Mike Hopkins said researchers have found that they have discovered cell death cascades that lead to physical and intellectual degeneration of Parkinson's disease.

Research Results, Published Nov. 2 in Science, Suggest promising new target drugs that can hinder Parkinson's disease progression.

According to the study, researchers say that the main driver of the parasymes disease marker nerve cells degeneration is a specialized "programmed" way toward the death of the oldest Greek intention, Philon. In addition, other forms of cell death, such as apoptosis (normal growth and development) and necroptosis (in general, cell death due to disease or injury) are transformed into the program. The first step in Parkinson's disease is Parkinson's disease in the brain neurons to accumulate wrong proteins. These proteins, which are considered alpha synclinics, have long been associated with progression of Parkinson's disease, but it is unclear how they affect their brain cells.

"The mucus of the disease cells in our hopes that we can ever treat and treat Parkinson's disease," said Dr. Didson, director of the legislative institute and professor of neurology. John Hopkins University School of Medicine

Learn more about what road cells die from Parkinson's cells, research group of molecular brain cells in laboratory growth with alpha synclinic teeth and made their reaction within 14 days. As brain cells die, researchers noted that they were "involved" propane "PARP1", which led to death by means of parantano.

They were then tested whether blocking PARP1 could save cells from certain deaths. In addition, researchers once again added alpha syndrome teeth to healthy mouse brain cells, and then cells treated with one of three drugs that result in PARP1 function: Veliparib (ABT-888), Maparabyar (AG-014699) or Thalaoperabi (BMN 673) , All currently used oncologist to treat breast and ovarian cancer. The researchers found that the cells were treated with these medicines within 14 days.

In order to test live mammals, the research team destroyed Alpas syncicin teeth genetically developed PARP gene in normal mice and mice brain. The researchers found that normal mice began to lose muscle weakness, loss of coordination and decrease movement, apparently in mice power tests and vertical polyclinics after three months of treatment. However, as PARS and PARP-blocking normal mice have not been detected.

"It shows that this basic step has been blocked by the safety of the passants on the path of the passantenosis is confirmed by the fact that Parkinson's disease kills cells by means of this mechanism," says Thea-Kem's Doctor, Institute for Research and Postdoctoral Patients at the John Hopkins Medical School of Cell Engineering.

Past studies have shown that PARP leads to neurons that form sugar that is called PAR, which strengthens alpha sicocin and increases the indicator of alpha scliccin which is a combination of proteins. KAMA was interested in whether or not PARP1 growth in Parkinson's cells resulted in similar results.

In order to test this hypothesis, researchers added PAR and Alpha Sinclinic's teeth in laboratory-raised mouse brain cells. They found that the combination of PAR and alpha syndeline formed the alpha syndicine coke, the more neurotoxic tension. The cells treated with this combination died 25 times faster than their colleagues alpha sinkokin.

To test these observations, the research team reiterated experimentation in normal mosaics. The researchers performed alpha synclinic clippings or more toxic PAR / alpha synclinic in the mice brain and still observed them in six months. Mice, who only have alpha syndiculin teeth, appear signs of degeneration six months after the start of treatment. However, mice who have experienced combination therapy have been experiencing twice as fast as only a three-month period of decentralization.

"PAR / alpha syndiculinary combination is not only faster than murders of neurons, it is a strong toxin," says K.

To ensure that this mechanism is in the case of human Parkinson's disease, researchers have collected 21 patients in Parkinson's disease in different phases of disease and liquid samples from 33 healthy people. The team evaluated each sample PAR. What was discovered was that the samples of people with Parkinson's disease were about twice as high as PAR.

"In addition, one of our 4 samples has been shown to be correlated between PAR concentrations and the progress of the disease," says K.

The researchers emphasized that more research should be done than their research can be used for human beings, but if further experiments support their outcomes, researchers hope that they are working with clinical trials to drug companies that are currently in drug-producing drugs. These drugs are slow or even stop at Parkinson's disease.

"If PARP inhibitors are working in patients with human Parkinson disease, they can protect the cells affected by Parkinson's disease, but slowly move these neurons into new cells," says Vina Doson, Doctor. , Professor of neurology at Johns Hopkins University School of Medicine.

Parkinson's disease is a progressive violation of the nervous system, which is about 1 million people in the US, according to Parkinson's Foundation. Early symptoms include traumas, sleeping breathing, constipation, and walking, which ultimately leads to more serious symptoms such as loss of losing function and talking and dementia. Much of the symptoms begin in the 60s, but the cases were reported at the age of 2 in patients.

This work was supported by neurological diseases and stroke institute grants (P50NS38377, R37NS067525, NS082205, U01NS082133 and U01NS097049, U01NS100610), JPB Foundation and Jane and Lee Seidman Foundation.

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