Category: Dementia

The young age at which amyloid protein, a hallmark of Alzheimer’s, begins to appear in the brain.

Amyloid protein, which is a hallmark of Alzheimer’s disease, has been detected in people as young as 20, a new study finds.

This is much earlier than any scientists previously thought.

Amyloid protein is strongly associated with Alzheimer’s disease.

It eventually forms in clumps outside the neurons.

Professor Changiz Geula, who led the study, said:

“Discovering that amyloid begins to accumulate so early in life is unprecedented.

This is very significant.

We know that amyloid, when present for long periods of time, is bad for you.”

Alzheimer’s study

The research looked at the brains of deceased people from ages 20 to 95.

Some had died young with no signs of dementia, while others had died later with or without Alzheimer’s.

The researchers focused on an area in the basal forebrain which is critical to memory and attention.

These neurons are the first to die in both normal ageing and in Alzheimer’s.

They found that the amyloid proteins began accumulating inside these neurons from as early as 20-years-old.

Together these proteins can form toxic lumps in the brain.

Older individuals and those with Alzheimer’s had larger toxic lumps of amyloid.

Professor Geula said:

“This points to why these neurons die early.

The small clumps of amyloid may be a key reason.

The lifelong accumulation of amyloid in these neurons likely contributes to the vulnerability of these cells to pathology in aging and loss in Alzheimer’s.”

The clumps damage the brain by killing neurons and by secreting more amyloid outside the cell.

Professor Geula said:

“It’s also possible that the clumps get so large, the degradation machinery in the cell can’t get rid of them, and they clog it up.”

The research is published in the journal Brain (Baker-Nigh et al., 2015)

MRI image from Shutterstock

Potential new treatment for Alzheimer’s and other cognitive disorders.

A life-extending protein called ‘klotho’ can increase learning and memory and ward off Alzheimer’s a new study reports.

Scientists at the University of California and the Gladstone Institutes have found that increasing the levels of klotho boosted learning and cognition in mice with Alzheimer’s toxins in their brains.

Klotho is an enzyme that naturally occurs in humans which is thought to be involved in the ageing process.

It takes its name from the entity in Greek mythology called ‘Clotho’, who was one of the ‘fates’ who were supposed to control the thread of people’s lives.

Dr Dena Dubal, who led the study, said:

“It’s remarkable that we can improve cognition in a diseased brain despite the fact that it’s riddled with toxins.

In addition to making healthy mice smarter, we can make the brain resistant to Alzheimer-related toxicity.

Without having to target the complex disease itself, we can provide greater resilience and boost brain functions.”

For the research, published in The Journal of Neuroscience, neuroscientists bred mice which had Alzheimer’s disease, but also had high levels of the klotho protein throughout their bodies (Dubal et al., 2015).

Normally mice with Alzheimer’s die earlier, have cognitive problems and abnormal brain activity, just like humans with the disease.

These mice, though, behaved normally and did not die prematurely.

Apparently the Klotho protein counteracted the effects of the Alzheimer’s disease.

Scientists are not yet sure why the klotho protein has these effects.

One theory is that klotho affects a neurotransmitter receptor in the brain called NMDA, which is crucial to learning and memory.

Professor Lennart Mucke, one of the study’s authors, said:

“We are encouraged in this regard by the strong similarities we found between klotho’s effects in humans and mice in our earlier study.

We think this provides good support for pursuing klotho as a potential drug target to treat cognitive disorders in humans, including Alzheimer’s disease.”

• See also: Longevity Gene May Enhance Cognition

MRI scan image from Shutterstock

How this feeling could protect you against depression and even Alzheimer’s disease.

Positive emotions, especially the feeling of awe, have been linked to lower levels of inflammatory cytokines by a new study.

The research suggests that the positive feeling from enjoying the beauty of nature or getting lost in a painting or symphony can actually help protect the body against heart disease, arthritis, depression, and even Alzheimer’s disease.

Dr Dacher Keltner, one of the study’s authors, said:

“That awe, wonder and beauty promote healthier levels of cytokines suggests that the things we do to experience these emotions — a walk in nature, losing oneself in music, beholding art — have a direct influence upon health and life expectancy.”

Across two different experiments, 200 people reported their emotions during the day, including the extent to which they felt:

• amusement,
• awe,
• compassion,
• contentment,
• joy,
• love
• and pride.

Their cheeks were also swabbed to get a measure of the cytokine, Interleukin 6, which is a marker of inflammation.

The results, published in the journal Emotion, showed that experiencing positive emotions was linked to lower levels of the inflammation marker (Stellar et al., 2015).

