I am working on peptide therapeutics for Alzheimer’s disease (AD). AD is a neurodegenerative disease in which the β-amyloid peptide (Aβ₄₂) aggregates in the brain to form amyloid plaques, which leads to the death of nerve cells. Currently, no therapeutic molecules are available in the market to treat AD patients. The approaches to disrupt Aβ₄₂ fibrillar aggregates are small molecules, nanoparticles, metal chelators, peptides, and chaperones, etc.

Our work comprises the design of peptide-based inhibitors especially cyclic peptides (CPs). We choose CPs because they are proteolytically stable, precise, and tight binding with Aβ₄₂ aggregates and they can cross the Blood-Brain Barrier (BBB). The inhibitor peptide sequences design from the amyloid core-forming segment ¹⁶KLVFF²¹as a template of Aβ₄₂. The synthesis of peptide inhibitors using peptide chemistry, and its characterization against Aβ₄₂ for fibrils disruption. The techniques we are using for peptide synthesis are solid-phase peptide synthesis. We purify peptides using high-performance liquid chromatography. Aβ₄₂ fibrils inhibition is studying by a dye-binding Thioflavin-T assay, Congo red, and ANS assay. Peptide conformational study by Circular Dichroism Spectroscopy, fibrils morphology by Transmission Electron Microscopy, and rescuing of Aβ₄₂ induced cell cytotoxicity of cyclic peptides are studying by MTT assay.

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