Risk gene for Alzheimer’s has early effects on the brain

A genetic predisposition to late-onset Alzheimer’s disease affects how the brains of young adults cope with certain memory tasks. Researchers from the German Center for Neurodegenerative Diseases (DZNE) and the Ruhr-Universität Bochum report on this in the scientific journal Current Biology. Their findings are based on studies with magnetic resonance imaging in individuals at the age of about 20 years. The scientists suspect that the observed effects could be related to very early disease processes.

The causes for Alzheimer’s in old age are only poorly understood. It is believed that the disease is caused by an unfavorable interaction of lifestyle, external factors and genetic risks. The greatest genetic risk factor for late-onset Alzheimer’s disease stems from inherited mutations affecting “Apolipoprotein E” (ApoE), a protein relevant for fat metabolism and neurons. Three variants of the ApoE gene are known. The most common form is associated with an average risk for Alzheimer’s. One of the two rarer variants stands for an increased risk, and the other for a reduced risk.

“We were interested in finding out whether and how the different gene variants affect brain function. That is why we examined the brains of young adults in the scanner while they had to solve a task that challenged their memory,” explained Dr. Hweeling Lee, who led the current study at the DZNE in Bonn.

Distinguishing similar events

The group of study participants comprised of 82 young men and women. They were on average 20 years old, and all of them were university students considered to be cognitively healthy. According to their genotype for ApoE, 33 of them had an average, 34 an increased and 15 a reduced risk of developing Alzheimer’s disease at a late age. During the study in the brain scanner, all individuals were presented with more than 150 successive images displayed on a monitor. These were everyday objects such as a hammer, a pineapple or a cat. Some pictures were repeated after a while, but sometimes the position of the displayed objects on the screen had changed. The study participants had to identify whether an object was “new” or had been shown before—and if so, whether its position had shifted.

“We tested the ability to distinguish similar events from one another. This is called pattern separation,” said Hweeling Lee. “In everyday life, for example, it’s a matter of remembering whether a key has been placed in the left or right drawer of a dresser, or where the car was parked in a parking garage. We simulated such situations in a simplified way by changing the position of the depicted objects.”

High-resolution through modern technology

Simultaneously to this experiment, the brain activity of the volunteers was recorded using a technique called “functional magnetic resonance imaging”. Focus was on the hippocampus, an area only a few cubic centimeters in size, which can be found once in each brain hemisphere. The hippocampus is considered the switchboard of memory. It also belongs to those sections of the brain in which first damages occur in Alzheimer’s disease.

When measuring brain activity, the scanner was able to show its full potential: It was an “ultra-high field tomograph” with a magnetic field strength of seven Tesla. Such devices can achieve a better resolution than brain scanners usually used in medical examinations. This enabled the researchers to record brain activity in various sub-fields of the hippocampus with high precision. “Up to now, there were no comparable studies with such level of detail in ApoE genotyped participants. This is a unique feature of our research,” said Hweeling Lee.

No differences in memory performance

There were no differences between the three groups of subjects with regard to their ability for pattern separation. “All study participants performed similarly well in the memory test. It did not matter whether they had an increased, reduced or average risk for Alzheimer’s disease. Such results are certainly to be expected in young healthy people,” said Nikolai Axmacher, Professor of Neuropsychology at the Ruhr-Universität Bochum, who was also involved in the current study. “However, there were differences in brain activity. The different groups of study participants activated the various subfields of the hippocampus in different ways and to varying degrees. Their brains thus reacted differently to the memory task. In fact, we saw differences in brain activation not only between people with average and increased risk, but also between individuals with average and reduced risk.”

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Dementia diet – the fruit juice you should use while cooking to avoid Alzheimer’s

Dementia is the name given to a group of symptoms linked to an ongoing decline in brain function. You could lower your risk of the neurodegenerative condition by simply using lemon juice with your cooking, it’s been claimed.

There are a number of different types of dementia, and the most common in the UK is Alzheimer’s disease.

Diagnosing the condition early could help to slow down the condition’s progress.

Making some small lifestyle changes could lower your chances of developing Alzheimer’s in later life.

One of the best ways to protect against dementia is to regularly use lemon juice as a marinade, it’s been claimed.

People with dementia have large quantities of advanced glycation end products (AEGs) in their brains, according to Dr Fox Online Pharmacy’s Dr Deborah Lee.

AEGs are a type of protein that accumulate in the body, that may be harmful in large quantities.

They’re also produced by cooking foods for long periods of time at high temperatures.

But one of the easiest ways to limit the amount of AEGs in your cooking, and subsequently your dementia risk, is to use lemon juice as a marinade, she said.

