Getting lost may be the first sign of Alzheimer’s, scientists discover

Losing your navigational skills or getting lost even though you are in a familiar setting may provide some of the first indications that Alzheimer’s disease could affect you in later life. This is a preliminary discovery of a remarkable long-term study being carried out by scientists who are searching to uncover how dementia first affects the brain.

The Prevent project – based at Edinburgh University, though it involves several other UK research centres – is intended to detect signs of Alzheimer’s in people while they are still relatively young. Usually, the disease does not show its symptoms until individuals are in their 60s, by which time it has already done profound damage to the brain.

“Alzheimer’s is considered to be a disease of memory but we now think from our early work that the difficulty people are really having – at least to begin with – is not to do with declining memories but to do with their declining ability to visualise the location of objects or themselves,” said Karen Ritchie, one of the researchers. “They are losing their ability to navigate.”

A classic example is the character of Alice Howland, played by Julianne Moore in the film Still Alice, said Ritchie.Alice first suspects she has Alzheimer’s when she gets lost, in familiar terrain, while jogging. “That early scene captures it perfectly,” said Ritchie, who was involved in setting up the project with Professor Craig Ritchie (no relation) of Edinburgh University. “It is a loss of navigational skill.”

The project – funded by the Alzheimer’s Society – involves the study of two groups. The first consists of people aged 41 to 59 with close relatives who have developed Alzheimer’s and who are considered to be at relatively high risk. The second is made up of individuals whose lives have not been touched by the disease.

One of the earliest findings, outlined in a paper to be published in the journal Alzheimer’s and Dementia, shows that those who were at higher risk were poorer at tests that measured ability to visualise their position. They also tended to have a small hippocampus, a region of the brain involved in navigation.

Julianne Moore on Still Alice: ‘The idea our inner self could be taken away is very frightening’

The Four Mountains test developed by Cambridge University neuroscientist Dennis Chan is a key ingredient. It involves showing people a picture of a mountain and asking them to identify it in a selection of four other landscapes. There is considerable variation in ability and it provides scientists with a powerful tool to pinpoint those suffering hippocampal degradation. “At present we use computer screens to administer the test but in future we plan to use virtual reality headsets,” said Ritchie.

Cate Latto, who volunteered to take part, feels that loss of navigational ability reflected an important symptom of Alzheimer’s. “My mother developed the disease in late life but even when she was relatively young she could never remember where she put her car keys or where she left her car. As children, we spent our lives hunting through car parks trying to find where she had left it.”

It remains to be seen how effective tests based on measuring navigational prowess will be in predicting who will develop Alzheimer’s in later life. It would also raise ethical issues. If there is no effective treatment for Alzheimer’s why pinpoint those at risk in middle age? What could be gained?

There are several answers, say scientists. Drugs that are currently ineffective may prove far more potent if given during the disease’s early stages. In addition, it is now known that regular exercise, healthy eating and giving up smoking – which improves cardiovascular health – can also help. “There are life-style changes that can help reduce the risk of the disease,” said Ritchie.

This point was stressed by Doug Brown, research director of the Alzheimer’s Society, which has just launched its Unite Against Dementia campaign. “Dementia isn’t just an issue for older people, it will affect us all, and all of us can help find the solutions. As this study shows – people in their 40s and 50s can make a huge research contribution that could help shape the future.”

Getting lost may be the first sign of Alzheimer’s, scientists discover

Adopt These 10 Habits to Stop Dementia or Alzheimer’s Before it Starts

Adopt These 10 Habits to Stop Dementia or Alzheimer’s Before it Starts

New Alzheimer"s test can predict age when disease will appear

Scientists have developed a new genetic test for Alzheimer’s risk that can be used to predict the age at which a person will develop the disease.

A high score on the test, which is based on 31 genetic markers, can translate to being diagnosed many years earlier than those with a low-risk genetic profile, the study found. Those ranked in the top 10% in terms of risk were more than three times as likely to develop Alzheimer’s during the course of the study, and did so more than a decade before those who ranked in the lowest 10%.

Rahul Desikan, of the University of California – who led the international effort, said the test could be used to calculate any individual’s risk of developing Alzheimer’s that year.

“That is, if you don’t already have dementia, what is your yearly risk for AD onset, based on your age and genetic information,” he said.

The so-called polygenic hazard score test was developed using genetic data from more than 70,000 individuals, including patients with Alzheimer’s disease and healthy elderly people.

It is already known that genetics plays a powerful role in Alzheimer’s. Around a quarter of patients have a strong family history of the disease, and scientists have shown this is partly explained by a gene called ApoE, which comes in three versions, and is known to have a powerful influence on the risk of getting the most common late-onset type of Alzheimer’s. One version of ApoE appears to reduce risk by up to 40%, while those with two copies (one from each parent) of the high-risk version can increase risk by 12 times.

The latest study takes a new approach, showing that, aside from ApoE, there are thousands of background genetic variations that each have a tiny influence on Alzheimer’s risk, but whose cumulative influence is substantial.

The researchers first identified nearly 2,000 single letter differences in the genetic code (known as SNPs) and, after ranking them for influence, developed a test based on 31 of the markers. The test was then used to accurately predict an individual’s risk of getting the disease in an independent patient cohort.

In people with the high-risk version of ApoE, those ranked in the top 10% of risk on the new test got Alzheimer’s at an average age of 84 years, compared with 95 years for those ranked in the lowest 10%.

James Pickett, head of research at Alzheimer’s Society, said: “Preventing the development of dementia symptoms is the holy grail of Alzheimer’s research but to succeed we first need accurate methods to predict who is most likely to develop the condition. This study’s approach was fairly successful at predicting the likelihood of someone developing dementia over the coming year, but needs to be tested further in mixed, non-US populations.”

Pickett added that, while the score could help to identify people for trials, it was too early to apply it as a genetic testing tool for use in the clinic.

Rosa Sancho, head of research at Alzheimer’s Research UK, said that while genetic makeup can influence the chances of developing dementia, a healthy diet, regular physical activity and remaining mentally active can also drive down the risk. “Genetics is only part of the story and we know that lifestyle factors also influence our risk of developing Alzheimer’s,” she said. “The best current evidence points to habits we can all adopt to help lower our risk and indicates that what’s good for your heart is also good for the brain.”

The findings are published in the journal PLOS Medicine.

New Alzheimer"s test can predict age when disease will appear

How to holistically prevent Alzheimer’s Disease

Alzheimer’s disease slowly destroys a person’s memory, their ability to think and eventually their ability to complete even the simplest of daily tasks. The disease is an irreversible, progressive brain disorder that affects more than five million Americans, according to the National Institute on Aging. There may be no cure and the causes are still being determined, but that doesn’t mean nothing can be done to prevent the onset of Alzheimer’s. Research suggests the following foods and spices might help keep the disease at bay.

Curcumin

Found in turmeric, curcumin is an ancient Indian herb used in curry powder. For centuries, Ayurvedic healers have used the spice, known to have anti-inflammatory properties, to treat a variety of conditions. Several studies suggest that regularly eating foods with this spice helps prevent the spread of the amyloid-beta plaque found in the brains of Alzheimer’s patients.  On top of that it also reduces the inflammation of neural tissue associated with the disease.

