Conclusion
In conclusion, progresses in the treatment of AD have been made upon discovering the pathogenesis of the disease. In particular, the discovery of protective mutation, A673T, has verified the possibility of BACE inhibitors to prevent the generation of beta amyloid plaques and that of PTI-125 is found to inhibit the toxic signalling cascade mediated by Aβ42 to prevent neurofibrillary tangles. Although there are challenges that prevent these compounds to be developed and used clinically, they are truly medical breakthroughs that provide clues for better cures of AD. In the near future, AD will no longer be a mysterious fatal disease which goes beyond our understanding and control.
In conclusion, progresses in the treatment of AD have been made upon discovering the pathogenesis of the disease. In particular, the discovery of protective mutation, A673T, has verified the possibility of BACE inhibitors to prevent the generation of beta amyloid plaques and that of PTI-125 is found to inhibit the toxic signalling cascade mediated by Aβ42 to prevent neurofibrillary tangles. Although there are challenges that prevent these compounds to be developed and used clinically, they are truly medical breakthroughs that provide clues for better cures of AD. In the near future, AD will no longer be a mysterious fatal disease which goes beyond our understanding and control.
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