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“When molecules collide within the bloodstream, sometimes sugars such as glucose, or fructose, stick themselves onto protein or fat particles,” she told Express Health.

“AEGs are produced by cooking for long periods and at high temperatures such as roasting, frying or barbecuing.

“When blood sugars are high, for example in prediabetes and diabetes, increasing numbers of AEGs are formed. AEGs are found in large quantities in the brains of people with Alzheimer’s disease.

“Marinade in lemon juice or vinegar before cooking [to reduce the number of AEGs].”

You could also protect against AEGs by steaming your vegetables, as opposed to frying them, she added.

Boiling or steaming vegetables reduces the number of AEGs by around 75 percent.

It’s a good idea to cook using lower temperatures, while processed foods are more likely to have higher quantities of AEGS.

You should cook from scratch wherever possible, and raw foods are better than cooked foods, she said.

There’s no certain way to prevent dementia from developing, but there are ways to lower your risk, said the NHS.

Eating a healthy, balanced diet should help to lower your chances of developing dementia.

It’s also important to do enough exercise. Everyone should aim to do at least 150 minutes of moderate-intensity activity every week.

There are around 850,000 people in the UK with dementia, and the condition affects one in every six people over 80 years old.

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A blood test for Alzheimer's that's almost 100% accurate

Scientists create a blood test for Alzheimer’s that’s almost 100% accurate and can spot the disease two decades before symptoms begin

  • Scientists can measure a hallmark protein of the disease years before symptoms 
  • The protein, called p-tau217, clumps abnormally in the brains of people with Alzheimer’s, causing memory loss, and some leaks into the bloodstream 
  • Researchers showed a blood test measuring levels of p-tau217 is 98% accurate
  • The step forward in research has been described as ‘extremely important’ 

A simple blood test can diagnose Alzheimer’s disease, sometimes decades before symptoms even begin.

Scientists revealed a protein involved in the damage of brain cells accumulates in the blood of patients up to 20 years before memory declines.  

P-tau217 clumps abnormally in the brains of Alzheimer’s patients — and some tiny fragments can leak into the bloodstream.

Researchers found a blood test that measured levels of the protein was 98 per cent accurate at identifying people with the memory-robbing disease. 

The breakthrough has been described as ‘extremely important’ for the development of treatments.

The cruel disease currently has no cure but finding one would be easier if trials may start on patients as early on in the disease as possible. 

The blood test could one day be used as a screening method to spot those at risk in a similar way that doctors look for high cholesterol or high blood pressure. 

It could be used by GPs in as little as five years once the test is refined, experts said.

But others were less optimistic, warning there are huge ethical concerns to tackle — telling people they will loose their memory will be devastating.  

A simple blood test is almost 100 per cent accurate at diagnosing Alzheimer’s disease, sometimes before symptoms even begin 

Some 850,000 people in the UK have dementia, the most common form of which is Alzheimer’s, accounting for around two thirds of patients. 

People with Alzheimer’s have tangles of proteins in the brain formed by tau proteins. They also have plaques formed by a protein called amyloid beta.

Amyloid beta and tau start to accumulate before any cognitive symptoms, such as memory loss and confusion, become apparent.

Tau is considered a hallmark protein of Alzheimer’s disease and other brain diseases.

It’s predominantly found in brain cells (neurons). But in people with Alzheimer’s disease, the proteins are misshapen.

 And Alzheimer’s disease is well known to feature tangles or clumps that are composed of tau protein. 

Scientists have long pointed to the importance of tau in Alzheimer’s because of evidence linking the spread of tau with disease progression. 

Another important protein is beta amyloid, the accumulation of which is largely completed at an earlier clinical stage known as mild neurocognitive disorder.

However, tau accumulation continues throughout the course of the disease, the Bright Focus Foundation reports.

Therefore, the total amount of abnormal tau in the brain is linked to disease stage and severity.

Tau clumps are not yet measurable with an available blood test, although research is ongoing. 

In the case of amyloid, a PET scan won’t identify disease severity because of amyloid’s early accumulation. 

Fluid from the spinal canal is taken to analyse for proteins related to dementia (known as a lumbar puncture). But this is not used routinely as a test for dementia and is more commonly used for research purposes.

But currently the disease can only be spotted when a person begins to show symptoms through an expensive brain scan, or a spinal tap — which takes fluid from the spine — to measure changing levels of the proteins in brain fluid. 

GPs in Britain currently rely on pen and paper memory tests to see if a patient’s decline in cognition matches up to typical scores of Alzheimer’s.

For many years, researchers have tried to develop blood tests that could detect Alzheimer’s.    