Cinnamon

A study published in the Journal of Alzheimer’s Disease found that two compounds found in cinnamon, cinnamaldehyde and epicatechin, protect a protein called tau. Tau plays a normal role in the structure and function of neurons, but this protein can be damaged and begin to accumulate and form the tangles in the brain that are characteristic of Alzheimer’s. Cinnamon’s compounds might prevent damage to the tau protein and thus, help prevent the onset of Alzheimer’s.  Some easy ways to increase your cinnamon intake include tossing a cinnamon stick into your coffee or tea, sprinkling it on your morning oatmeal, or using it to spice up your favorite recipes.

Omega-3

Omega-3 fatty acids are essential fats that your body needs, but can’t make. Therefore, they must be obtained from food. Some research indicates that Omega-3 can lower blood levels of beta-amyloid, a protein involved in Alzheimer’s. The Alzheimer’s Society supports a diet — often referred to as a Mediterranean diet — of fish like salmon, mackerel, herring, sardines, albacore tuna and lake trout that are rich in Omega-3 fatty acids, along with lots of vegetables. They also recommend limiting intake of saturated fats, red meat and dairy products.

Staying healthy as you age generally requires a nutritious diet, physical activity, social involvement and mental stimulation.  The simple addition of any of the foods and spices mentioned above may also help reduce the risk of Alzheimer’s disease.

References:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781139/

http://www.lifetimedaily.com/will-a-gluten-free-diet-protect-against-alzheimers/

http://blog.thealzheimerssite.com/rosemary-memory-effects/

How to holistically prevent Alzheimer’s Disease

Alzheimer’s Disease Development – Don’t Blame Beta-Amyloid

Beta-amyloid accumulation in the brain is popularly believed by many scientists and experts from various disciplines to be the sole cause of Alzheimer’s disease. This article explains that this idea can actually be very misleading. Please read on.

What is Alzheimer’s disease (AD)? It is a neurodegenerative disorder that leads to memory loss, cognitive decline, and death.  AD can occur in anyone at any age, however, it is most common among the elderly and is less prevalent in younger people.

No Cure (?)

There is no proven medication to cure or prevent the disease, possibly due to a lack of knowledge regarding the molecular mechanisms underlying the origination and development of AD.

CDC states,

Scientists do not yet fully understand what causes Alzheimer’s disease. There probably is not one single cause, but several factors that affect each person differently.

The CDC statement is surely a conclusion based on many studies that have been performed to date. Then, why do many scientists, doctors, and experts in various disciplines still put the blame on beta-amyloid as if it were the cause of AD?

Amyloid Hypothesis

Many scientists and experts alike have accepted the ‘amyloid hypothesis,’ in which the development of AD is believed to be triggered by the accumulation of the amyloid beta (Aβ, commonly known as beta-amyloid) protein in the central nervous system (CNS).

Generally, amyloid refers to misfolded peptides or proteins that demonstrate a stable and resistant to breakdown to smaller compounds. Amyloidosis is a condition in which amyloid, is abnormally deposited in various tissues or organs.

Thus, amyloid is thought to alter the normal function of tissues and cause serious changes in tissues and organs of the body. The amyloid hypothesis, however, has shifted in recent years to suggest soluble beta-amyloid oligomers, rather than plaques, are responsible for neurodegeneration.

Almost all clinical trials of new drugs to combat AD have so far failed. Is that so?

Breakthrough

Time and again you have heard constant promises of a breakthrough. Unfortunately, when you check back a few months later all mention of the drug would typically vanish. It is publicized perhaps for a brief story about a failed trial.

The failure is not for lack of budget. Drug companies have poured billions into amyloid-blocking drugs with little success. In fact, the pharmaceutical industry has spent billions into research.

Eli Lilly alone, for instance, is said to have spent £3 billion over three decades trying to develop a successful drug.  The US National Institutes of Health has spent more than 500 hundred million dollars in pursuit of AD treatments.

Read these in order to know more about the drug companies’ failure,

Eli Lilly’s Alzheimer’s Antibody Does Not Work

After 190 Tries, Are We Any Closer to a Cure for Alzheimer’s?

Most research has focused on hypothetical disrupting sticky plaques caused by beta-amyloid accumulation outside neurons (a type of brain cells). When the plaques clog up the brain and destroy brain cells, neurons cannot transmit neurotransmitters to the next ones as they should which in turn impairs mental and cognitive functions.

Get Rid of The Plaque and You Get Rid of The Disease

The plaques are a build-up of beta-amyloid, so it is this very substance that most of the researchers have been trying to deal with. They think if they develop drugs that successfully inhibit from accumulating on the outside of the neurons, then Alzheimer can be prevented. Their uses in people with an early stage of Alzheimer’s are expected to slow down the disease progression and prevention may even be possible.

Back to Eli Lily’s story. The company’s researchers tried to attack the beta-amyloid precursors, in the hope beta-amyloid is not present to entangle with neurons.

Billed as the best hope yet, on the other hand, after the trial, the company concluded that the results of the early trial have failed to justify putting a drug on the market.

Was that a sign of the end of the amyloid hypothesis? Definitely, no.

Bryce Vissel, a professor of neuroscience at the University of Technology in Sydney and director of Neuroscience and Regenerative Medicine in the Faculty of Science was quoted as saying that researchers must urgently get back to the biology of this disease, He further asserted that it doesn’t mean throwing out the enormous body of work on beta-amyloid with the bathwater. Any holistic view of the data will have to account for it.

Not all Alzheimer’s patients found to have accumulated beta-amyloid in their brain and there are people with accumulated beta-Amyloid but without Alzheimer’s symptoms!

If accumulated beta-amyloid is to blame for Alzheimer’s development, then all people found to have built-up beta-amyloid in their brain are supposed to experience Alzheimer’s. Unfortunately, that’s not the case.

No Significant Effect

Karl Herrup, a neuroscientist at the Hong Kong University of Science and Technology, argues that the simple linear model that goes directly from amyloid to dementia has to be rejected because it has been tested in the clinic and in mouse models and proven to be untrue.

He further asserted that if the hypothesis were true, you would think that if you took healthy people and put amyloid into their brains, they would get Alzheimer’s disease. And, in fact, the evidence suggests that they do not.

Furthermore, doing the reverse by taking amyloid out of the brains of individuals with Alzheimer’s disease has been shown to have no significant effect on the symptoms or progression of the disease, he added.

He concluded that scientists need to stop using amyloid to define Alzheimer’s disease. It plays a role in the disease, but so do lots of other things. Scientists need to look at all the cause of Alzheimer’s disease if they’re going to make progress against this truly dementing illness.

What’s Good for Your Heart, It Turns Out, is Good For Your Brain

According to CDC, scientists are finding more evidence that some of the risk factors for heart disease and stroke such as high blood pressure, high cholesterol, and low levels of the vitamin folate may also increase the risk of Alzheimer’s disease. Evidence is also growing for physical, mental, and social activities as protective factors against Alzheimer’s disease.

