Extraordinary memory or poor memory.

Extraordinary memory or poor memory.

“Apple. Table. Chair.”

Remember those objects.

The substance of memory prompts fascinating questions, conjectures and also quandaries.

“For me, it’s how extraordinary our memory can be in some cases and how impossibly poor it can be in other cases,” said Dr. David E. Dr. Warren, an assistant professor in the Department of Neurological Sciences at the University of Nebraska Medical Center where he specializes the application of scientific findings to clinical treatment.

Dr. Warren’s fascination with memory stems from the surprising intricacies of its functions as well as the limits of its capabilities. A person can remember details of childhood with what seems like perfect clarity, while at the same time they might forget where they parked the car at the grocery store.Helderberg Memory Centre Chris Verster

“It’s that discrepancy between the extraordinary capacity to store information and its every day failures that interests me,” Dr. Warren underscored.

When it comes to advancing the research of a severe brain disorder like Alzheimer’s disease, Dr. Warren’s interest and dedication to understanding memory embodies the type of individual you want standing in your corner.

Thanks to a significant grant from the Fremont Area Alzheimer’s Collaborative, a new pilot-study under development hopes to make forward strides in understanding how the initiation and progression of Alzheimer’s disease assaults specific areas of the brain; and how those clinical impacts might reveal more about the way the disease diminishes cognitive and behavioral functions of the brain.

Marv Welstead, a progressive and well-known advocate of Alzheimer’s research and treatment, and honorary member of the Fremont Area Alzheimer’s Committee, presented the check for $24,318 to Dr. Warren Friday morning during an interview with the Fremont Tribune.

“The goal (of the Fremont Area Alzheimer’s Collaborative) is that through the Fremont Area Memory Walk, 40 percent of the money we raise is for caregiver education and programming … and 60 percent is used for institutions conducting cutting-edge research in Alzheimer’s,” Welstead said, referring to dollars raised each year at the Fremont Area Memory Walk in October.

The Fremont Area Alzheimer’s Collaboration grant represents the 4th grant to UNMC with regards to memory and Alzheimer’s research. All totaled the Collaboration has donated approximately $100,000 to research into Alzheimer’s at UNMC. Welstead explained that this research proposal represents an innovative method in analyzing Alzheimer’s disease. It serves as a way for research institutes like UNMC to advance research by stimulating further, and larger grant funding from places like the National Institutes of Health. The grant is provided through a component fund managed by the Fremont Area Community Foundation.

“The Fremont Area Community Foundation is proud to support the groundbreaking research being performed by Dr. Warren and his team at UNMC. Thanks to supporters of the Fremont Area Alzheimer’s Fund … we are helping to advance promising research in the search for a cure,” said Melissa Diers, executive director of the Foundation.

Those types of grants enable scientists to lay a foundation for further research known as ‘seed’ funding. This funding of pilot projects carries a critical importance for scientific research because the National Institutes of Health and other funding organizations require researchers to demonstrate supporting evidence or data with their research proposals.

“You have to come in with a great idea and evidence to back it up,” Dr. Warren said. “With seed money … a great idea can turn into a study; and a study can turn into a translational finding that we could potentially apply to patient care to improve the outcomes of patients with Alzheimer’s disease.”

Using high-tech, non-invasive neuro-imaging, neuro-stimulation and neuro-psychological techniques the research project plans to investigate how the disease impacts memory and cognitive functions of the hippocampus.

With Magnetic Resonance Imaging (MRI) researchers will delve deep into the inner workings of live, thinking brains. It will analyze the hippocampus and surrounding brain regions involved in memory formation and processing. Moreover, researchers will attempt to discover ways to improve early detection of the disease and compare healthy brains to those with Alzheimer’s disease.

Scientists will monitor the moment-to-moment activation of certain brain structures to determine how those activations cascade into other structural areas. Such analysis permits scientists to form better pictures of how the whole brain “network” interacts in both healthy and Alzheimer’s-infected individuals.