Awe, in particular, had a strong association with lower cytokine levels.

Dr Jennifer Stellar, the study’s lead author, said:

“Awe is associated with curiosity and a desire to explore, suggesting antithetical behavioral responses to those found during inflammation, where individuals typically withdraw from others in their environment.”

In depression, for example, the pro-inflammatory cytokines are thought to be important as they tend to block key hormones and neurotransmitters, like dopamine and serotonin, which affect memory, sleep, appetite and mood.

People who are depressed have been found to have higher levels of certain inflammatory cytokines.

The study can’t yet tell us what causes what, though, as Dr Stellar explained:

“It is possible that having lower cytokines makes people feel more positive emotions, or that the relationship is bidirectional.”

Nevertheless, this is one of the first studies to link positive emotions to a boost in the body’s defences against both mental and physical illness.

Woman and sunset image from Shutterstock

Study finds compound in this alcoholic drink may have protective effect against neurodegenerative diseases.

A compound found in beer could help protect the brain from diseases like Alzheimer’s and Parkinson’s, a new study suggests.

Xanthohumol is a compound found in hops which has already been linked to anti-inflammatory and anti-cancer effects.

The study’s authors explain:

“Hops from dried female clusters of the hop plant are widely used in beers and a few types of soft drinks.

In traditional Chinese medicine, hops have been used to treat a variety of ailments for centuries.

The presence of a high concentration of Xn [Xanthohumol] in beers might be linked to the epidemiological observation of the beneficial effect of regular beer drinking.

Xn has attracted considerable interest because of its multiple pharmacological functions, including anti-oxidation, cardiovascular protection, anticancer and cancer chemoprevention, antivirus, anti-obesity, and anti-inflammation.”  (Yao et al., 2015).

The new study, published in the Journal of Agricultural and Food Chemistry, tested Xanthohumol on the brain cells of lab rats.

Researchers found that Xanthohumol helped to reduce oxidative stress on the brain cells.

Oxidative stress refers to the stress on cells caused by highly reactive ‘free radicals’ which are byproducts of the body’s normal process of producing energy.

The study’s authors write:

“As neuronal cells are particularly vulnerable to oxidative stress and have limited replenishment during the entire lifespan, increasing evidence has supported oxidative stress as one of the pathogenic causes in the neuropathology of adult neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease.”

Naturally this is only an early study, and it is far from showing that drinking a pint of beer a day will stave off Alzheimer’s and Parkinson’s.

But it may well help lead the way to producing new drugs to help the fight against neurodegenerative diseases.

Image credit: Alzheimer’s photo from Shutterstock

The non-prescription drugs which new study links to dementia risk.

Commonly used antidepressants and hayfever drugs, among others, have been linked to an increased risk of developing dementia, a new study finds.

The drugs are often taken by older people, as Professor Shelly Gray, the study’s first author, explained:

 “Older adults should be aware that many medications — including some available without a prescription, such as over-the-counter sleep aids — have strong anticholinergic effects.

And they should tell their health care providers about all their over-the-counter use.

But of course, no one should stop taking any therapy without consulting their health care provider.

Health care providers should regularly review their older patients’ drug regimens — including over-the-counter medications — to look for chances to use fewer anticholinergic medications at lower doses.”

Four commonly used drugs which have strong anticholinergic effects are:

1. Doxepin (Sinequan) – an older antidepressant.
2. Chlorpheniramine (Chlor-Trimeton) – an antihistamine used to treat hayfever.
3. Diphenhydramine (Benadryl) – another antihistamine often used to treat hayfever and sometimes used to aid sleep.
4. Oxybutynin (Ditropan) – for bladder control.

The study, which is published in JAMA Internal Medicine, tracked 3,434 people over the age of 65 who had no signs of dementia (Gray et al., 2015).

They were followed up over 7 years, during which time 797 developed dementia.

The results showed that the more of these drugs people took, the greater their risk of developing dementia.

One-fifth of the drugs had been bought over-the-counter without prescription.

The authors suggest that taking any of these drugs would put people at greater risk if taken for three years or more at these doses:

• 10 mg/day of doxepin,
• 4 mg/day of chlorpheniramine,
• or 5 mg/day of oxybutynin.

The first three can be substituted for other drugs which do not carry the dementia risk, the third cannot.

Unfortunately, the study also suggests that the damage caused by taking these medications may be irreversible.

Professor Gray said:

“If providers need to prescribe a medication with anticholinergic effects because it is the best therapy for their patient, they should use the lowest effective dose, monitor the therapy regularly to ensure it’s working, and stop the therapy if it’s ineffective.”

Image credit: JLA