You don’t have to wait for the Anti-Alzheimer’s Drugs or use inflammatory drugs suggested by your doctor. In fact, you can prevent and slow down AD by adopting a healthy lifestyle that includes doing things that prevent inflammation and don’t do things that promote inflammation.

By doing that, it not only help you steer clear of heart disease but may also help prevent and slow down the progression of AD.

Can Coconut Oil Ease AD?

Families who’ve given it to loved ones swear by it. Watch this video of how Dr. Mary Newport has discovered the benefits of using coconut oil to treat her husband’s Alzheimer’s Disease.

Pomegranate is stated in three different chapters in The Quran, the central religious text of Islam. Muslims believe that a three-time-mention of pomegranate in the Quran indicates its importance as a beneficial fruit to be used by humans for health maintenance and treating ailments.

From to time, studies have shown its many health benefits. That includes a study in 2014 that suggested that the anti-inflammatory punicalagin in pomegranates could battle Alzheimer’s.

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Alzheimer’s Disease Development – Don’t Blame Beta-Amyloid

Study Links Noodles to Weight Gain, Inflammation, Parkinson’s, and Alzheimer’s

Study Links Noodles to Weight Gain, Inflammation, Parkinson’s, and Alzheimer’s

Science Proves Rosemary Can Help Fight Dementia and Alzheimer’s

Science Proves Rosemary Can Help Fight Dementia and Alzheimer’s

People with Alzheimer’s who enjoy singing songs from their youth | Letter

I read the heartwarming letter (29 November) in which Dennis Ruston said that even when his late wife had advanced Alzheimer’s she loved to join in the hymns on TV’s Songs of Praise and was word-perfect. Singing for the Brain groups, organised by the Alzheimer’s Society, allow people with dementia to join in songs from their youth. They normally each have a carer with them to support and encourage them to sing. Researchers have found that the brain’s musical pathways remain relatively unscathed by the illnesses that affect normal speech, and people who have lost their speech because of dementia, stroke and other conditions can often still access the words of songs. In such cases, singing is one of the few remaining activities that a dementia patient and their spouse can enjoy equally together.
Ann Wills
Ruislip, Middlesex

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People with Alzheimer’s who enjoy singing songs from their youth | Letter

Music shone through my wife’s Alzheimer’s | Letters

Laura Barton’s description of Hannah Peel’s relationship with her gran through music (Waking moments, G2, 23 November) brought back so many memories of my wife’s struggle with Alzheimer’s. Denise died last year having struggled with Alzheimer’s for five years. She had been a music teacher and church organist in her early life but, even though I was able to care for her at home until the end, her memory and recognition failed early on in the disease. However, even when she slept most of the time, hymns would sometimes bring a smile to her lips, not least the weekly Songs of Praise on a Sunday afternoon. Such was the awakening that she would join in with most hymns and was word perfect. As the final credits rolled Denise would close her eyes and return to her abyss of darkness.
Dennis Ruston
Derby

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Music shone through my wife’s Alzheimer’s | Letters

The long, difficult search for a drug to treat Alzheimer’s and dementia

Most of us forget names, dates or places from time to time. But Hilary Doxford never did. While the rest of us smile about our common inadequacy, she knew she was experiencing a genuine malfunction of her high-performance brain. “I did have a really good memory and didn’t need to write things down,” she says. “And I used to be able to multiply two four-digit numbers together almost instantaneously.” But one day, she started getting the sums wrong.

The doctors sent her away at first. So you can’t remember names or multiply 3,765 by 1,983 any more? Oh well, that’s middle age for you. But Doxford, who was then in her late 40s, knew differently. “My benchmark is myself,” she says. “Even now, when I tell people, everybody says: ‘I would never have known.’ What I’m doing is no different from what other people are experiencing. But when I compare it to how I used to be … I can’t multiply a two-digit number by a one-digit number. I can do it if I add them – like 27 times three. It’s my short-term memory – when you need to hang on to a number because you need to use it. That’s what’s gone.”

Doxford went to the GP because her partner, Peter, had asked her to marry him. She wanted to be sure she would not be sentencing Peter to looking after a woman whose brain was deteriorating. “My GP said: ‘It’s normal – off you go.’”

Three years later, then a married woman, she went back. “All the symptoms were getting worse,” she says. Doxford is the general manager of a medical research charity.“I forgot the surnames of some of my staff. I started finding it hard to concentrate and focus. Then I started avoiding taking responsibility for things unless I absolutely had to.”

The GP said it was probably stress and sent her home again. But then she had a long, difficult business meeting with somebody, and when he greeted her three weeks later, she had no recollection of having met him before. This time she was sent for tests. She scored incredibly highly on the IQ part and incredibly poorly on memory, and was given an MRI scan. “The diagnosis was Alzheimer’s,” she says, matter-of-factly.

‘My benchmark is myself. When I compare it now to how I used to be’ … Hilary Doxford, who was diagnosed with Alzheimer’s in her early 50s. Photograph: Lydia Goldblatt for the Guardian

Dementia will take hold of one in three people who passes the age of 65, and costs the UK more than £26bn a year. This week the Office for National Statistics announced it is now the commonest cause of death in England and Wales, passing cancer and heart disease. People with dementia lose the ability to care for themselves and can become malnourished, while their immune system weakens. Infections such as pneumonia may be the actual agent of death, but dementia is the underlying cause.

It is a cruel disease, which takes away the person their families love and know, leaving a stranger who looks at them with confusion. And while there are are some drugs that will temporarily alleviate symptoms in some people, there is no cure. But dementia, of which Alzheimer’s is the commonest form, has finally begun to get the attention it deserves. In December 2013, the G8 countries, meeting in London, agreed to set an ambition to cure or come up with a significant treatment for Alzheimer’s by 2025. Last year David Cameron announced that the UK would set up a dedicated dementia research institute, with initial funding of £150m, and a further £100m from Alzheimer’s charities. Although the UK was already spending £300m on dementia research, Cameron believed it should be afforded the same level of resources as Aids and climate change. That was welcome news to campaigners, although, they say, the sum is still much less than that invested in cancer research (£590m in 2010).

Doxford, now 56, was glad to have a diagnosis. “On the one hand, it was a relief, because it explained all the problems I’d been having just doing normal stuff. On the other hand, ‘Oh shit’. The first question I asked the consultant was: ‘How long have I got being normal?’ He was implying that I only had two to three years, but then he said: ‘I do know somebody who is eight years down the line and she is pretty much OK.’” Others Doxford has met have since told her of people managing fine 10 to 15 years after diagnosis. For her, it has now been nine.

Initially she was put on Aricept (the brand name of donepezil), one of the few Alzheimer’s drugs currently available. These drugs help some people by delaying the worsening of symptoms, although they progress faster later on. But they do not work for everyone.

“It was pretty horrendous,” says Doxford. “I seemed to get all the side effects on the packet.” She began falling over. The worst was when she was tying up the boat that she and her husband kept. “We were in the marina and I had the rope in my hand. The next thing I knew, I was in the water.” They sold the boat, fearing for her safety. The consultant gave her another drug, but it was worse. “The first day I took it, I thought I was dying,” she says. She decided drugs were not for her.