Anyone who was detected as a patient could begin treatment or be enrolled on drug trials in the early stages of the disease, when drugs are likely to be more effective and before the brain has suffered significant damage.

It is important to note, however, that there is no cure or treatment for Alzheimer’s. 

The research, by an international team from Sweden and the US, comprised of two studies which were presented today at the Alzheimer’s Association International Conference. 

It looked at a sub-group of tau, called p-tau217. 

Researchers in the US found p-tau217 accumulates in the cerebrospinal fluid — a clear, colorless body fluid found in the brain and spinal cord — of Alzheimer’s patients before the onset of cognitive symptoms.

Levels increase with disease progression, and can accurately predict the formation of amyloid plaques seen in patients’ brain scans.

The researchers developed a method to measure the amount of p-tau217 and other tau fragments in as little as 4ml of blood.

They found that, similar to cerebrospinal fluid, p-tau217 levels in the blood were extremely low in healthy volunteers but elevated in patients with amyloid plaques.

This was the case even in those who had yet to develop cognitive symptoms, according to the study published in the Journal of Experimental Medicine.

Lead researcher Randall Bateman, professor of neurology at Washington University School of Medicine in St Louis, said: ‘Our findings support the idea that tau isoforms in the blood are potentially useful for detecting and diagnosing Alzheimer’s disease pathology.’   

Scientists at Lund University, Sweden, found that levels of p-tau217 are seven times higher in the blood of people with Alzheimer’s than those without the condition.

Levels of the protein increase in the blood up to 20 years before the onset of dementia symptoms, well before the disease is visible in brain scans.

More than 1,400 people were enrolled in the study, according to the publication in the medical journal JAMA. 

It revealed the blood test was between 89 and 98 per cent accurate at identifying which patients had Alzheimer’s, depending on how far advanced their disease was.

Lead author Dr Oskar Hansson said: ‘This test, once verified and confirmed, opens the possibility of early diagnosis of Alzheimer’s before the dementia stage, which is very important for clinical trials evaluating novel therapies that might stop or slow down the disease process.’ 

Independent experts were excited about the study findings, but cautioned there was still work to be done before a blood test is viable.

HOW TO DETECT ALZHEIMER’S 

Alzheimer’s disease is a progressive brain disorder that slowly destroys memory, thinking skills and the ability to perform simple tasks.

It is the cause of 60 percent to 70 percent of cases of dementia.

The majority of people with Alzheimer’s are age 65 and older.

More than five million Americans have Alzheimer’s.

It is unknown what causes Alzheimer’s. Those who have the APOE gene are more likely to develop late-onset Alzheimer’s.

 Signs and symptoms:

  • Difficulty remembering newly learned information
  • Disorientation
  • Mood and behavioral changes
  • Suspicion about family, friends and professional caregivers
  • More serious memory loss
  • Difficulty with speaking, swallowing and walking

Stages of Alzheimer’s:

  • Mild Alzheimer’s (early-stage) – A person may be able to function independently but is having memory lapses
  • Moderate Alzheimer’s (middle-stage) – Typically the longest stage, the person may confuse words, get frustrated or angry, or have sudden behavioral changes
  • Severe Alzheimer’s disease (late-stage) – In the final stage, individuals lose the ability to respond to their environment, carry on a conversation and, eventually, control movement

Dr Amanda Heslegrave, Senior Research Fellow, UK Dementia Research Institute at University College London (UCL), said: ‘Since the methods previously used to measure these proteins such as lumbar puncture for CSF measurement or scans are either invasive or extremely costly, this is important.

‘While these are exciting results you could not say that they indicate a definitive test for potential Alzheimer’s disease is available right now.’  

Clive Ballard, a professor of age-related disease, University of Exeter Medical School, said although the research looked ‘promising’, ‘it could still be at least five years before we see an accurate blood biomarker test for dementia it in the clinic’. 

David Curtis, an honorary professor in genetics at University College London, said: ‘The results seem to be robust. From a clinical point of view, this kind of research is enormously important.

‘This will entail mass-screening, just as is now done to detect people with high cholesterol.

‘Unfortunately we do not yet have treatments to prevent Alzheimer’s disease, although tests such as this will greatly facilitate developing them. 

‘For now, the potential implications of such predictive tests could raise some challenging issues for society. There may well be some difficult ethical issues to think about.’

Professor Tara Spires-Jones, UK Dementia Research Institute at the University of Edinburgh, who said the results are ‘very solid’, added: ‘It is important to note that this blood test is not fool proof – there are some people with Alzheimer’s in the studies who have test results in the same ranges as healthy people.’ 

