HealthCare

A Mumbai-based scientist's path-breaking research on rogue proteins in human brain that cause Alzheimer's has brought new hope in the global quest for finding a treatment for the degenerative disorder previously thought to be incurable.

Dr Sudipta Maiti, a professor at the Department of Chemical Sciences, TATA Institute of Fundamental Research (TIFR), and his team have found that it is possible to reverse the behaviour of Amyloid Beta protiens that cause Alzheimer's when they depart from their prescribed function of aiding human memory and cognitive behavior. These renegades join hands with other similarly misbehaving protiens, and together they attack brain cells impairing speech, judgement, memory, perception and behaviour.

Dr Maiti's research showed that when these gangs of bad-boy Amyloid Beta protiens are separated from each other, they return to their original form and resume originally prescribed functions, mainly related to aiding human memory and cognitive behavior. So far it was believed that the Amyloid Beta oligomers - science jargon for gangs of bad-boy protiens - were a stable bunch and did not return to their normal state. With Dr Maiti's research, this thinking is bound to change. Alzheimer's Disease International, a federation of non-profit organizations promoting awareness about the disease, has estimated that as of 2010, there were 35.6 million people with dementia worldwide. By 2050, it is projected that this figure will have increased to over 115 million. Since Alzheimer's is an old-age disease and India's life expectancy has been rising rapidly, one is likely to hear more about it in the coming years.

Dr Maiti's team demonstrated the mob mentality of Amyloid Beta protiens gone bad by creating Alzheimer's disease in a test tube. They placed monomers (single units) of Amyloid Beta in a water-based solution at a normal concentration of 100 nm (nanomolar), mimicking the human brain fluid (cerebro spinal fluid). "When we increased the concentration of the fluid above normal, we observed that the Amyloid Beta protein started forming oligomers (multiple units). These oligomers, together, were toxic enough to cause Alzheimer's," he said. However, when the concentration of artificial brain fluid was lowered to normal again, Amyloid Beta oligomers split back into individual units, lost their toxicity and, in fact, returned to performing their original assigned tasks.

"We were able to reverse the Alzheimer's disease in the test tube. We discovered that after seven days of lowering the concentration of the brain fluid, the oligomers became unstable and broke out from the group to form harmless monomers of the protein found in healthy brains," Maiti said.

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The small biotechnology company and the Swiss pharmaceutical giant will develop Evotec has signed a new agreement with partner Roche to develop a compound with potential in Alzheimer's disease, replacing an antidepressant programme which was dropped in May.

The German biotechnology company said it will receive $10 million in upfront licensing fees as a result of Roche's decision to collaborate on the development of the new compound, a monoamine oxidase type B inhibitor codenamed EVT-302.

The agreement could also see Evotec receive development and milestone payments up to $820m and tiered double-digit royalties on sales should the drug candidate reach the market. Proof-of-concept clinical trials are scheduled to start next year.

As a result of the latest deal Evotec has raised its revenue forecasts for 2011 to 77-79 million euros from an earlier prediction of 70-72 million euros. MAO-B inhibitors are thought to work in Alzheimer's disease by blocking the breakdown of neurotransmitters and interrupting the formation of reactive oxygen species (ROS) involved in the inflammation and degeneration of neurons which are the hallmark of Alzheimer's disease.

"For these reasons, the selective MAO-B inhibitor is targeted to treat AD symptoms and potentially slow disease progression," said Evotec in a statement.

EVT-302 joins other programmes at Roche targeting two other key characteristics of Alzheimer's disease, namely amyloid plaques and tau proteins.

The Swiss drugmaker's lead programmes are gantenerumab and RG7412, both of which are monoclonal antibodies targeting the amyloid pathway which are currently in Phase II trials.

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Under the terms of the agreement, Roche will pay Evotec an upfront fee of $10 million, which analysts view as the main reason for the steep share gains.

Evotec could then receive further development and commercial milestone payments of up to $820 million, as well as tiered double-digit royalties on sales. Roche will initiate studies in 2012 to demonstrate proof of concept and will be responsible for all clinical development, manufacturing and commercialization activities.

Evotec, which generated revenue of EUR55.3 million in 2010, has been continuing to seek alliances with large pharmaceutical companies due to the risks and high costs involved in developing new drugs.

"This shift in strategy away from the cost-intensive own research is paying off," said an analyst, who wished to remain anonymous. "Roche is a major partner and Alzheimer's a widespread disease in the center of research," he said.

At 1000 GMT, Evotec shares traded up as much as 16% at EUR2.14, while the TecDAX was up 0.2%.

Alzheimer's disease is the most common cause of dementia and, according to the World Health Organization, affects around 35 million people worldwide.

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