There ought to be big money in Alzheimer’s drugs. It is more than a century since abnormal protein deposits in the brain were identified by the German psychiatrist Alois Alzheimer as a likely cause of neurodegeneration. Over the past few decades, drug research has focused largely on attempts to clear the amyloid-beta peptides and tau proteins believed to cause these deposits, which gradually shut down the brain’s normal workings.

But there has been a very high failure rate, often at a late stage of development, when companies have spent a great deal of money – in some cases as much as $ 300m – on research and development. Dr Eric Karran, formerly the director of research at Alzheimer’s Research UK and now leading the efforts of drug company Abbvie to find a cure, says that yes, it’s difficult, but too often in these failed trials, the preparatory work has not been thorough enough.

“Some people in the field would say that [the failure rate] has been a disaster,” he says. They suggest that the underlying concept, that Alzheimer’s is caused by amyloid plaque, may be wrong. “I would not subscribe to that view. There has been some sloppy science. We would not expect such trials to work anyway. In some cases there has been a very strong commercial push. In other cases, there has been a strong desire to get something into [human trials] because we have so little.”

Nobody would say research into Alzheimer’s is easy, says Dr Mike Hutton, chief scientific officer for neuroscientific drug discovery at the pharmaceutical company Lilly. “Amyloid accumulates in the brain for 10 to 15 years before you see clinical symptoms. There is a worry that we’re focusing on populations that are too far advanced.” Ideally, scientists must figure out who is most likely to get Alzheimer’s – then see if they can prevent healthy brains from developing it. But although there are some predictive tests available, it is hardly ethical to offer them to people when medical science cannot offer them treatment.

So the trials must be done in people with the earliest stages of dementia. And this year, for the first time, the results of two separate early trials have suggested that it may be possible to find drugs that might slow down the decay for people with mild dementia. Small wonder there have been wild headlines about a cure – a bit of good news is desperately wanted. One, Lilly’s solanezumab, a monoclonal antibody, failed in a large 2012 trial to slow the deterioration in most people with Alzheimer’s, but there was some improvement in those with the mildest form of the disease. Results from a new trial of more than 2,000 people with early-stage Alzheimer’s are eagerly anticipated, and due before the end of the year.

Another drug, Biogen’s aducanumab, made headlines in September. Trial results showed it almost completely cleared amyloid from the brains of a group of early Alzheimer’s patients,and that the expected deterioration slowed down significantly. The trial was small (166 people), and at the high doses that produced the best results, there were side effects such as headaches, but there was excited talk of “a game-changer”.

There has been such hype before, but David Reynolds, chief scientific officer of Alzheimer’s Research UK, says he is reasonably confident that the solanezumab results in December will also show an improvement in the symptoms of dementia, or at least a slowing of the decline. Sadly, there still seems little hope for those who already have moderate to severe dementia, beyond care and compassion.

In a nursing home in Hertfordshire, surrounded by trees and green spaces, James Gatesman, a former coroner’s officer and enthusiastic allotment gardener, spent the last years of his life in bed, his long legs angled to the wall, under a framed photograph of his Metropolitan police class at Hendon College. A yellow spot attached to the glass identified his own face in the picture.

Deborah Gateman with her father, James, before he died. Photograph: Lydia Goldblatt for the Guardian

You could still see the fine figure of a man that Gatesman had been – 6ft 2in with broad shoulders and a strong, handsome face. But he had ceased to speak, and could no longer move his own limbs. His daughter Deborah and his wife, Doreen, could only communicate with him through touch, or his occasional grunts, moans and howls.

“I always talk to him and treat him as if he understands us,” said Deborah, shortly before her father died. “I think of it as almost like locked-in syndrome – that he is in there. I worry about what we discuss in front of him.” When his wife paid for him to have music therapy, Gatesman responded to the Gilbert and Sullivan tunes he used to love with noises and movement of his hands. That confirmed Deborah’s belief that he was more aware than he seemed.

Gatesman was diagnosed in 2003, but Doreen recalls odd behaviour on a holiday in Australia in 1996, when he wandered away from their group and nobody knew where he was. In later years, his behaviour became unpredictable, and he refused to go to a doctor. “That was probably the worst time,” she said. “Where do you go for help?”

Eventually Gatesman had to see a GP because of an ear infection, and ended up in the memory clinic. He had a brain scan and was diagnosed with Alzheimer’s. The progression was slow but inexorable. He was on Aricept for a year, but that was stopped when he was sent to a residential assessment centre – a care home where people with dementia spend some weeks or months while their condition and needs are determined. Instead, he was put on the drugs that are too often used to control the sometimes bizarre and agitated behaviour of dementia patients – antipsychotics. “He was throwing chairs around and he did pull a handrail off the wall,” Doreen says. When they visited him, he was no longer walking, but sitting in a reclining chair. “He was a bit of a dribbling mess,” said Deborah. “The antipsychotics were turning him into a zombie.” By the time he was moved to the long-term home in Hertfordshire, he was underweight. Doreen insisted the antipsychotics were stopped, and he regained not just his weight, but his spirit. Then “they had quite a lively character on their hands. He would run off down the corridors,” said Deborah. Or he would speak to the Polish nurses in the Flemish and German he had learned while in the RAF, in the war.

The Alzheimer’s Society has campaigned to reduce the use of antipsychotics – often referred to as the “chemical cosh” – in care homes. Dr Doug Brown, the organisation’s research director, says prescriptions have markedly reduced as a result, though “we wouldn’t say the problem has gone away. We still need to keep an eye on it”. The Society has piloted staff training in more than 100 care homes for “person-centred care”, which appears to cut the use of drugs dramatically. It involves taking the trouble to understand the triggers for an individual’s distress – such as the man who gathered all his furniture in the centre of his room every day and became upset when staff put it back. He was a decorator. Given a brush and a bucket of water, he spent contented hours thinking he was painting the walls.

The overuse of antipsychotics is one outcome of the past neglect of dementia, and further evidence of the real need for a drug that will do more than just quieten patients down – one that will slow the progress of a devastating disease and eventually, hopefully, cure it.

The long, difficult search for a drug to treat Alzheimer’s and dementia

Dementia and Alzheimer"s leading cause of death in England and Wales

Dementia and Alzheimer’s disease has become the leading cause of death in England and Wales for the first time, figures show.

An ageing population and better diagnosis of the condition has led to dementia and Alzheimer’s knocking ischaemic heart disease from the top spot, statisticians said.

Of the 529,655 deaths registered in England and Wales in 2015, 11.6% were attributable to dementia or Alzheimer’s, according to the Office for National Statistics (ONS).

Among those aged 80 or over, dementia and Alzheimer’s accounted for 13.7% of male deaths and 21.2% of deaths among women.

Meanwhile, the mortality rate for dementia and Alzheimer’s has more than doubled over the past five years, the figures show.

But due to improvements in treatment, diagnosis and awareness, the mortality rates for the other top five leading causes of death – including ischaemic heart disease, chronic lower respiratory disease, lung cancer and cerebrovascular diseases such as strokes – have fallen since 2001.

