Normal proteins, if misfolded, form insoluble aggregates or fibrils, resistant to proteolytic degradation. Such proteins, named amyloid proteins, share a common structural motif, called the cross β sheet structure. The insoluble β-amyloid fibrils have been implicated in neurodegenerative diseases such as Alzheimer's disease (AD). Prions have structural similarities with β-amyloid fibrils. As microbial keratinases can degrade prions, we investigated the possible capacity of microbial keratinases, purified in our lab, for degrading β- amyloid fibrils. Lysozyme is a model system to study protein misfolding. β-Amyloid fibrils of lysozyme were prepared by treating Hen Egg White Lysozyme (HEWL) with 8M Urea for 48 h at 55°C. The fibril formation was confirmed by formation of a fibrous precipitate, immunoblotting with anti β-amyloid antibody, High Performance Liquid Chromatography (HPLC), and Congo Red Absorption spectroscopy. Using Q Sepharose Column Chromatography, two microbial keratinases, Ker1 and Ker2 were purified from an actinomycete strain, Amycolatopsis sp. MBRL 40, previously isolated in our laboratory (MBRL). β-amyloid fibril degrading activity of these keratinases were investigated both in solution or as reconstituted form on cationic/neutral liposomes. Both soluble and reconstituted Ker1 degraded β-amyloid fibrils as confirmed by loss of fibrous precipitate of β-amyloid fibrils, changes in the spectra as observed in HPLC and Congo Red Absorption spectroscopy and loss of signal when immunoblotted with anti β-amyloid antibody. Details of the findings on degradation of β-amyloid degradation by keratinase (Ker1) of indigenous Amycolatopsis sp. MBRL 40 obtained in our laboratory and its potential as a therapeutic option for neurodegenerative diseases shall be presented in this oral paper. Many drugs for treating Alzheimer's disease (AD) are in various stages of clinical trials. These drugs either inhibit the activity of acetylcholinesterase or inhibit the formation of Aβ plaques and their downstream effects e.g. Ca++ channel antagonists, nonsteroidal anti-inflammatory drugs, antioxidants, iron chelators, hypolipidemic drugs etc. Microbial keratinases are novel molecules in this sense as they haven't been investigated so far and we propose these enzymes as new potential therapeutic interventions for neurodegenerative diseases such as AD.