Bioenergetics breakdown in Alzheimer's disease: targets for new therapies.

摘要: Alzheimer's disease is rapidly growing worldwide and yet there no cure for it. Currently available drugs only provide symptomatic relief do not intervene in process sufficiently enough to prevent or Characteristic features of this are decline neuronal mass cognitive functions. The most dominant hypothesis proposed pathogenesis called “amyloid hypothesis". It states that excessive production amyloid peptides abeta (Aβ) the underlying cause death dysfunction. However, recent designed based on have failed clinical trails, demanding fresh assessment. Early persistent molecular events progression energy deficiency high oxidative stress neurons. Our review will put together a model known human animal data with regards breakdown generation. integrate deficits as dysfunction peptide culminating catastrophic loss Finally, model, we also suggest enzyme targets bioenergetics pathway design development new modifying therapies.