The ONS data shows that for 2015, ischaemic heart disease was the second leading cause of death, accounting for 11.5% of deaths.

But when the figures are broken down by gender, they show that heart disease is still the leading cause of death for men and dementia and Alzheimer’s disease were certified as the main cause of death among women.

“In 2015, dementia and Alzheimer’s disease became the leading cause of death in part because people are simply living longer but also because of improved detection and diagnosis,” said Elizabeth McLaren, the head of life event statistics at the ONS.

The figures also show large variation among age groups – people over 80 were more likely to die from dementia and Alzheimer’s – while suicide was the leading cause of deaths for people aged under 35.

Meanwhile, breast cancer remains the leading cause of death for women, aged 35 to 49.

But when all forms of cancer are grouped together, cancer was the most common cause of death in 2015, accounting for 27.9% of all deaths.

Dementia and Alzheimer"s leading cause of death in England and Wales

Alzheimer"s treatment within reach after successful drug trial

An Alzheimer’s drug has been shown to successfully target the most visible sign of the disease in the brain, raising hopes that an effective treatment could be finally within reach.

A small trial of the drug was primarily aimed at assessing safety, but the findings suggest it effectively “switched off” the production of toxic amyloid proteins that lead to the sticky plaques seen in the brains of Alzheimer’s patients.

If the tablet, produced by pharmaceutical giant Merck, is also shown to slow the pace of mental decline – a crucial question that a major clinical trial should answer when it reports next year – it could be the first treatment for Alzheimer’s to be licensed in more than a decade.

Prof John Hardy, a neuroscientist at UCL who first proposed that amyloid proteins play a central role in Alzheimer’s disease, welcomed the results. “People are excited,” he said. “This is a very nice drug and I’m sure Merck are feeling very pleased with themselves.”

Matt Kennedy, who led the trial at Merck, said: “Today there are very limited therapeutic options available for people with Alzheimer’s disease, and those that exist provide only short-term improvement to the cognitive and functional symptoms. They do not directly target the underlying disease processes. There is an urgent need for [these].”

How BACE1 blocking drug could reduce toxic proteins in Alzheimer’s patients

The new therapy is designed to do this by halting the steady production of amyloid-beta proteins, which are known to clump together in sticky plaques in the brains of Alzheimer’s patients. A leading theory of Alzheimer’s is that the accumulating proteins kill off healthy neurons, eventually leading to memory loss, cognitive decline and changes to personality.

Kennedy said it was too early to predict when a drug might reach the market if the next step is successful. “We are eagerly awaiting the results of the phase three clinical trials,” he said. “It is premature to speculate on availability.”

In the trial, published in the journal Science Translational Medicine on Wednesday, 32 patients with early stage Alzheimer’s disease were given the drug, called verubecestat, daily for seven days. Healthy volunteers were also given the drug for up to two weeks.

This was not long enough to show visible changes to the accumulation of plaques in the brain, by MRI scans for instance. However, samples taken from the fluid surrounding the brain showed the drug had reduced the levels of two compounds that are known to be the building blocks for abnormal amyloid proteins.

Hardy said that the changes to the biomarkers convince him that the drug is successfully targeting the buildup of plaques in the brain. The real remaining uncertainty, he said, was whether this would convert into cognitive benefits for patients.

“What we have to be worried about is that the plaques have set off other pathologies – that it is too late,” he said.

The drug works by blocking a brain enzyme called BACE1, which fuels the production of two small molecules that link together to form amyloids. Mutations in genes related to BACE1 have been found in people who appear to be protected against Alzheimer’s disease.

There have been previous attempts to develop drugs that inhibit BACE1, but these have mostly failed due to unacceptable side-effects, such as liver toxicity and eye problems.

The Merck drug appears to have very few side-effects and it will be the first of its kind to make it into a large efficacy trial. The company is running two phase three trials, in 1,500 patients with mild to moderate Alzheimer’s and in another 2,000 patients in the earliest stage of the disease. The results of the first of these are due to be reported in July 2017.

There are 850,000 people with dementia in Britain, and this figure is expected to reach one million by 2025. Alzheimer’s is the most common form of the condition.

Rosa Sancho, head of research at Alzheimer’s Research UK, welcomed the findings, adding that the Merck drug is one of several that are heading into the final stages of clinical testing. “There is a wave of potential new treatments currently being tested for dementia, with the results of these studies hotly anticipated over the course of the coming months and years,” she said.

Competing drugs include one developed by the biotech firm Biogen, which reported promising results in August and which also targets the plaques. The Biogen drug aims to sweep the proteins away once they appear rather than halting the production of proteins in the first place, however.

“With us, it’s a question of switching off the tap. With them it’s mopping up the water,” said Ian McConnell, a spokesman for Merck.

Hardy suggested that Merck’s drug is likely to be far cheaper and easier to produce than the Biogen therapy, which involves injecting patients with antibodies.

Alzheimer"s treatment within reach after successful drug trial

A decade of deadlock over Alzheimer"s treatment may be drawing to a close

When Terry Pratchett was diagnosed with Alzheimer’s he recalled his wife’s relief that he hadn’t got a brain tumour. “All I could think then was, ‘I know three people who have got better after having a brain tumour. I haven’t heard of anyone who’s got better from Alzheimer’s,’” the late author wrote in 2008.

Nearly a decade on, not much has changed for people facing a new diagnosis of Alzheimer’s. Unlike patients with heart disease, cancer or diabetes, there is no well-trodden medical track to follow and no treatments that can slow the disease’s devastating progress.

Between 2002 and 2012, 99.6% of drugs studies aimed at preventing, curing or improving Alzheimer’s symptoms were either halted or discontinued. The consistent failure of trials, at vast financial cost to drugs companies, caused many to shut down dementia programmes as a result.

The latest trial results from Merck, together with other drugs in the final stage of development, provide hope that the years of deadlock may be drawing to a close.

The Merck trial may be preliminary, in the clinical sense, but it represents an entire career’s work for some of the scientists involved. “We’re 16 years into the program,” said Matt Kennedy, the neuroscience director at Merck who led the research. “It’s a good example of how long it takes.”

How BACE1 blocking drug could reduce toxic proteins in Alzheimer’s patients.

The first challenge scientists faced was creating a compound that would get through the blood-brain barrier, without also causing toxic side-effects or damaging healthy structures in the brain. Simply optimising the structure of the compound to do this took a decade, Kennedy said.

The latest results appear to show that the scientists got this bit right – the drug appeared to have few side-effects and it substantially lowered levels of toxic amyloid compounds.

The real question, which the next phase of the trial should answer, is whether the formation of plaques are a root cause of the disease or simply a visible symptom. Previous drugs aimed at clearing abnormal tangles of proteins from the brain have not been successful, and some argue that by the time the plaques are present irreparable brain damage may have already occurred.

It is possible that previous drugs based on the so-called amyloid hypothesis, were given to patients whose disease was too far advanced for them to benefit. Merck hopes that its drug, which acts at an earlier stage in the disease process by shutting down the production of the misshapen proteins rather than clearing them once they appear, will fare better.

