Category: Dementia

Damage to the brain can occur 15 to 20 years before the clinical symptoms appear.

A disrupted body clock, leading to sleep problems, could be an early sign of Alzheimer’s, research finds.

Changes in the sleep cycle occur much earlier than memory problems or other symptoms of dementia.

The finding is an important sign because damage to the brain can occur 15 to 20 years before the clinical symptoms appear.

Dr Erik S. Musiek, the study’s first author, said:

“It wasn’t that the people in the study were sleep-deprived.

But their sleep tended to be fragmented.

Sleeping for eight hours at night is very different from getting eight hours of sleep in one-hour increments during daytime naps.”

Studies in people and animals have now linked poor sleep to higher levels of amyloid protein build-up in the brain.

Amyloid is thought to be a cause of Alzheimer’s.

Dr Musiek said:

“Over two months, mice with disrupted circadian rhythms developed considerably more amyloid plaques than mice with normal rhythms.

The mice also had changes in the normal, daily rhythms of amyloid protein in the brain. It’s the first data demonstrating that the disruption of circadian rhythms could be accelerating the deposition of plaques.”

For the study, 189 normal older adults with an average age of 66 were tracked.

50 of these turned out to have problems with sleep.

Dr Yo-El Ju, study co-author, said:

“In this new study, we found that people with preclinical Alzheimer’s disease had more fragmentation in their circadian activity patterns, with more periods of inactivity or sleep during the day and more periods of activity at night.”

It is not yet known if poor sleep is contributing to Alzheimer’s or whether it is a symptom of the disease’s early stages.

Dr Ju said:

“At the very least, these disruptions in circadian rhythms may serve as a biomarker for preclinical disease.

We want to bring back these subjects in the future to learn more about whether their sleep and circadian rhythm problems lead to increased Alzheimer’s risk or whether the Alzheimer’s disease brain changes cause sleep/wake cycle and circadian problems.”

The study was published in the journal JAMA Neurology (Musiek et al., 2018).

Dementia risk doubled in people with high on this major personality trait.

Being neurotic may double the risk of developing dementia later in life, research reveals.

The major personality trait of neuroticism involves a tendency towards worry and moodiness.

People who are neurotic are more likely to experience negative emotions like depression, anxiety, guilt and envy.

However, the link between neuroticism and dementia only occured in people experiencing long-standing stress.

In other words, neurotic people are particularly sensitive to chronic stress.

Neurotic people not exposed to excessive stress were at no greater risk of dementia.

Dr Lena Johannsson, the study’s first author, said:

“We could see that the women who developed Alzheimer disease had more often been identified in the personality test 40 years earlier as having neurotic tendencies.

We found a clear statistical correlation for the women who had at the same time been subject to a long period of stress.”

The study followed 800 women with an average of 46 for almost four decades.

They were asked if they had experienced prolonged periods of stress.

This meant a month or more of ongoing stress related to family, work or health that created feelings of nervousness, fear and irritability.

Thirty-eight years later, one-in-five had developed dementia.

The risk was substantially higher, though, in those who were neurotic.

An even more vulnerable group were those who were both neurotic and introverted — women with this combination were at the highest risk.

Dr Johannsson said:

“We know that many factors influence the risk of developing dementia.

Our personality may determine behavior, lifestyle and how we react to stress, and in this way affect the risk of developing Alzheimer disease.”

However, neuroticism can be changed by therapy and its effects can be reduced.

Dr Johannsson said:

“Some studies have shown that long periods of stress can increase the risk of Alzheimer disease, and our main hypothesis is that it is the stress itself that is harmful.

A person with neurotic tendencies is more sensitive to stress than other people.”

The study was published in the journal Neurology (Johansson et al., 2014).

90% use too much of an everyday substance that can cause inflammation of blood vessels in the brain, which is linked to dementia.

A high-salt diet is linked to cognitive decline and possibly dementia, research finds.

Salt causes the delicate lining of the brain’s blood vessels to inflame, because of signals sent from the gut.

Fully 90 percent of Americans consume above the recommended dietary maximum of 2,300 mg per day.

Dr Costantino Iadecola, study co-author, said:

“We discovered that mice fed a high-salt diet developed dementia even when blood pressure did not rise.