Additionally, using a form of neuro-stimulation, Dr. Warren’s team plans to explore the viability of remediating memory impairment caused by Alzheimer’s disease.

He cited previous evidence from research that demonstrated the means through which neuro-stimulation promotes improvements in certain kinds of memory function for healthy individuals.

Similarly, Dr. Warren’s team is interested to discover if neuro-stimulation techniques might carry the same potential improvements for Alzheimer’s patients.

Dr. Daniel L. Murman, director of the Behavioral and Geriatric Neurology program at UNMC, explained the study represents cutting edge investigation. It could lead to a better grasp of how Alzheimer’s effects certain brain areas. Further, it holds the promise of allowing researchers the ability to intervene with neuro-stimulation.

“Someday, instead of telling the patients with memory impairment to do crossword puzzles to improve their cognitive function, we may be able to stimulate the brain to improve memory,” Murman said.

Dr. Warren reiterated the complexity of memory. It comes in all forms he explained. And Alzheimer’s progresses through stages, impairing different types of memories along its devastating path. Simple memory tests can diagnose the disease. Dr. Warren cautioned doctors and patients must remain mindful in differentiating the normal, age-related decline of memory function experienced by most people to the more rapid and severe decline in Alzheimer’s.

“And this is a challenge, because almost every older adult that I speak to complains about their memory, so how do you distinguish between pathological problems and … changes in memory related to normal aging,” Dr. Warren said.

The key is to ask, “Does it interfere with your daily life?”

And that’s where those three arbitrary objects mentioned in the first sentence return. They probably have no impact on your life, so if you can’t remember them, chances are you’re just getting old.

OTC drugs implicated in cognition testing

OTC drugs implicated in cognition testing

So-called anticholinergic drugs, easily available treatments widely known by trade names associated with treatments for sleep disorder, hypertension, heart disease and COPD, have been linked with cognitive impairment and a higher risk of developing dementia, according to research concluded at the Indiana University School of Medicine. As reported on the CNN website, study subjects were assessed on a range of memory and cognitive tests and, with the aid of PET and MRI imaging technology, they were scored for impact on brain structure and metabolism.

Female Chemist Looking At Products In Pharmacy

It was determined that research subjects who had been taking the anticholinergic drugs performed worse on short-term memory tests while also exhibiting lower levels of glucose metabolism in the brain overall and, markedly, within the hippocampus – the part of the brain associated with the earliest stages of Alzheimer’s.

Please contact the Helderberg Memory Centre in Somerset West – Western Cape- and become part of our clinical trials.

What is Alzheimer’s Disease?

What is Alzheimer’s Disease?

Alzheimer’s disease is a type of dementia and also the most common cause of dementia.   Dementia refers to a number of symptoms that include loss of memory (especially short-term memory) as well as problems with the use of language.  Further symptoms include difficulties with thinking, problem-solving or language.

The disease is caused by a build-up of proteins in the brain. ‘Plaques’ and nerve ‘tangles’ are formed and these impact on the connections between nerve cells in the brain, eventually causing the death of some of these cells.IMG_5768

Brain function is also dependent on chemical transmitters and some these also become depleted in Alzheimer’s Disease.

Alzheimer’s Disease typically has a gradual progression and it is often difficult to determine exactly when the illness started.

A further characteristic of Alzheimer’s Disease is that it is a disease of the elderly. It is relatively rare below the age of 60, and becomes progressively more common as age increases.


Want to be part of our Clinical Trials?

The Cognitiv|AD clinical trial is evaluating the safety and effectiveness of a study medication used in mild to moderate Alzheimer’s disease patients currently or previously taking:

  • Aricept (Donepezil Hydrochloride)
  • Reminyl (galantamine)
  • Exelon (rivastigmine)

Patients eligible for the Cognitive|AD Clinical trial could create hope for the future!

