What is Alzheimer's Disease?

Scientists aren’t absolutely sure what causes cell death and tissue loss in the Alzheimer's brain, but the plaques and tangles are prime suspects.

Does Memory Loss Always Mean Dementia?

Dementia is a broad category of symptoms that affect the brain and causes memory loss.

Early onset Alzheimer's

Although, Alzheimer’s is viewed as a disease of the elderly, up to 5% of Americans with Alzheimer’s have the early-onset variety, which can start to show symptoms as early as one’s 30s.

Showing posts with label Risk factors. Show all posts
Showing posts with label Risk factors. Show all posts

Saturday, January 26, 2019

Poor sleep increases Alzheimer’s brain proteins

poor sleep

A single night of poor sleep can cause a spike in brain proteins linked to Alzheimer’s disease, a new study reports.


Researchers from the U.S. and the Netherlands have found that sleep helps the body clear away two compounds in the brain, called amyloid and tau, and interrupted, poor sleep may cause too much of them to build up.

While the study doesn't show that poor sleep causes Alzheimer's, it adds one more piece to the puzzle of what causes dementia. [Read more Study:Access to nature makes men and seniors sleep better]
The team believes that the findings back the notion that chronic poor sleep in midlife could elevate the risk of developing Alzheimer's later in life.


“When people had their slow-wave sleep disrupted, their amyloid levels increased by about 10 percent,” says study leader Dr. Yo-El Ju of Washington University in St. Louis.

Although scientists knew there was a connection between dementia and poor sleep, it wasn’t clear whether dementia was driving insomnia or vice versa.

The study was jointly conductedby researchers from Washington University School of Medicine in St. Louis; Stanford University in California, in the U.S., and Radboud University Medical Centre in the Netherlands.

Alzheimer’s disease is a neurodegenerative disease that progresses rapidly. It is the most common cause of dementia, accounting for about 70% of all dementia cases. The disease affects memory, decision-making, language, thinking, and speech.

The brains of people with Alzheimer's disease feature two hallmarks of the disease – plaques of amyloid protein and tangles of tau protein. These plaques and tangles causes neuron cells to die.
In the UK, around 850,000 people are currently living with dementia, and the majority have Alzheimer’s disease, for which there is no cure. Although the number of dementia cases is dropping as people adopt healthier lifestyles, the number of people living with the illness is expected to rise to 1.2 million by 2040 because of the ageing population. [Read more Whatcauses aging? Can the process be slowed?]

More than a third of Britons also sleep for less than 6 hours a night, according to The Sleep Council.
For their study, the researchers sought to identify the most important phase of sleep.

“What we did was allow people to sleep a normal amount of time, but we prevented them from getting deep sleep or what is called slow-wave sleep,” Ju told NBC News.

“When we interrupted just the slow-wave sleep part, they still had an increase in amyloid. So this tells us it's getting the deep slow-wave sleep that's important for reducing the levels of amyloid.”
Ju and colleagues recruited 22 healthy adults aged between 35 and 65. All the participants reported experiencing no sleep problems and had no cognitive impairments.

The participants showed up in a controlled sleep lab. Half were allowed to sleep normally, while the other half were constantly kept in shallow sleep. [Read more Newprotein target may reverse memory loss in Alzheimer’s]

poor sleep

“As soon as they got into slow-wave sleep, they got a beep. And the beeps got louder and louder and louder until they came out of the deep sleep,” says Prof. Ju.

“It was pretty harsh.”

The participants didn’t realize their sleep had been interrupted, and this went on for the entire night.
The participants’ spinal fluid was analyzed in the morning.

“When people had their slow wave sleep disrupted, their amyloid levels increased by about 10 percent,” Prof. Ju says.

The subjects were also fitted with sleep monitors to measure theirsleep at home. Participants who experienced poor sleep at home were found to have higher levels of a second Alzheimer’s related protein called tau. [Read more Scientistsreport significant breakthrough in anti-aging]

Prof. Ju says they were not surprised to see that tau levels didn’t increase after only one night of poor sleep whereas this did cause amyloid levels to rise, since tau levels tend to change more slowly.
“But we could see, when the participants had several bad nights in a row at home that their tau levels had risen,” she adds.