There is no guarantee that the drug will ultimately make it to market, but in a field that has seen such scant progress, the fact that a major clinical trial is underway is welcome news.

Professor John Hardy, a neuroscientist at University College London and pioneer in the study of Alzheimer’s disease, said: “Conveying some excitement isn’t the wrong thing to do in this case.”

A decade of deadlock over Alzheimer"s treatment may be drawing to a close

How to Support a Loved One Who Has Alzheimer’s

How to Support a Loved One Who Has Alzheimer’s

Alzheimer’s Patient Reverses Symptoms by Applying Coconut Oil On A Daily Basis

Carolyn, the devoted daughter of an 88-year-old women who has Alzheimer’s recently decided to take charge of her mother’s care. The almost immediate results she saw were drastic and inspiring.

Additionally, the simple change she implemented in her mom’s life is available for any family struggling and suffering from Alzheimer’s to try for themselves.

Her mother spent the last seven years in a nursing home. As the years wore on and her mother’s condition deteriorated, Carolyn started to worry that her mother was being neglected and potentially abused.

Carolyn decided it was time to make a change and take matters into her own hands. She removed her ailing mother and devoted herself to being her mother’s full-time primary caregiver. On February 14, 2016, Carolyn made the hardest and probably the most important decision for her mother and removed her from the toxic nursing home environment and took her home to care for her.

While in the care of the nursing home, Carolyn’s mother was diagnosed with stage 6 Alzheimer’s. Stage 6 is also known as the “severe decline” stage. In stage 6 most patients need help with day-to-day life activities and near constant supervision. For the last two years, Carolyn’s mother struggled to speak and did not remember people, names, faces, and words. Reading had become almost impossible for her mom due to her memory issues. Communication was becoming a real struggle for Carolyn’s mother.

Coconut oil, the wonder drug

Carolyn had read about and was familiar with the benefits of coconut oil. Immediately after her mother’s liberation from the nursing home, Carolyn started liberally applying coconut oil. She would do this twice a day, after bathing in the morning and again at night before bedtime.

Within 5 days she started noticing an immediate and drastic improvement in her mother’s condition. Her mother started remembering people and names she hadn’t in years. She was able to communicate again. Carolyn was amazed when her mother was able to read, out loud, a Bible storybook and only struggled with a couple of words.

Alzheimers and coconut oil, science backs it up

These results may have been shocking, but they are no surprise given the results of a recent Spanish clinical trial. In December 2015, a clinical trial was published on the effects of coconut oil being used to treat patients who have Alzheimer’s.

The study included giving 40 ml, approximately 2.7 tablespoons, of coconut oil a day to one of two control groups. Both control groups were made up of people of varying ages and genders in various stages of Alzheimer’s. One control group received the coconut oil and the other did not.

The study concluded that there was a statistically significant increase in test scores demonstrating improved cognitive status in the control group that received the coconut oil. The study clearly demonstrated the potentially powerful positive effects of coconut oil on patients struggling with Alzheimer’s.

In addition, a US study currently being conducted in Florida is scheduled for publication in late 2016. The health, wellness, and Alzheimer’s communities are eagerly awaiting those results.

Big Pharma doesn’t welcome the idea

The pharmaceutical industry is the one industry that stands to lose the most if the new studies collaborate Spanish study findings. Alzheimer’s disease affects millions of seniors and is a rapidly increasing disease. Pharmaceutical companies have been working for years to develop a vaccine but to date have come up empty handed. Pharmaceutical companies may be left out in the cold if the connection between coconut oil and cognitive ability increase in Alzheimer patients is proven.

For Carolyn and her mother there is no doubt that coconut oil has made a huge impact in their daily lives. Carolyn and her mother are enjoying this additional time together, their newfound freedom, and their ability to communicate with one another.

Sources:      

http://healthimpactnews.com/2016/88-year-old-woman-recovering-from-alzheimers-and-diabetes-using-coconut-oil/

http://healthimpactnews.com/2015/study-coconut-oil-improves-cognitive-functioning-in-alzheimers-patients/

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Alzheimer’s Patient Reverses Symptoms by Applying Coconut Oil On A Daily Basis

Study Shows THC Could Remove Alzheimer’s Plaques From The Brain

Alzheimer’s disease is a progressive brain disorder that leads to memory loss and can seriously impair a person’s ability to carry out daily tasks. Salk Institute scientists have found evidence that tetrahydrocannabinol (THC) compounds found in marijuana can promote the cellular removal of amyloid beta protein in the brain — the brain plaques which are linked with the progression of Alzheimer’s disease.

What Study Shows?

Alzheimer’s affects more than five million Americans according to the National Institutes of Health, and is a leading cause of death. It is also the most common cause of dementia and its incidence is expected to triple during the next 50 years. It is strongly associated with the build-up of amyloid-beta proteins in the brain, forming plaques that are thought to somehow damage neurons and cause their demise. As a result, key brain regions like the hippocampus can decrease in volume, leading to severe learning and memory defects.

How it Works?

The compound works by passing from the lungs to the bloodstream, where it attaches to two types of receptors, cannabinoid receptor (CB) 1 and 2, which are found on cell surfaces all over the body.

Receptors in the brain can be activated by endocannabinoids, which are a class of molecules made in the body that signal between brain cells. THC works similarly to endocannabinoids by activating the same receptors in the brain, which produces the drug’s psychoactive effects.

“Inflammation within the brain is a major component of the damage associated with Alzheimer’s disease, but it has always been assumed that this response was coming from immune-like cells in the brain, not the nerve cells themselves,” first author Antonio Currais, a postdoc researcher in Schubert’s laboratory, said in the release.

The researchers found that high levels of amyloid beta were associated with cellular inflammation and higher rates of neuron death. They demonstrated that exposing the cells to THC reduced amyloid beta protein levels and eliminated the inflammatory response from the nerve cells caused by the protein, thereby allowing the nerve cells to survive.

What they found was that not only did the THC cause a breakdown of the protein buildup, but a reduction in inflammation in the cells. Inflammation is bad because it makes it harder for your neurons to communicate with one another correctly.

Sources:

-http://www.popsci.com/marijuana-compound-removes-alzheimers-plaque-from-brain-cells-study

-https://www.salk.edu/news-release/cannabinoids-remove-plaque-forming-alzheimers-proteins-from-brain-cells/

-http://www.iflscience.com/brain/thc-may-weapon-against-alzheimer-s/

-http://www.sciencealert.com/marijuana-compound-removes-toxic-alzheimer-s-protein-from-the-brain?0_8852473623119295=

Study Shows THC Could Remove Alzheimer’s Plaques From The Brain

Trial shows tantalising signs that new Alzheimer"s drug could benefit early-stage patients

A trial of a new Alzheimer’s drug has shown it could benefit patients in the earliest stages of the disease, raising hopes that a treatment for the devastating condition may finally be on the horizon.

While the trial was designed to assess the safety of the treatment and not whether patients fared better on the drug, an “exploratory analysis” of the data revealed that the treatment appeared to slow the mental decline of patients who responded to the therapy.

