Published: 00:59 BST, 18 August 2026 | Updated: 06:49 BST, 18 August 2026
Ask a firefighter if you can put out a blaze by only tackling the smoke, and not the flames themselves, and you can imagine their response.
Yet this is the same situation neurologists have been facing for decades when treating Alzheimer’s disease: merely being able to temporarily treat the ‘smoke’ of the disease – the symptoms.
I have been a neurologist for more than 40 years, and specialise in treating people with Alzheimer’s and other neurodegenerative diseases.
When I lecture around the world about the ‘smoke, not fire’ challenge, people ask me about the slow pace of research to find an effective treatment.
Why, they ask, if drug companies have been pouring billions of dollars into Alzheimer’s research, have scientists not yet found something to cure, or even prevent, this pernicious disease?
The short answer I believe is because researchers have been focused on the wrong issue when it comes to Alzheimer’s.
We have been told effective treatment for the disease requires the removal of beta- amyloid plaques in the brain that are common in patients.
But while beta-amyloid plaques do contribute to Alzheimer’s, by increasing inflammation, they are not the root cause of it.
Dr David Perlmutter, a neurologist for more than 40 years, says researchers have been focusing on the wrong area when trying to treat Alzheimer's
Dr Perlmutter argues the fundamental cause of Alzheimer’s lies in the activation of the brain’s specialised resident immune cells, called the microglia
Instead – as I discuss in my new book, Brain Defenders: Harness The Power Of Your Immune Cells To Protect Your Brain For Life – the fundamental cause of Alzheimer’s almost certainly lies elsewhere: in the activation of the brain’s specialised resident immune cells, called the microglia. They clean up dead cells, fight infections and help keep brain tissue healthy.
But studies also show that chronic (rather than acute, i.e. short term) activation of these immune cells by, for example, having type 2 diabetes or obesity – can drive increased beta-amyloid production, as well as impair its clearance.
So beta-amyloid build-up in Alzheimer’s patients is a consequence of the behaviour of the microglia – and research, then, should have been focusing on ways to target this behaviour as a way to treat the condition effectively.
Yet the ‘amyloid hypothesis’, as it is known, continues to wield incredible influence – something I find shocking considering the often serious side-effects caused by the medications created to ‘treat’ amyloid plaques, including brain bleeds and swelling.