Contact us – Helderberg Memory Centre -Somerset-West – and find out how you can be part of our clinical trials.

How to cure Alzheimer’s Disease

How to cure Alzheimer’s Disease

Putting the pieces together on how to cure Alzheimer’s Disease.  The most common form of dementia is Alzheimer’s disease, a progressive disorder of the human brain which over time reduces a person’s cognitive abilities to the point that they cannot carry out the most basic tasks. This terrible disease was thrust back into the national conscious as the result of the death of Nancy Reagan. No retelling of the lief of Mrs. Reagan would be complete without mention of her fairy tale love affair with President Ronald Reagan, or President Reagan’s long battle with Alzheimer’s disease.

With this in mind we thought we might take a moment to review what scientists know about Alzheimer’s disease and what treatments and cures are currently being pursued.

Alzheimer’s and Risk Factors

The National Institute on Aging estimates that there are more than five million Americans who may suffer from Alzheimer’s, which accounts for anywhere from 60 percent to 80 percent of all cases of dementia in the U.S. Alzheimer’s causes the buildup of amyloid plaques and tau tangles in the brain tissue of an affected individual, killing off brain cells for years before symptoms of memory loss start to occur.

Alzheimer’s disease is such a difficult medical problem to answer in part because the damage is irreversible, but also because there are so many scientific unknowns involved in the process. Researchers still have very little understanding of the underlying causes for Alzheimer’s, which is a major reason why no cure exists yet. An editorial published in a recent issue of the Journal of Alzheimer’s Disease theorizes that microbes in the brain could be a contributing factor, but this theory has proven to be controversial in the past.  The major risk factors for Alzheimer’s are related to aging and genetics, factors which cannot be changed through conventional medicine. Regular physical exercise, challenging mental activity and overall diet are thought to help improve overall health and thus the risk of developing Alzheimer’s, but it’s not known what can be done to directly prevent the formation, or slow the progression, of the damage once it starts.

A good attention to proper oral care and hygiene may be another way to encourage the best possible prognosis for Alzheimer’s patients, according to a study published in the peer-reviewed open access scientific journal PLOS ONE. Researchers from the University of Southampton and King’s College London contributing to the study found a steep decline in the mental activity of Alzheimer’s patients among those who had gum disease. The findings support the notion that the immune system response triggered by bacteria reaching the brain, including certain inflammatory effects, may be strongly linked to the progression of Alzheimer’s disease.

Computer usage may also be an indicator of Alzheimer’s in people of advanced age, according to research performed at Oregon Health and Science University and also published in the Journal of Alzheimer’s Disease. A demonstrated link between computer use and hippocampal volume, which is a major factor affecting human memory, was found in healthy adults of at least 65 years of age. Smaller hippocampal volume is thought to be an indicator of Alzheimer’s.


Early Diagnosis of Alzheimer’s

Earlier diagnoses can give Alzheimer’s patients more time to plan for their long-term care and explore treatment options. A new type of blood test developed by German scientists could increase the maximum amount of time for early detections up to 15 years before clinical symptoms begin to appear. The study results, published in a March issue of Biophotonics, discuss a test involving an infrared sensor which is able to detect the misfolding of amyloid-beta peptides which gradually form into amyloid plaques, causing brain damage. The earlier detections could help doctors prescribe medications that would delay the onset of brain damage; once clinical symptoms appear, a great deal of irreversible damage has already been done.

Early detection of Alzheimer’s could also be bolstered by innovative medical science research taking place at the University of Southern California. A study published in the scientific journal Trends in Cognitive Science identifies the locus coeruleus as the first part of the human brain which is affected by the onset of Alzheimer’s. The locus coeruleus regulates blood vessel interactivity throughout the brain and releases norepinephrine, a neurotransmitter which affects attention, cognition and memory. The way that the locus coeruleus interacts with the rest of the brain makes it more susceptible to toxins as well as infections in other areas of the brain, the researchers found.