The small study of only 165 people with mild symptoms of the disorder found that a dozen monthly injections of the antibody aducanumab removed clumps of protein that build up in the Alzheimer’s brain.

A leading theory of the disease holds that the steady accumulation of a protein called amyloid-beta in the ageing brain kills off healthy neurons and brings about the memory and cognitive impairments experienced by Alzheimer’s patients.

In the trial, the strongest glimpse of mental improvement was seen in patients who had the highest dose of drug and who showed the greatest reduction in amyloid plaque proteins in follow-up brain scans. These patients did not worsen at all after six months of treatment. But the small number of patients enrolled in the study means that two much larger trials, which are now recruiting 2,700 patients in 20 countries, are needed to confirm whether the tantalising signs of benefit are real.

Alzheimer’s experts welcomed the results, but cautioned that it is too early to know whether the drug will be a help for patients. Other antibody treatments have looked impressive in early studies only to fail later on in larger trials.

Comparison brain scans, with amyloid beta protein shown in red. The different dosages of aducanumab being tested are shown on the right. Photograph: Ayres, Michael/Sevigny et al/Nature

John Hardy, a neuroscientist at UCL who first proposed that amyloid was a driver of Alzheimer’s disease, said: “It’s very interesting and nice to see all these positive data, and it has caused genuine excitement in the field, but it’s a very small number of patients and too small to draw any definitive conclusions from.”

The results from the trial led by the US biotech firm, Biogen, and a Swiss company called Neurimmune, are reported in the journal Nature. The data were first released at a scientific conference in March last year.

Aducanumab was hailed as a potential treatment for Alzheimer’s when scientists found the antibody in people who aged without suffering the sort of mental decline that goes hand in hand with old age. It appeared that the antibody prevented the build-up of amyloid plaques and staved off dementia.

When injected into Alzheimer’s patients, one or two in every thousand of the antibodies enter the brain where they latch on to wayward amyloid-beta proteins. Researchers at Biogen believe that other cells called microglia then arrive and clear the aberrant proteins from the brain. The drug appears to be most effective if the accumulation of amyloid protein is blocked before it causes too much damage. The process may start 15 years before people show symptoms.

In the latest trial, some patients experienced side effects. MRI scans showed a shift in the brain fluid that was more common at high doses and in people who carry the APOE type-4 gene, which is a major risk factor for Alzheimer’s disease. The scientists are now working on ways to avoid the side effect or diminish the problems by reducing the doses patients receive.

David Allsop, professor of neuroscience at Lancaster University, said the side effects will have to be overcome if the therapy is to find widespread clinical use. “Nevertheless, these findings could be a gamechanger if the effects on memory decline can be confirmed in more extensive follow-on studies.”

There are 850,000 people with dementia in Britain, a number that is expected to reach one million by 2025. Alzheimer’s is the most common form of the condition. “If this drug works, we’ll have a treatment for patients suffering from this devastating disease,” said Biogen’s Alfred Sandrock.

“These results provide tantalising evidence that a new class of drug to treat the disease may be on the horizon, said David Reynolds at Alzheimer’s Research UK.

James Pickett at the Alzheimer’s Society was similarly optimistic: “These results are the most detailed and promising that we’ve seen for a drug that aims to modify the underlying causes of Alzheimer’s disease.”

Trial shows tantalising signs that new Alzheimer"s drug could benefit early-stage patients

Black Currant: Natural Rescue from Alzheimer’s and Dementia

The epidemic of Alzheimer’s takes an enormous toll. The disease ravages the brain, robbing people of memory and awareness, and disconnecting them from those they love. And it’s increasing: according to the Alzheimer’s Association, Alzheimer’s is now the 6^th leading cause of death in the U.S. Some 5.4 million Americans now suffer from it, affecting millions of households. But the race to find treatments is uncovering many promising new developments, including black currants. The powerful antioxidants in these tiny, dark berries may help slow the disease’s damage, and prolong lives.

An Assault on the Brain

Of all the dementia cases in the U.S., Alzheimer’s accounts for some 80 percent. The disease results in badly reduced mental abilities and tragic, debilitating memory loss. Researchers have linked Alzheimer’s to abnormal clumps in the brain, known as amyloid plaques, and tangled bundles of fibers called neurofibrillary tangles. The specific role these plaques and tangles play in the disease is not entirely known. But scientists believe they help block communication among nerve cells and disrupt the vital processes those cells need to survive. The death of these nerve cells is what causes the devastating symptoms of Alzheimer’s.

Protection in Black Currant Extract

What makes black currant so promising in the fight against Alzheimer’s is its concentration of potent anti-oxidants. These anthocyanins may help prevent the degradation of blood vessels and Alzheimer’s-related dementia. Cholesterol build-up in the walls of blood vessels causes a reduced flow of blood to the brain, which can cause vascular dementia.

Researchers presented a promising paper to the American Heart Association, showing that anthocyanins from black currant extract may have beneficial effects. A membrane-enriched black currant extract, supplied by Iprona AG under their BerryPharma brand, was tested for its effect on the arteries. The study compared the effects of the extract to the effects of a placebo. The extract helped improve flow, and resulted in a decrease of the plaques associated with the disease.

Reducing Protein Levels in the Brain

A study on mice with Alzheimer’s disease was recently published in the Journal of Nutritional Biochemistry. Researchers fed one group of mice anthocyanin-enriched bilberry and black currant extracts, and the other group a control diet. As a result, the mice fed the extracts showed far lower brain protein levels than the mice fed the control diet. These proteins — called asamyloid precursor proteins (APP) — are thought to be a key risk factor for Alzheimer’s. The mice who were fed the extracts also showed far less spatial memory loss than the mice fed the control diet.

Delaying the Damages of Aging

Tufts University research, published in the Journal of Alzheimer’s Disease, studied the effects of high-antioxidant fruits  on oxidative stress in brain cells — another factor linked to risk of Alzheimer’s. The study found that these fruit extracts (such as black currant, boysenberry, cranberry, strawberry, dried plum, and grape) had a strong protective effect. It was noted that the high levels of anthocyanins and polyphenols in dark berries may help protect aging brain cells, slowing the onset of Alzheimer’s.

A Traditional Cure

Black currant has long been a traditional cure, used to treat digestive ailments, colds, and flu. Black currant seed oil is an increasingly popular anti-inflammatory. But now it’s clear that this little berry may also help fight the devastating effects of cognitive decline. We’re learning more about ways to help stay healthy as we age, including the importance of keeping our minds and bodies busy. We’re also learning about the power in natural ingredients. By midcentury, reports the Alzheimer’s Association, someone in the U.S. will develop the disease every 33 seconds. The news that black currants hold so much potential is promising indeed.

Black Currant: Natural Rescue from Alzheimer’s and Dementia

New research hints at pattern of Alzheimer"s spread in the brain

Scientists say that they have discovered a possible explanation for how Alzheimer’s disease spreads in the brain.

Alzheimer’s is linked to a buildup of protein plaques and tangles that spread across particular tissues in the brain as the disease progresses. But while the pattern of this spread is well-known, the reason behind the pattern is not.