Professor John Gallacher, director of Dementias Platform UK, Department of Psychiatry, University of Oxford, said: ‘We remain a long way from a blood test to detect Alzheimer’s disease. 

‘Simply, the predictive value of a test is much lower in a general population than in the laboratory, and the ethical concerns of getting it wrong much greater. The search continues.’ 

Despite the potential barriers ahead, Dr Rosa Sancho, head of research at Alzheimer’s Research UK said: ‘A reliable blood test for Alzheimer’s disease would be a huge boost for dementia research, allowing scientists to test treatments at a much earlier stage which in turn could lead to a breakthrough for those living with dementia.’

Dr Fiona Carragher, director of research and influencing at Alzheimer’s Society, said: ‘A cost effective, accurate and non-invasive diagnostic test is a vital step in developing new treatments for the 850,000 people living with dementia in the UK today.’

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Adults with Alzheimer’s risk factors show subtle alterations in brain networks despite normal cognition

Researchers at McGill University and the Douglas Mental Health University Institute, in collaboration with the StoP-AD Center, have published a new paper in the Journal of Alzheimer’s Disease, examining how a known genetic risk factor for late-onset Alzheimer’s disease (AD) influences memory and brain function in cognitively intact older adults with a family history of AD.

For their study, the researchers looked at a specific gene, called apolipoprotein E (APOE), which has three allelic variants: e2, e3 and e4. Of these genetic variants, previous studies have shown adults with a single APOE e4 (+APOEe4) gene are at higher risk of developing AD. In this study, Drs. Sheida Rabipour, Maria Natasha Rajah and collaborators used functional magnetic resonance imaging (fMRI) to explore whether having a +APOEe4 genotype altered brain activity during memory task performance in older adults who may be at risk of developing AD.

“It turns out that the +APOEe4 variant, most strongly associated with AD development, doesn’t directly affect memory performance or brain activity in cognitively intact older adults,” explains Dr. Rabipour, a postdoctoral researcher in the lab of Dr. Rajah, and the study’s first author. “Rather, +APOEe4 seems to influence the brain regions and systems that older at-risk adults activate to support successfully remembering past events.”

Specifically, older adults with +APOEe4 use different brain regions, such as the parietal cortex, to support successful memory encoding, compared to adults without this genetic risk factor. In contrast, older adults without the APOEe4 genetic risk for AD use traditional memory-related brain regions, such as the medial temporal lobes and prefrontal cortex, to support successful memory encoding. The findings suggest that the role of +APOEe4, when examined over and above the influence of family history, is subtle, and affects the correlation between brain activity and memory performance.

Drawing on existing cohort for data

To complete their study, the researchers examined the influence of +APOEe4 in 165 healthy older adults from the PREVENT-AD cohort, factoring out age and family history, which are also important risk factors for AD. The team used a powerful multivariate analytical approach, enabling them to objectively disentangle people’s general sense of familiarity from specific recollection of an event and its associated context.

“We used a robust data-driven method that does not focus on any particular brain region, but rather examines the whole brain patterns of activity across the different stages and processes required to complete the memory task we designed,” says Dr. Rabipour.

The team was able to identify a distinct relationship between performance and brain activity patterns for recognition memory, even in cognitively normal older adults, based on +APOEe4 genotype. “In other words, even though all our participants were cognitively normal and performed well on the memory task, we were still able to detect a difference in the brain systems supporting memory function based on having a copy of +APOEe4,” notes Dr. Rabipour.

Moving forward

The findings of the study show that there are differences in the relationships between recognition and associated brain activity patterns based on genetic risk for AD and that these differences are measurable even in cognitively normal older adults, when accounting for family history of AD. Additionally they show that the tasks used to measure memory performance are important to consider when examining the nuances between different types of memory and how they may be affected by AD risk factors. Finally, the results suggest that family history and APOE genotype should be considered separately when examining AD risk.

“Understanding the ways in which different genotypes influence—or don’t influence—behavior and brain activity has important implications on the way we design treatments for AD-related memory impairments as well as our approach to preventing and delaying AD development,” explains Dr. Rabipour. “Using our task, we were also able to support a leading theory that memory systems for general familiarity are distinct from those that underlie detailed recollection of a past event. This could imply different approaches to diagnosing and treating conditions that impact one memory system compared to the other and may also help develop tools or strategies to enhance these types of memory as we age.”

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Dementia: The diet shown to be a ‘powerful weapon’ against brain decline

Dementia comes in numerous forms but the most common is Alzheimer’s disease. The symptoms of Alzheimer’s disease develop gradually over many years and eventually become more severe. Memory problems – usually the first sign – can begin with forgetting a recent conversation and may culminate in forgetting who your loved ones are. The decline is heartbreaking but research suggests you can (to an extent) protect yourself against it.

