New Scientist - USA (2021-11-06)

6 November 2021 | New Scientist | 49

single night without sleep can increase levels

of beta-amyloid in our brains. But lack of

sleep can also promote tau accumulation

and inflammation in the brain. Additionally,

the mechanisms controlling our body clock

may play a role in the development of

neurodegenerative disease, says Erik Musiek

at Washington University in St Louis, Missouri,

by regulating sleep patterns and inflammation.

Drugs currently used to treat sleep disorders

such as insomnia could be useful against

Alzheimer’s as well, says Musiek. Mouse

studies have shown that a type of drug known

as an orexin antagonist reduces beta-amyloid

levels in the brain. A clinical trial in humans

is expected to start this month.

Musiek says that working out how sleep

and our body clock protect our brains is

important for finding new treatments. “If

we knew that when we sleep it activates this

particular pathway in this particular kind of

cell, and that’s why [sleep] is protective, then

you could just make a drug that does that.”

In the meantime, there is plenty we can do to

improve the quality of our sleep, which, unlike

prescription drugs, has no negative side effects.

The American Academy of Sleep Medicine

recommends getting at least 7 hours per night

and adopting good habits such as maintaining

a consistent sleep schedule and avoiding bright

light and caffeine in the evenings.

A blow to the head

We now know that brain injury can increase

the risk of developing dementia later in life:

one study of more than 350,000 people found

that even mild head injuries more than double

the risk of dementia. While Alzheimer’s is the

most common form of dementia, there isn’t

conclusive evidence that head injury leads to

it specifically, says Kristen Dams-O’Connor,

a neuropsychologist and specialist in brain

injury at Mount Sinai Hospital in New York.

There is overlap between Alzheimer’s

symptoms and those experienced after

traumatic brain injury “which can make

it difficult to disentangle them”, she says.

It is important to stress that brain injuries

are just one of many risk factors, and even

if people who have had a traumatic brain

injury (TBI) are, on average, at a greater risk

But what kicks off inflammation and TNF

production in the first place? While genes

are one factor, Tansey’s research also suggests

that diets high in fat and sugar can lead to

inflammation and immune dysregulation,

including in the brain. Blocking TNF can

prevent many of these effects, she says.

It remains to be seen if these findings can be

translated into treatments. Until then, there

may be other ways to reduce inflammation.

While there are some exceptions, research

generally shows that exercise and diets low

in red meat, saturated fat and sugar support

healthy brain function as we age.

Off to sleep

Again and again, studies have linked

Alzheimer’s disease and sleep problems,

but the nature of this relationship isn’t fully

understood – and probably goes both ways.

While we sleep, potentially harmful proteins

are flushed away by the brain’s waste-removal

apparatus, the glymphatic system. Even a

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“ Alzheimer’s, as currently understood,

is really not a single disease”

While many scientists
study factors that increase
our risk of developing
Alzheimer’s disease,
others are interested in
factors that promote
resilience to it. One way to
study this is by looking at
families with rare genetic
mutations that almost
always lead to early-onset
Alzheimer’s. Occasionally,
someone will inherit this
mutation but won’t go on
to develop the disease.
In one case, a woman
had another rare genetic
mutation called the
Christchurch mutation in

the APOE gene, which

appeared to be protective.

APOE plays a role in

Alzheimer’s (see main

story) and studying its

harmful and protective

functions may lead to

therapies.

Another research group

has identified resilient

individuals who don’t

carry the Christchurch

mutation, hinting that

other genetic protective

factors may be at play too.

We can’t change our

genes (at least not yet).

However, several studies

have suggested that

people with higher

cognitive reserve are

more resilient to cognitive

decline related to

Alzheimer’s disease,

meaning they maintain

normal functioning

despite build-up of

plaques in their brains.

Cognitive reserve

appears to be at least

partially under our

control, factors like

higher education and

bilingualism and even

whether you have a

stimulating job seem

to promote resilience to

dementia symptoms.

Reserve and

resilience