration, proliferation and location. This can be achieved by labeling the neuronal stem cells with Iron, which can be observed with MRI. After the cells are implanted we see that the concentration of cells diminishes in the implantation area and increases in the final location of destination.
“The vaccine PD01 takes advantage of the fact that accumulations and the associated deposition of alpha-syn in the brain are partly responsible for the progression of Parkinson’s disease. A reduction in the alpha-syn concentration in the brain should therefore have a positive effect on the clinical progression of Parkinson’s. It is precisely here where PD 01 acts, as the vaccine triggers an effective immune response to the harmful alpha-syn, as a result of which the body’s own immune system reduces the alpha-syn. AFFiRiS is now able to announce the successful outcome of the preclinical phase confirming the effectiveness of this principle.”
To quote Dr Frank Mattner, CSO: “Alpha-syn is an attractive target for treating Parkinson’s causally and not just symptomatically. However, it must be remembered that alpha-syn is an endogenous protein belonging to a family of proteins whose members have extensive sequence homologies. For example, as a so-called neuroprotective factor, the member of this protein family known as beta-syn is important for a healthy body. A vaccination aimed at reducing alpha-syn must therefore ensure that the triggered antibody immune response exclusively addresses alpha-syn, but leaves beta-syn untouched. Our AFFITOM(R) technology allows us to develop vaccines that guarantee this high level of specificity to alpha-syn. During 2010 we will complete the preliminary work for the clinical trial”.
March 28, 2010
ScienceDaily (Mar. 26, 2010) – Scientists at UCSF reported improving the motor deficits of experimental parkinsonism in rats using embryonic medial ganglionic eminence (MGE) cells transplanted to the striatum. In a report published in Cell Stem Cell (vol. 6, issue 3, 2010) transplanted neurons migrated, integrated into local circuits, and matured into GABAergic inhibitory interneurons, resulting in improved motor function in this animal model.
“University of California, Berkeley, biologists have found a signal that keeps stem cells alive in the adult brain, providing a focus for scientists looking for ways to re-grow or re-seed stem cells in the brain to allow injured areas to repair themselves.
The researchers discovered in fruit flies that keeping the insulin receptor revved up in the brain prevents the die-off of neural stem cells that occurs when most regions of the brain mature into their adult forms.”
26 Mar 2010
“UCSF scientists report that they were able to prompt a new period of “plasticity,” or capacity for change, in the neural circuitry of the visual cortex of juvenile mice. The approach, they say, might some day be used to create new periods of plasticity in the human brain that would allow for the repair of neural circuits following injury or disease.
The strategy – which involved transplanting a specific type of immature neuron from embryonic mice into the visual cortex of young mice – could be used to treat neural circuits disrupted in abnormal fetal or postnatal development, stroke, traumatic brain injury, psychiatric illness and aging.”