Now scientists say they have uncovered a potential explanation as to why certain tissues of the brain are more vulnerable to Alzheimer’s disease.

The vulnerability appears to be linked to variations in the levels of proteins in the brain that protect against the clumping of other proteins – variations that are present decades before the onset of the disease.

Related: Hope for Alzheimer’s treatment as researchers find licensed drugs halt brain degeneration

“Our results indicate that within healthy brains a tell-tale pattern of protein levels predicts the progression of Alzheimer’s disease through the brain [in those that are affected by the disease],” said Rosie Freer, a PhD student at the University of Cambridge and first author of the study.

The results could open up the possibility of identifying individuals who are at risk of developing Alzheimer’s long before symptoms appear, as well as offering new insights to those attempting to tackle the disease.

Charbel Moussa, director of the Laboratory for Dementia and Parkinsonism at Georgetown University Medical Center said that he agreed with the conclusions of the study. “It is probably true that in cases of diseases like Alzheimer’s and Parkinson’s we may have deficiencies in quality control mechanisms like cleaning out bad proteins that collect in the brain cells,” he said, although he warned that using such findings to predict those more at risk of such disease is likely to be difficult.

But others are less convinced by the results. “This might be part of the explanation as to why Alzheimer’s disease kills some cells and not others, but it is undoubtedly a complex problem and this is only part of the answer to that problem,” said John Hardy, professor of neuroscience at University College London. “This paper has only looked at a few brain regions and really only at a few cell [types],” he added. “So it points towards the idea that there is an intrinsic reason for selectivity but it does not really prove it.”

Related: GM worm study provides ‘powerful first step’ towards preventing Alzheimer’s

Published in the journal Science Advances by scientists from the University of Cambridge, the research involved the analysis of data relating to more than 500 brain tissues from six healthy individuals, aged between 24 and 57 years of age.

The team looked at the levels of a family of molecules known as mRNA, that are encoded by genes and which are required to produce proteins. From this analysis, the researchers found that they were able to predict the levels of proteins across the brain, allowing them to map the levels of proteins associated with Alzheimer’s disease.

The scientists found that regions of the brain with higher levels of proteins prone to clumping in plaques and tangles corresponded to regions that generally show early evidence of Alzheimer’s disease.

The team also found a link between the susceptibility of regions to Alzheimer’s disease and levels of a group of proteins that are known to affect the clumping of those that form plaques and tangles.

The scientists found that the “vulnerability map”, produced by looking at the levels of these proteins in the brains of healthy individuals, is consistent with the map of how Alzheimer’s progresses.

Related: Alzheimer’s researchers find molecule that delays onset of disease

That, the researchers say, suggests that the vulnerability of particular tissues to Alzheimer’s disease could, in part, be down to a combination of higher levels of plaque and tangle-forming proteins and problematic levels of proteins that affect their clumping.

The scientists say the findings could lead to new ways to predict an individual’s risk of developing Alzheimer’s disease.

“Although we all have these patterns, in some people the patterns are more extreme, and in some others are less. Those in which the imbalance is greater, are more at risk,” said Michele Vendruscolo, co-author of the research, although he stresses that research to back up the suggestion has yet to be carried out.

Dr David Reynolds, chief scientific officer at Alzheimer’s Research UK, said: “These findings suggest that our susceptibility to Alzheimer’s may not only be dictated by abnormal changes in the brain, but by how our brains are hardwired to react to those changes.”

“Understanding the molecular mechanisms that underpin susceptibility to diseases like Alzheimer’s has the potential to open the door to new treatment and prevention approaches,” he added. “Building a complete picture of the biology driving a complex disease like Alzheimer’s gives scientists the best chance of developing effective treatments against it.”

New research hints at pattern of Alzheimer"s spread in the brain

Examine finds important oils might improve cognitive functioning in Alzheimer’s sufferers!

Alzheimer’s Disease is the only cause of death in the top ten that cannot be prevented or cured.  For many families, a diagnosis of Alzheimer’s Disease is more devastating than any other diagnosis.(1)

Many people are searching for holistic options that may help improve symptoms or slow progression of the disease.  Essential oils have been used for generations to manage symptoms of depression, anxiety and even insomnia.  Caregivers are finding comfort in using oils to treat similar symptoms in relationship to Alzheimer’s Disease.(2)

Essential oils provide sensory stimulation that helps decrease agitation, improves sleep and overall quality of life associated with Alzheimer’s Disease or dementia!

Oils can be applied to the skin, inhaled or even placed in food or beverages if the oils are safe for human consumption.  In addition to the benefits associated with the oils themselves, studies also show that sensory stimulation helps decrease agitation, improves sleep and improves the overall quality of life associated with the disease.(2)

One study found that used rosemary, lemon, lavender and orange essential oils for 28 days on patients with Alzheimer’s Disease.  All patients showed significant improvement in cognitive function following aromatherapy.  Researchers used the Gottfries, Brane, Steen scale, Functional Assessment Staging of Alzheimer’s disease, and the Touch Panel-type Dementia Assessment Scale to assess progress following aromatherapy.(3)

Study found that essential oils was an effective non-pharmacological therapy for dementia and may have potential for improving cognitive functioning in patients with Alzheimer’s Disease!

Patients experienced no known side effects associated with the aromatherapy.  The study concluded that aromatherapy was an effective non-pharmacological therapy for dementia and may have potential for improving cognitive functioning in patients with Alzheimer’s Disease.(3)

Seven essential oils that could provide comfort for patients diagnosed with Alzheimer’s Disease or dementia!

If you or someone you love is struggling with dementia or Alzheimer’s, consider using the following oils.

1. 
   Lavender:  Lavender is thought to help calm and balance emotions and has been found helpful in managing depression, anger, irritability and insomnia.(2)


2. 
   Peppermint:  Peppermint can be used to energize and stimulate the mind, as well as calm nerves. (2)


3. 
   Rosemary:  Rosemary is similar to peppermint and can be used to stimulate the mind and body.  It may help improve cognitive performance and mood. (2)


4. 
   Bergamot:  Bergamot is a citrus oil that can help relieve anxiety, agitation, mild depression and stress. (2)


5. 
   Lemon Balm or Melissa Oil:  This is one of the more expensive oils but has been shown through studies to be effective in calming and relaxing people who deal with anxiety and insomnia.  It also may help improve memory and ease indigestion.(2)


6. 
   Ylang Ylang:  Ylang Ylang can help ease depression and promote quality sleep.(2)


7. 
   Ginger:  Ginger is helpful to digestions or loss of appetite or even constipation. (2)

If someone you know is diagnosed with Alzheimer’s or dementia, consider the benefits of aromatherapy.  It may help your loved one find more comfort within their diagnosis.

Sources included:

(1) http://www.alz.org/facts/

(2) http://www.alzheimers.net/10-10-14-essential-oils-dementia

(3) http://www.ncbi.nlm.nih.gov/pubmed/20377818

Examine finds important oils might improve cognitive functioning in Alzheimer’s sufferers!