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Research shedding light on one of the factors that causes Alzheimer’s has also presented new ways of safeguarding against it.

In a research paper conducted by Professor Michael T. Heneka, of the Department of Neurology, University Hospital Bonn, Germany, and his co-authors, inflammation in the brain – known as neuroinflammation, was highlighted as a marker of Alzheimer’s disease.

According to Dr. Scuderi and her co-authors in the research paper, inflammation is an important component of Alzheimer’s disease because of the body’s immune reaction to initial abnormal deposits in brain cells.

Rather than making things better, however, this immune reaction that causes inflammation can rapidly develop to the point where it promotes the progression of Alzheimer’s disease, the research states.

This development has prompted researchers to investigate ways to counter brain inflammation.

According to Dr Fred Pescatore, a natural health physician based in New York and bestselling author of ‘The A List Diet’ and ‘Feed Your Kids Well’, one of the most promising countermeasures is to eat a ketogenic diet.

“The ketogenic diet is one of your most powerful weapons against brain inflammation,” he said, speaking exclusively to Express.co.uk.

The ketogenic diet is a very low-carb, high-fat diet that involves drastically reducing carbohydrate intake and replacing it with fat.

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This reduction in carbs puts your body into a metabolic state called ketosis, which can supply energy to your brain.

As Dr Pescatore reported, in a recent pilot study, researchers placed 15 subjects with mild Alzheimer’s on a ketogenic diet for three months.

They assessed cognitive function before the diet period, immediately after the diet period, and then a month later once the subjects had resumed their usual diets.

“Among these subjects, ten were able to achieve sustained ketosis,” he said.

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These patients showed significant cognitive improvement when compared to the five patients who didn’t follow the diet closely enough, noted Dr Pescatore.

Those who achieved sustained ketosis experienced a four-point increase in the Alzheimer’s Disease Assessment Scale-Cognitive Subscale Test (ADAS Cog), which is used to measure memory, language, and praxis, he said.

Other tips to reduce your risk

The latest research suggests that other factors are also important, although this does not mean these factors are directly responsible for causing dementia.

These include:

  • Hearing loss
  • Untreated depression (although this can also be a symptom of dementia)
  • Loneliness or social isolation
  • A sedentary lifestyle

The research concluded that by modifying all the risk factors we are able to change, our risk of dementia could be significantly reduced.

Furthermore, there’s some evidence to suggest that rates of dementia are lower in people who remain mentally and socially active throughout their lives.

Interventions such as “brain training” computer games have been shown to improve cognition over a short period, but research has not yet demonstrated whether this can help prevent dementia.

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It’s not just Alzheimer’s disease: Research highlights form of dementia

The long-running study on aging and brain health at the University of Kentucky’s Sanders-Brown Center on Aging Alzheimer’s Disease Center has once again resulted in important new findings—highlighting a complex and under-recognized form of dementia. The work was recently published in the Journal of the American Medical Association (JAMA): Neurology.

“One of the things that we’ve learned in the last decade or so is that a lot of people that we think have dementia from Alzheimer’s disease, actually don’t. There are other brain diseases that cause the same kind of symptoms as Alzheimer’s, including some that we only recently figured out existed,” said Erin Abner an associate professor at the University of Kentucky’s Sanders-Brown Center on Aging (SBCoA) and College of Public Health, who helped lead the recent study.

Abner collaborated with several of her colleagues at SBCoA for the study, which used brain autopsy data from 375 older adults within the University of Kentucky Alzheimer Disease Center Brain Bank. This work builds on the work done last year by Dr. Pete Nelson and his team to discover another form of dementia caused by TDP-43 proteinopathy now known as LATE.

Abner refers to misfolded TDP-43 protein, which was discovered in 2006, as the “newest brain bad guy.” She says although TDP-43 exists normally in a non-disease causing form, it is seen in multiple debilitating diseases in addition to LATE, including ALS and frontotemporal dementia. She says as she and the team at SBCoA reviewed clinical and brain autopsy data for research participants, they noticed there were significantly more people than expected that had not only Alzheimer’s pathology but also pathology indicating Lewy bodies (alpha synuclein), and the ‘newest brain bad guy’—TDP-43.

“They had every neurodegeneration causing pathology that we know about. There was not a name for this, so we came up with one: quadruple misfolded proteins, or QMP,” stated Abner.

The group then obtained more data to conduct a study of how often QMP occurred and what that meant for the participant with QMP. The study found that about 20% of the participants with dementia had QMP, and their dementia was the most severe.

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