27-NOV-2018: AMU researchers claim to find immune-suppressive agent to check Alzheimer's disease
ALIGARH November 27: Dr Shadab Kazmi and Mr Anzar Abdul Mujib, research fellows associated with Prof M Owais' laboratory, Interdisciplinary Biotechnology Unit, Aligarh Muslim University have "established" potential of a new formulation for treatment of Alzheimer's and other related amyloid-associated neurological diseases. Result of decades of painstaking efforts, a new research approach has brought the Aligarh Muslim University one step closer to a remedy that targets the neurological hallmarks of Alzheimer's disease and prevention from this disease may soon become a possibility.
Explaining the fresh research inputs, Prof Owais said that current treatments for Alzheimer's hardly make any impact on its progression, so the search for effective alternatives is an ongoing binge. It is speculated that targeting amyloid buildup might make it possible to stop Alzheimer's in its tracks. Many scientists are on the hunt for a remedy. However, in their latest research paper published in Nature's Scientific Reports, Dr Shadab Kazmi and Mr Anzar Abdul Mujeeb have suggested a new approach to prevent progression of the disease.
Excited by the findings, Prof Owais said, "This study is the culmination of a decade of research that has repeatedly demonstrated that this technique can effectively and safely target in animal models what we think may cause Alzheimer's disease," adding, "I believe we are getting closer to testing this therapy in humans".
He said that the researchers started testing various small peptides for their putative anti-amyloid activity. A novel formulation based on immune-suppressive agent cyclophosphamide was developed by injecting DNA coding for amyloid into the skin rather than the muscle. By its specific interaction with amyloid intermediates, the cyclic peptide seems to regulate fibrillation process in concentration dependent manner. The present study further suggests that exposure to peptide during initial phase ensues in reversal of beta-amyloid fibrillation process. This cyclic peptide sparked generation of antibodies that target ab42. The peptide prevented the buildup of amyloid plaques and also indirectly prevented the build up of another protein that play crucial role in induction of Alzheimer's disease.
"The current study examined this response in mice and found that the strategy induces reduction in beta-amyloid formation and significantly, there were no adverse immune reactions", added Prof Owais.
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Related PicturesMr Anzar Abdul Mujib