ABSTRACT
Tau is an axonal protein known to form abnormal aggregates and is the biomarker of Alzheimer’s disease. Metal-based therapeutics for inhibition of Tau aggregation is limited and rarely reported in the contemporary science. Here, the first example is reported of a rationally designed molecular cobalt(II)-complexes for effective inhibition of Tau and disaggregation of preformed Tau fibrils. The mechanistic studies revealed that the prevention of Tau aggregation by CBMCs is concentration-dependent and Tau seldom exhibits conformational changes. Interestingly, CBMCs play a dual role by causing disassembly of preformed aggregates as well as complete Tau inhibition. We believe that this unprecedented finding by the newly developed molecular complexes has a potential to lead to developing innovative metal-based therapeutics for Alzheimer’s disease.
Abbreviations used
- AD
- Alzheimer’s Disease;
- Aβ
- Amyloid β;
- CBMCs
- Cobalt-Based Metal Complexes;
- NFTs
- Neurofibrillary Tangles;
- MTs
- Microtubules;
- PHFs
- Paired Helical Filaments;
- APP
- Amyloid Precursor Protein