There are grounds for optimism here. Many experts assert that the reason so many previous drugs have failed to tackle Alzheimer’s is that they’ve been targeting the wrong thing. For years it was assumed that a key element in someone developing the disease was the presence of amyloid plaques, big clumps of excess protein that gather between the neurons in the brains of the afflicted. It makes sense: having big hunks of unyielding proteins gathering around the delicate neural connections is bound to be disruptive to the finer neurological processes, surely? So if you get rid of them, the brain should be able to function better.
And yet, that didn’t seem to happen: drugs that supposedly remove amyloid plaques don’t appear to cause any subsequent improvement in cognitive functioning. Could the whole premise that amyloid plaques cause Alzheimer’s be flawed?
According to many, yes. In more recent years, focus has shifted to other candidates, one of which is the build-up of misshapen proteins inside the brain cells, not between them. Neurofibrillary tangles, for example, occur when proteins become misshapen inside the neurons and potentially undermine the delicate cellular support systems.