Category: Dementia

The simple self-treatment that prevents Alzheimer’s disease.

A simple daily regimen of the common painkiller ibuprofen along with dietary adjustments could prevent the onset of Alzheimer’s disease, new research concludes.

Ibuprofen is a widely available nonsteroidal anti-inflammatory that does not require a prescription.

The drug, along with adopting the Mediterranean diet and a healthy intake of antioxidants, could stop the disease in its tracks.

Until recently the problem has been identifying the disease early enough to take action.

Alzheimer’s is thought to begin around 10 years before any cognitive symptoms are noticeable.

The author of the new research, Dr Patrick McGeer (and colleagues), have developed a simple saliva test that can predict the onset of Alzheimer’s.

Dr Patrick McGeer, study co-author, explained:

“Knowing that the prevalence of clinical Alzheimer’s Disease commences at age 65, we recommend that people get tested ten years before, at age 55, when the onset of Alzheimer’s would typically begin.

If they exhibit elevated Abeta 42 levels then, that is the time to begin taking daily ibuprofen to ward off the disease.

Abeta 42 refers to a protein secreted in the saliva that is elevated in people at risk of developing Alzheimer’s.

It could provide the vital clue to start treatment early, Dr McGeer said:

“Unfortunately, most clinical trials to date have focused on patients whose cognitive deficits are already mild to severe, and when the therapeutic opportunities in this late stage of the disease are minimal.

Consequently, every therapeutic trial has failed to arrest the disease’s progression.

Our discovery is a game changer.

We now have a simple test that can indicate if a person is fated to develop Alzheimer’s disease long before it begins to develop. Individuals can prevent that from happening through a simple solution that requires no prescription or visit to a doctor.

This is a true breakthrough since it points in a direction where AD can eventually be eliminated.”

The study was published in the Journal of Alzheimer’s Disease (McGeer & McGeer, 2018).

When the microglia stop working properly, the brain begins to degrade.

A low-fat diet and restricting calorie intake helps reduce brain aging in mice, new research finds.

Eating around 40% less food helped preserve the brain in old age even better than exercise.

Dr Bart Eggen, who led the study, said:

“Obesity and aging are both prevalent and increasing in societies worldwide, but the consequences for the central nervous system are not well understood

We determined if a high- or low-fat diet, in combination with exercise and food restriction, impacted microglia during aging in mice.”

The microglia are cells in the brain that help regulate normal functioning.

When these cells stop working properly, the brain begins to degrade.

For the study mice were either fed a high- or low-fat diet — with some receiving 40% fewer calories than normal.

Some also did plenty of exercise.

Dr Eggen explained the results:

“Aging-induced inflammatory activation of microglia could only be prevented when mice were fed a low-fat diet in combination with limited caloric intake.

A low-fat diet per se was not sufficient to prevent these changes.”

The researchers hope to look at the effects of different diets.

Dr Eggen said:

“Nevertheless, these data do show that, in mice, the fat content of a diet is an important parameter in terms of the detrimental effects of aging on the brain, as well as caloric intake.

Only when fat content and caloric intake are limited, can aging-induced changes in microglia be prevented.”

The study was published in the journal Frontiers in Molecular Neuroscience (Yin et al., 2018).

There are around 5.5 million Americans living with Alzheimer’s and deaths have almost doubled in two decades.

Exercise could be the lifesaving ingredient that prevents Alzheimer’s disease, new research finds.

Higher levels of fitness were linked to less deterioration of critical nerve fibers in the brain, the so-called ‘white matter’.

The brain’s white matter is the bundle of nerve fibers the neurons use to communicate with each other.

People with lower levels of fitness had weaker white matter and lower brain function.

Dr Kan Ding, the study’s first author, said:

“This research supports the hypothesis that improving people’s fitness may improve their brain health and slow down the aging process.”

The scientists measured people’s cardiorespiratory fitness along with carrying out brain scans.

Dr Rong Zhang, study co-author, said:

“Evidence suggests that what is bad for your heart is bad for your brain.

We need studies like this to find out how the two are intertwined and hopefully find the right formula to help prevent Alzheimer’s disease.”

Further research at the O’Donnell Brain Institute at The University of Texas Southwestern Medical Center is now examining how much exercise works and whether it is ever too late.

The study will also look at the effects of cholesterol levels and blood pressure on preserving brain function.

Dr Ding said:

“A lot of work remains to better understand and treat dementia.

But, eventually, the hope is that our studies will convince people to exercise more.”

The study was published in the journal Journal of Alzheimer’s Disease (Ding et al., 2017).

The first time scientists have been able to completely clear the brain of Alzheimer’s-related protein tangles.

Alzheimer’s has been reversed in mice for the first time, raising the hopes of a drug to combat the disease.

Decreasing the levels of a key enzyme — called BACE1 — reduced the levels of amyloid plaques, which are linked to Alzheimer’s.

The mice’s brains were eventually completely free of these tangles and their cognition improved.

This is the first time scientists have been able to clear the brain of these protein tangles.

It is possible a drug could be developed to help target this enzyme.

Professor Riquiang Yan, who led the study, said:

“To our knowledge, this is the first observation of such a dramatic reversal of amyloid deposition in any study of Alzheimer’s disease mouse models.”

For the study, the scientists created mice that produce lower levels of the BACE1 protein over time.

The mice were also engineered to develop Alzheimer’s.

After developing Alzheimer’s at 75 days old, these mice were then clear of the plaques in their brain at 10 months old.

Effectively, one genetic abnormality cured the other.

Their cognition was also improved, although not fully.

