Immunotherapies that target aggregation of amyloid-β in order to treat Alzheimer’s disease have a long and expensive history of failure. The tide finally seems to be turning, however, with the advent of several treatments that can reduce amyloid-β levels without resulting in an unacceptable level of risk for the patients. This newfound incremental success is taking place at the same time as the years of frustration with the lack of progress have finally blossomed into a variety of alternative theories on the causes of Alzheimer’s disease, such as blocked drainage of cerebrospinal fluid or persistent microbial infection, some of which have advanced to the point of development of therapies.
The challenge for amyloid-β clearance therapies is now to show benefits in patients, and there are good reasons to believe that this will be challenging in the late disease state. The present consensus on Alzheimer’s disease is that amyloid-β accumulation is an early phase, damaging yes, but nowhere near as damaging as the tau aggregation that occurs later on. Further, Alzheimer’s patients also tend to have other forms of neurodegeneration, such as vascular dementia, that are unlikely to be greatly affected by amyloid-β
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