This was surprising since, in humans, the deleterious effects of salt on cognition were attributed to hypertension.”

The effect was quickly reversed by lowering salt intake.

The conclusions come from a study in which mice were fed a high-salt diet that is equivalent to a high-salt diet in humans.

Subsequently, the mice had much worse cognitive function.

Their brains showed 28 percent less activity in the cortex and 25 percent less in the hippocampus.

They had problems getting around a maze and did not show the usual interest in new objects placed in their cage.

They also had poorer blood flow in their brains and the integrity of the blood vessels there was worse.

However, these changes were reversed once the mice were returned to a normal diet.

The scientists found that these changes had nothing to do with higher blood pressure.

Worse cognitive functioning in the mice was seen even when the mice had normal blood pressure.

They were the result of signals sent from the gut to the brain.

These activated an immune response in the brain which increased levels of interleukin-17.

This eventually resulted in the inflammation of the delicate lining of the brain’s blood vessels.

The study was published in the journal Nature Neuroscience (Faraco et al., 2018).

Usually neurons shrink while we sleep, allowing waste products to clear.

A single night of lost sleep increases proteins in the brain linked to Alzheimer’s, research shows.

People not allowed to sleep for one night showed elevated levels of beta amyloid, the clumps of protein seen in the brains of people with Alzheimer’s.

As these build up, they hamper the brain’s ability to function.

Dr Ehsan Shokri-Kojori, the study’s first author, said:

“We certainly show that even oe night of sleep deprivation can increase the levels of these harmful beta amyloid compounds.

That’s a very logical assumption, I would say, and it’s consistent with prior research.”

The researchers recruited 20 healthy people who were allowed to sleep normally one night and were kept up the next night.

Brain scans were used to assess levels of beta amyloid.

Dr Ehsan Shokri-Kojori explained:

“…the beta amyloid increases were observed in regions of the brain important to memory and thought.

These included the hippocampus, which has been tied to memory, and the thalamus, which is an important hub for relaying sensory information to the brain.”

Usually, while we sleep, neurons in the brain get smaller, which allows waste products to be cleared.

Dr. Andrew Varga, a sleep scientist not connected to the study, said:

“It makes intuitive sense that if you have chronically high levels of beta amyloid they would congregate together and form plaques, but that piece of it is not fully fleshed out.”

The study was published in the journal Proceedings of the National Academy of Sciences (Shokri-Kojori et al., 2018).

The fruits and vegetables that provide the highest protection against cognitive decline.

Certain fruits and vegetables that contain antioxidant flavonols appear to protect against cognitive decline.

Flavanols, which are a type of flavonoid, are found in nearly all fruits and vegetables, as well as in tea.

Consuming around one cup of dark leafy greens each day is linked to retaining stronger cognitive abilities with age.

Kaempferol and myricetin

A flavanol called kaempferol was linked to the highest level of protection by the research.

Typical foods that contain high levels of kaempferol include beans, tea, kale, spinach and broccoli.

Another flavanol called myricetin was also protective, although not quite to the same extent as kaempferol.

Typical foods that contain high levels of myricetin include wine, tea, kale, oranges and tomatoes.

Quercetin, which is found in tea, apples, kale and tomatoes was also protective, but at a still lower level.

Dr Thomas M. Holland, the study’s first author, said:

“It’s exciting that our study shows making specific diet choices may lead to a slower rate of cognitive decline.

Something as simple as eating more fruits and vegetables and drinking more tea is an easy way for people to take an active role in maintaining their brain health.”

Slowing cognitive decline

For the study, almost 1,000 people were divided into groups based on the amount of flavanols in their diet.

The group consuming the most flavanols got 15 mg a day — the amount that would come from a single cup of dark leafy greens.

Study participants were tracked over an average of 7 years and given regular cognitive tests.

These revealed that people who consumed the highest levels of flavanols experienced the slowest decline in their cognitive abilities.

The study’s authors explained:

“Results suggest dietary intakes of total flavonols and several flavonol constituents may be associated with slower decline in global cognition and multiple cognitive abilities with older age.”

As with any correlational research like this one, the study cannot prove that there is a link, merely that there is an association.

Related

• People who eat more foods containing flavanols have a lower risk of developing Alzheimer’s.

The study was published in the journal Neurology (Holland et al., 2022).