Professor Yan said:

“Our study provides genetic evidence that preformed amyloid deposition can be completely reversed after sequential and increased deletion of BACE1 in the adult.

Our data show that BACE1 inhibitors have the potential to treat Alzheimer’s disease patients without unwanted toxicity.

Future studies should develop strategies to minimize the synaptic impairments arising from significant inhibition of BACE1 to achieve maximal and optimal benefits for Alzheimer’s patients.”

The study was published in the Journal of Experimental Medicine (Hu et al., 2018).

Could this discovery show the way to reversing dementia?

A build-up of toxic urea in the brain is a major cause of dementia, according to new research.

Toxic levels of urea have newly been linked to Huntington’s, a type of dementia.

Recent research has also linked urea to Alzheimer’s, the most common form of dementia.

Urea and ammonia — which are usually excreted in urine — can also build up in the brain, especially if the kidneys are unable to filter them out.

Drugs that are now commonly used to target urea could one day be used to help treat dementia.

Professor Garth Cooper, who led the study, said:

“This study on Huntington’s Disease is the final piece of the jigsaw which leads us to conclude that high brain urea plays a pivotal role in dementia.

Alzheimer’s and Huntington’s are at opposite ends of the dementia spectrum – so if this holds true for these types, then I believe it is highly likely it will hold true for all the major age-related dementias.

More research, however, is needed to discover the source of the elevated urea in HD, particularly concerning the potential involvement of ammonia and a systemic metabolic defect.

This could have profound implications for our fundamental understanding of the molecular basis of dementia, and its treatability, including the potential use of therapies already in use for disorders with systemic urea phenotypes.”

The study looked at brains donated by families for medical research along with genetically modified sheep.

Professor Cooper said:

“We already know Huntington’s Disease is an illness caused by a faulty gene in our DNA – but until now we didn’t understand how that causes brain damage – so we feel this is an important milestone.

Doctors already use medicines to tackle high levels of ammonia in other parts of the body Lactulose – a commonly used laxative, for example, traps ammonia in the gut.

So it is conceivable that one day, a commonly used drug may be able to stop dementia from progressing.

It might even be shown that treating this metabolic state in the brain may help in the regeneration of tissue, thus giving a tantalising hint that reversal of dementia may one day be possible.”

The study was published in the journal PNAS (Renee et al., 2017).

The sign comes 10 years before memory and thinking problems are obvious.

A worsening of anxiety symptoms could be an early sign of Alzheimer’s in older people, new research finds.

The symptom could help to diagnose the disease 10 years before problems with memory and thinking are obvious.

In this ‘preclinical’ phase, up to 10 years before disease onset, deposits of amyloid and tau proteins build up in the brain.

The study found that the greater these build-ups, the higher the symptoms of anxiety people experienced.

Dr Nancy Donovan, the study’s first author, explained:

“Rather than just looking at depression as a total score, we looked at specific symptoms such as anxiety.

When compared to other symptoms of depression such as sadness or loss of interest, anxiety symptoms increased over time in those with higher amyloid beta levels in the brain.

This suggests that anxiety symptoms could be a manifestation of Alzheimer’s disease prior to the onset of cognitive impairment.”

The conclusions come from a study of 270 people aged 62-90 years-old, who were followed over five years.

Their anxious-depressive symptoms predicted the build of amyloid plaques in the brain, which are, in turn, linked to the onset of Alzheimer’s disease.

Dr Donovan said:

“If further research substantiates anxiety as an early indicator, it would be important for not only identifying people early on with the disease, but also, treating it and potentially slowing or preventing the disease process early on.”

The study was published in the American Journal of Psychiatry (Donovan et al., 2018).

Alzheimer’s linked to condition that affects 1 in 5 people in the US.

Insomnia leads to a build up of the proteins linked to Alzheimer’s, new research finds.

Insomnia is thought to affect around 1 in 5 people in the US — somewhere between 50 and 70 million people.

In addition, around one-third of Americans do not get enough sleep.

A wakeful brain, though, produces more amyloid beta than the brain’s waste disposal system can cope with.

This could eventually lead to Alzheimer’s disease.

Professor Randall Bateman, who led the study, said:

“This study is the clearest demonstration in humans that sleep disruption leads to an increased risk of Alzheimer’s disease through an amyloid beta mechanism.

The study showed that it was due to overproduction of amyloid beta during sleep deprivation.”

The study looked at the effects of sleeping poorly on the brain in the short term.

Three groups were compared: some slept normally, some stayed up all night and others were given a sleeping aid.

Those who stayed up had amyloid beta levels some 25-30% higher.

This level is on a par with those genetically predisposed to Alzheimer’s.

Dr Brendan Lucey, the study’s first author, said:

“I don’t want anyone to think that they are going to get Alzheimer’s disease because they pulled an all-nighter in college.

One night probably has no effect on your overall risk of Alzheimer’s.

We are really much more concerned about people with chronic sleep problems.”

Amyloid beta is a normal byproduct of brain activity.

However, without adequate sleep, the brain cannot clear it away.

Dr Lucey said:

“Understanding how lack of sleep relates to the concentrations of amyloid beta in the brain will help direct future research into therapeutics.

This information could help us figure out how to reduce amyloid beta deposition over time in people whose sleep is chronically disrupted.”

Sleep medication may not provide much benefit, the study suggests.

Dr Lucey said:

“We were looking at healthy, well-rested adults.

This suggests that if you already are getting enough sleep, getting more sleep with the help of medication may not provide any benefit.”

The study was published in the journal Annals of Neurology (Lucey et al., 2017).