Prof. Ju concludes by saying:

“At this point, we can't say whether improving sleep will reduce your risk of developing Alzheimer's. All we can really say is that bad sleep increases levels of some proteins that are associated with Alzheimer's disease. But a good night's sleep is something you want to be striving for anyway.”
Next, the team plans to study whether treating obstructive sleep apnea will improve people's slow-wave sleep and affect amyloid levels. Sleep apnea is a common cause of sleep disruption. People with this condition have a higher risk of developing dementia.

The study was published in the journal Brain.

Family History of Alzheimer’s May Explain Link of Metabolic Gene that Raises Risk for Disease

family history

Years of conflicting research that failed to pinpoint the missing link between a mitochondrial gene and the risk of Alzheimer’s may have finally been resolved by the scientists of Iowa State University (ISU) in the U.S. The researchers say that family history of Alzheimer's disease may be the missing link. It shows that having a family history of Alzheimer's disease appears to alter the behavior of the gene called TOMM40.

Lead researcher AurielWillette, assistant professor of food science and human nutrition at ISU, says the initial discovery of the gene TOMM40 gave the scientists impression that it raises the risk of Alzheimer’s. But the findings were later dismissed when several studies failed to replicate the results.
However, Willette and his colleagues weren’t convinced that the gene was a total failure, so they decided to examine other elements that may be producing the mixed results.

The researchers discovered a startling difference in the gene’s effect on cognitive function, memory and risk based on a family history of Alzheimer’s disease and the length of a specific part of the gene.
“It was kind of a shot in the dark, but we found if you don’t have a family history of Alzheimer’s disease, then having a longer version of the gene is a good thing. It is related to better memory up to 10 years later and about one-fifth of the risk for developing Alzheimer’s disease,” said Willette, who is also an adjunct assistant professor of neurology at the University of Iowa.

“However, if your mom or dad has Alzheimer’s, then having a long version is bad. It’s a complete polar opposite.”

The main pathological hallmarks ofAlzheimer’s disease are amyloid-β (Aβ) plaques, and neurofibrillary tangles, caused by tau protein. These plaques and tangles around the neurons eventually cause the neurons to die.

Outward symptoms start with mild memoryloss. As the symptoms progress, the person finds it increasingly difficult to hold a conversation or carry out everyday tasks such as button a shirt.
Although numerous studies being conducted worldwide are providing new clues, scientists still do not know the exact causesof Alzheimer's disease. They think that there are various factors, and some of these affect different people in different ways, according to the study.

family history of alzheimer's

Family history of Alzheimer’s and TOMM40

The researchers designed the study to explore the magnitude to which family history regulated the effects of TOMM40 on symptoms of Alzheimer's disease, such as thinking and memory loss.
They used data from two large studies of Alzheimer's disease. One set of data came from 912 adults in the Wisconsin Registry for Alzheimer's Prevention – a study which is following middle-aged adults at risk of developing Alzheimer's and following changes in cognitive function and memory loss, based on assessments carried out every 2 years for up to a decade.

The other set of data came from 365 participants in the Alzheimer's Disease Neuroimaging Initiative – a study which is monitoring similar changes in older adults with and without the disease.
The researchers found that having a family history of Alzheimer's disease appears to make a big difference in how TOMM40 affects memory and thinking, and that the difference depends on the length of a particular portion of the gene. [Read more Study:Access to nature makes men and seniors sleep better]

Prof. Willette and his team found that having the longer version of the gene, together with no family history of Alzheimer's, was linked to around a one-fifth lower risk of developing Alzheimer's disease and better memory up to 10 years later.

Family history was focused particularly on whether Alzheimer’s disease was found in a participant’s parents. The researchers also discovered a link between the family history, gene, and mitochondrial function, which produces energy to power the cells. Age, gender and education were controlled for in the examination of TOMM40 gene and family history in the participants.

The team is also involved in another project which is investigating factors that affect how the body makes and uses energy, such as insulin resistance, as well as proteins and enzymes that affect energy regulation.

Studies like these are slowly uncovering what happens to thinking and memory when there is not enough energy for brain cells to perform properly.

The study was published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.