I was sitting in a conference in August, drifting as I so often do between listening to what was on stage and pretending to be doing important work on my laptop (by which I mean sending memes on WhatsApp).
All of a sudden, from the stage, the renowned biologist came out with a sentence that made every single person in the room sit up and pay attention: 鈥淥f course,鈥� she said, 鈥渨e now know that 础濒锄丑别颈尘别谤鈥檚 starts in the nose.鈥�
I鈥檓 sorry, what? Starts in the nose? I didn鈥檛 know 础濒锄丑别颈尘别谤鈥檚 starts in the nose.
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My own lovely dad died from 础濒锄丑别颈尘别谤鈥檚 last year, and ever since his diagnosis, I鈥檝e done an incredible amount of digging into the disease, trying to understand what was happening to him. I was astonished I鈥檇 never come across this idea.
And perhaps you haven鈥檛 either. Which is why I want to share my astonishment at discovering that Aviv Regev was right 鈥� not only is 础濒锄丑别颈尘别谤鈥檚 closely associated with our sense of smell, but there is a growing body of research suggesting that our noses might have something to do with why the disease develops in the first place.
The first bit you might already know: people with 础濒锄丑别颈尘别谤鈥檚 tend to lose their sense of smell, sometimes years before any symptoms of memory loss start to show up. But it turns out that our ability to smell is a surprisingly good indicator of our overall health (looking at you, covid-19). One study from 2014 found that of whether they would be dead within five years than a cancer diagnosis.
It鈥檚 not that losing your sense of smell itself will kill you. More that the olfactory nerves are deeply intertwined with some of the most important memory structures in the brain, so when they start to deteriorate, it can be an early warning that something much more serious is going on.
And this connection seems to work in both directions. One intriguing study (admittedly with quite a small sample size) , thus exposing them to all kinds of wonderful scents while they slept. After six months, the people who had the olfactory enrichment performed better on memory tests than those in a control group.
All very interesting. But not what Regev had been suggesting. Her words seemed to imply that noses are actually responsible for the trouble in the first place.
It turns out that the reason scientists are even entertaining this possibility is because of how fiercely our brains are protected from the outside world. Our skulls are like an actual fortress: even our blood isn鈥檛 allowed in without passing a particularly fussy bouncer called the blood-brain barrier.
One of the only real exceptions is a little bit of bone right at the top of your nose that is riddled with holes. It鈥檚 called the cribriform, and it鈥檚 where the olfactory fibres dangle down into your nose to give you your sense of smell 鈥� a bit like if you pushed some Play-Doh through a sieve.
And that means that, despite all the elaborate defences protecting your brain, there is a potential route in, sitting right in the middle of your face.
So, here鈥檚 the idea. Maybe the beta-amyloid plaques, the sticky little protein fragments that appear to play such a key role in the cascade of 础濒锄丑别颈尘别谤鈥檚 in the brain, are what鈥檚 left over after the brain has fought an infection. And maybe the nose is how the infection arrives.
To see if this held any water, in 2022, a group of scientists of some mice.
(I should add, for the sake of the mice鈥檚 reputation, that it was actually Chlamydia pneumoniae, a cousin of the bacterium that causes the STI. But I hope you鈥檒l forgive me the less scientifically accurate version. In a long career, you get very few chances to write sentences that good, and I wasn鈥檛 about to waste mine.)
The remarkable thing, though, was that within 72 hours, the bacteria had travelled up the nerves in the nasal cavity and got through to the brain. What鈥檚 more, the infection triggered the accumulation of beta-amyloid. Now that鈥檚 not definitive proof of how 础濒锄丑别颈尘别谤鈥檚 starts in humans. But there is some other, rather unsettling evidence that infections aren鈥檛 the only unwelcome visitors that manage to get in that way.
A group in Mexico . Inside the dogs鈥� brains, they found microscopic particles of metals 鈥� that seem to have entered through the nose 鈥� wrapped in pockets of inflammation and that same beta-amyloid protein. You don鈥檛 see the same thing in dogs that lived in cleaner, more rural environments.
Now these studies have been extended to who died from gun violence or car accidents 鈥� and they find something similar. Tiny, metal鈥搑ich particles, thought to originate from exhausts and brake dust, turned up in their brain tissue, alongside inflammation and accumulations of beta-amyloid. The very sorts of changes associated with 础濒锄丑别颈尘别谤鈥檚, appearing in brains that were sometimes only a few years old. Put together, it implies that the disease might have an environmental cause, one that begins much much earlier than we thought.
So, where does 础濒锄丑别颈尘别谤鈥檚 start? The answer is no one nose (pun very much intended). There is still a great deal we don鈥檛 understand, but the implications from all this research are rather extraordinary. What if the beta-amyloid plaques we鈥檝e spent so long trying to get rid of are, at least sometimes, the aftermath of the brain trying to protect itself? And what if, rather than focusing entirely on clearing up the damage, we could work out what set it off in the first place?
But more than anything, I can鈥檛 help but laugh as I think about all this in the context of my dad, who had many wonderful qualities, but a discreet nose wasn鈥檛 one of them. We used to say that his nose would enter a room 15 minutes before he did. He would have found it very funny indeed if it turned out to have been the cause of his downfall.
