Researchers at the Indian Institute of Technology (IIT), Guwahati claimed to have developed ways to prevent or reduce short-term memory losses associated with Alzheimer's disease.
The team claims their research has provided a different path that may extend the onset of Alzheimer's disease.
The four-member team has studied neurochemical principles of Alzheimer's to explore new ways to prevent accumulation of neurotoxic molecules in the brain, that are associated with short-term memory loss due to Alzheimer's.
The study has been published in reputed international journals including ACS Chemical Neuroscience, RSC Advances of Royal Society of Chemistry, BBA and Neuropeptides.
"The development of a cure for Alzheimer's disease is important especially for India, which has the third highest number of Alzheimer's patients in the world, after China and US, with more than four million people falling prey to the memory loss associated with it. While current treatments only alleviate some of the symptoms of the disease, there is no disruptive therapeutic approach yet that can treat the underlying causes of Alzheimer's," said Vibin Ramakrishnan, Professor at the institute's Department of Biosciences.
"Approximately hundred potential drugs for treatment of Alzheimer's disease have failed between 1998 and 2011, which shows the gravity of the problem. We have explored interesting methods such as application of low-voltage electric field and the use of 'trojan peptides' to arrest aggregation of neurotoxic molecules in the brain," he added.
According to Harshal Nemade, Professor at Department of Electronics and Electrical Engineering, the team found that application of a low-voltage, safe electrical field can reduce the formation and accumulation of toxic neurodegenerative molecules that cause short-term memory loss in Alzheimer's disease.
"We found that external electric or magnetic field modulates the structure of these peptide molecules, thereby preventing aggregation. Upon exposure to electric field, we could retard the degeneration of nerve cells to an extent of 17 35 per cent. Objectively, this would translate to about 10 years delay in the onset of the disease.
"However, it would take testing in animal models and clinical trials before bringing in such new therapeutic approaches into human treatment," he added.
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