July 3: US researchers have developed an experimental drug that potentially slows down the progression of Parkinson's disease as well as its symptoms.

In experiments performed with cultures of human brain cells and live mouse models, researchers from the Johns Hopkins University in Maryland reported that the drug blocked the degradation of brain cells that is the hallmark of Parkinson's disease. 

"It is amazingly protective of target nerve cells," said Ted Dawson, Professor at the University's School of Medicine.

The drug, named NLY01, is similar to compounds used to treat diabetes and is expected to move to clinical trials this year. 

If successful in humans, it could be one of the first treatments to directly target the progression of Parkinson's, not just the muscle rigidity, spasmodic movements, fatigue, dizziness, dementia and other symptoms of the disorder, Dawson said in the paper published in the journal Nature Medicine

In a preliminary experiment in laboratory-grown human brain cells, Dawson's team treated human microglia -- a brain cell type that sends signals throughout the central nervous system in response to infection or injury -- with NLY01 and found that they were able to turn the activating signals off. 

Further, the researchers injected the mice with alpha-synuclein -- the protein known to be the primary driver of Parkinson's disease -- and the mice treated with NLY01 maintained normal physical function and had no loss of dopamine neurons, indicating that the drug protected against the development of Parkinson's disease.

In another experiment, the team used mice that were genetically engineered to naturally produce more human-type alpha-synuclein typically used to model human Parkinson's disease that runs in families. 

While under normal conditions, these so-called transgenic mice will succumb to the disease in 387 days, those treated with NLY01 extended the lives by over 120 days.

However, the experimental drug must still be tested for safety as well as effectiveness in people, Dawson cautioned.

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Mumbai (PTI): The Mumbai-bound carriageway of the Mumbai-Pune Expressway connecting link was opened to vehicular traffic on Saturday noon after a delay caused by the dismantling of inauguration infrastructure and cleaning work, a day after the Pune section became operational.

The 13.3 km-long "missing link", which bypasses a section of the Bhor Ghat stretch of the expressway and cuts travel time between Mumbai and Pune by 25 to 30 minutes, was inaugurated a day earlier by Chief Minister Devendra Fadnavis in the presence of Deputy CMs Eknath Shinde and Sunetra Pawar.

The Pune-bound carriageway of the corridor was opened to traffic immediately; however, the Mumbai-bound section remained closed to traffic for several hours after the inauguration.

An official of the Maharashtra State Road Development Corporation told PTI on Saturday that the opening of the Mumbai-bound carriageway was delayed mainly due to the dismantling of the inauguration infrastructure and cleaning work.

The removal of the stage and other decorations was completed in the morning. The work to load and transport the material slightly delayed the opening of the carriageway.

Vehicular movement on the carriageway began after all the remaining material was cleared and road cleaning was completed, the official added.

The expressway control room said that despite significant vehicular movement, the access-controlled highway has not witnessed any major traffic snarls since Friday evening, after the Pune-bound carriageway of the missing link was opened to traffic.

The Missing Link project connects Khopoli (in Raigad) on the Mumbai side to Kusgaon near Lonavala in Pune district and is expected to make the expressway fully access-controlled, easing congestion in the ghat section.

Developed by the MSRDC and dubbed an "engineering marvel", the project includes two tunnels, two viaducts and a cable-stayed bridge over Tiger Valley. It bypasses the steep, accident-prone ghat section, where frequent traffic snarls are reported during weekends and on public holidays.