This article was taken from: https://www.theguardian.com/commentisfree/2018/sep/25/cure-for-alzheimers-new-drug
By Dean Burnett
The headlines claim treatment will be available within six years. The reality is a lot more complex
A new study has inspired headlines claiming a cure for Alzheimer’s disease could be available within six years – but are we genuinely on the verge of an effective treatment?
Given the physical, emotional and financial cost that Alzheimer’s and similar dementias inflict – something that’s only going to get worse as the population ages – this would obviously be a massive boon. But as always, the picture is a lot more complex.
In fairness to the researchers at Cambridge and Lund universities, the press release itself shies away from such definite claims, only going so far as to say that trials for a drug modelled on their results could begin within two years. The more grandiose claims seem to come from a lead author on the study making (personal?) comparisons with similar trials’ progress.
So is this yet another bold prediction that will end in crushing disappointment, as seems to be happening a lot lately?
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.
However, many others, including those behind the current study, assert that its oligomers – even smaller molecules that occur naturally in neurons and similar – that are causing the damage, and that the tangles and plaques are consequences of this. Ergo, removing those larger molecular deposits is tantamount to clearing the dead fish away from the town’s water supply: they’re not helping matters, but they’re clearly not what’s poisoning it. This new study suggests we could have drugs that tackle the source, not the downstream effects.
But, as ever, a note of caution is advisable amid all the hype. We’re talking about interfering with the intricate molecular processes that take place in every brain cell here; however necessary and useful that may be, the potential for harmful side effects is undoubtedly vast, so rushing ahead and hoping for the best is a very risky strategy.
There’s also the questionable use of the term “cure” in the many reports around this. Even if the drug works 100% effectively as hoped, the damage to the brain inflicted by Alzheimer’s and similar diseases is widespread and severe. And the human brain, particularly if it’s quite old already, has limited scope for repair in such circumstances. The human brain works thanks to complex and specific networks and connections between the various areas, and these are the result of a lifetime of development and experience.
Alzheimer’s causes widespread damage and destruction to neurons, and while stopping the process causing it will prevent things from getting worse, it won’t automatically mean things will get better. Even if we could somehow replace the lost brain cells in the damaged regions (which we can’t), to claim a full “cure”, we’d need to somehow shape and connect them so they’re exactly as they were.
Still, any progress is good at this juncture. But are we close to a cure for Alzheimer’s? As trite as it may be to end on such a scientific cliche, sometimes it’s just the truth: further research is needed.
• Dean Burnett is a doctor of neuroscience. He discusses ageing and dementia in his latest book, The Happy Brain