Protein Aggregation and Neurodegeneration

We also have abundant experience in developing new peptide drugs to stop abnormal protein aggregation which is seen in various forms of neurodegenerative diseases like Parkinson’s disease, Alzheimer’s disease, and Amyotrophic lateral sclerosis (ALS). Using the high-throughput peptide array technology, we can efficiently find the minimum peptide sequence required for the self-binding of pathogenic proteins, and then effectively inhibit the protein aggregation by applying the synthetic peptide to the cells to interfere with protein-protein interaction. The peptide will be linked with a membrane-permeable sequence so that it is capable of penetrating the blood-brain barrier and the neuronal plasma membrane. One of such kind of interference peptides we have developed effectively inhibit the aggregation of TAR DNA-binding protein 43 (TDP-43), a nuclear protein that abnormally aggregates in the cytoplasm in ALS patients and thereby causes progressive deterioration of motor nerve cells in the brain and spinal cord.

TDP43