For over a decade, scientists have thought that if amyloid protein is the primary problem in dementia, the key to treatment must be drugs which reduce its production or stimulate its clearance from the brain. Initial efforts however, whilst they reduced the amount of protein, did little to improve clinical symptoms and outcomes.
Studies are ongoing to determine whether giving drugs very early in the condition (in people for example with evidence of amyloid in their brains but no symptoms of dementia) can halt or even prevent it. Let’s hope they yield positive results.
However, what if amyloid isn’t in fact causing the problem, but is simply associated with it? Cause and association are not the same thing, as I mention regularly when describing clinical trials. Around 25% of patients with amyloid in their brains at post mortem have no evidence of dementia when alive. In addition, around a third of patients with overt dementia have no evidence of amyloid on brain scans. This scenario is common in…
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