Indian Institute of Technology Guwahati (IIT-G) on Wednesday said its researchers have discovered new ways that can help prevent or reduce short-term memory losses associated with the Alzheimers disease.
The research team explored new ways to prevent the accumulation of neurotoxic molecules in the brain that are associated with short-term memory loss due to Alzheimer’s disease.
They reported some methods such as the application of low-voltage electric field and the use of ‘trojan peptides’ to arrest aggregation of neurotoxic molecules in the brain.
The idea of using ‘Trojan peptide’ comes from mythological “Trojan Horse” used as subterfuge by the Greeks in the battle of ‘Troy’.
“Approximately hundred potential drugs for the treatment of Alzheimer’s disease have failed between 1998 and 2011, which shows the gravity of the problem,” lead researcher Vibin Ramakrishnan, Professor, Department of Biosciences & Bioengineering, IIT-G, said in a statement.
A defining hallmark of Alzheimer’s is the accumulation of Amyloid beta peptides in the brain. The research team seeks methods to reduce the accumulation of these peptides, in order to arrest the progression of Alzheimer’s.
Last year, the IIT-G researchers found that application of a low-voltage, the safe electrical field can reduce the formation and accumulation of toxic neurodegenerative molecules that cause short-term memory loss in Alzheimer’s disease.
They found that external electric/magnetic field modulates the structure of these peptide molecules, thereby preventing aggregation.
“Upon exposure to an electric field, we could retard the degeneration of nerve cells to an extent of 17–35 per cent. This would translate to about 10 years delay in the onset of the disease,” said Dr Ramakrishnan.
Working further in this area, the research team explored the possibility of using ‘Trojan peptides’ to arrest aggregation of these neurotoxic molecules.
They have designed ‘Trojan peptides’ by adopting a similar approach of ‘deceit’ to impede the aggregation of the amyloid peptide, arrest the formation of toxic fibrillar assemblies, and reduce poisoning of nerve cells that leads to memory loss.
“Our research has provided a different path that may extend the onset of Alzheimer’s disease. However, it would take testing in animal models and clinical trials before bringing in such new therapeutic approaches into human treatment,” the researchers noted.