Research into Alzheimer’s

A new defense against the formation of amyloid-beta into hardened plaques could have come from a team of Swiss scientists working at the École Polytechnique Fédérale de Lausanne. A study published in the neurology journal Brain discusses an implantable capsule containing cells which have shown themselves to be effective at counteracting the process by which amyloid-beta uses to clump together. The researchers have been able to produce the amyloid-beta countering effects by implanting the capsule into mice. The semi-permeable capsule, which measures 27 millimeters (mm) long by 12 mm wide by 1.2 mm thick, includes a hydrogel shielding the cells from the body’s immune system while allowing the cells to draw nutrients from the body.

Snake venom could prove to be an unlikely source for an Alzheimer’s treatment, but that could be the case thanks to research taking place at Australia’s Monash University. Scientists at that institution were able to isolate a molecule from the venom of a poisonous snake, Bothrops asper, which stimulated enzymes helping to fight the plaque created by amyloid-beta deposits. The compound has also shown some effectiveness in being used to treat bleeding caused by wounds.

Techniques for unraveling the tau tangles which are another element of Alzheimer’s progression in patients could be coming if a drug developed by a Singapore-based pharmaceutical firm continues to have successful trials. TauRx Pharmaceuticals, founded in 2002, has produced a drug called LMTX which helped to produce better cognitive scores in Alzheimer’s patients in early trials. The results are based on three decades of research performed by Claude Wischik, currently a professor at the University of Aberdeen in Scotland.

The brain damage caused by Alzheimer’s might be irreversible, but a study produced by researchers at the Massachusetts Institute of Technology (MIT) and published in Nature gives rise to the notion that a person’s memories could still be retrieved even after Alzheimer’s has damaged brain tissues. The researchers identified dentate gyrus (DG) neurons which, when activated, were able to retrieve memories in mice which were formed during contextual fear conditioning. Researchers also ablated the DG neurons using diphtheria toxin and found that the mice couldn’t retrieve the same memories. There are likely differences in the brain functions of human Alzheimer’s patients and engineered mice, researchers warn, but this finding would provide further evidence of the important role played by the hippocampus, where the DG neurons are located.

Future developments that could link vascular disease to the development of Alzheimer’s could come from Emory University in the coming years. The academic institution recently received a five-year, $5.2 million grant for greater exploration into any possible connection between the regulation of blood pressure and Alzheimer’s. It’s hoped that the research will lead to potential new treatments for the disease, specifically ones which may target the renin-angiotensin system and endothelial cells.

“Contact us to find out more about our Alzheimer’s Trial program from Helderberg Memory Centre

Resource:  http://www.ipwatchdog.com/2016/03/27/putting-the-pieces-together-on-how-to-cure-alzheimers/id=67404/

Controversial New Push to Tie Microbes to Alzheimer’s Disease

Controversial New Push to Tie Microbes to Alzheimer’s Disease

A journal article says herpes virus and Lyme disease bacteria are behind the mind-robbing illness, but not all researchers are convinced.

Scientists have long puzzled over the root causes of Alzheimer’s disease, a devastating and typically fatal condition that currently denies more than five million Americans their cognition and memory. But in a provocative editorial soon to be published in the Journal of Alzheimer’s Disease, a cadre of scientists argue that the complex disease may have a surprisingly simple trigger: tiny brain-infecting microbes. This controversial view, which is not new, has long been dismissed as outlandish, but a growing body of work suggests it may be worth considering and further studying. If researchers can prove the theory and iron out the many argued-over details—both formidable tasks, as brain infections are difficult to study—Alzheimer’s could become a preventable illness.

The editorial, signed by 31 scientists around the world, argues that in certain vulnerable individuals—such as those with the APOE ε4 gene variant, a known Alzheimer’s risk factor—common microbial infections can infect the aging brain and cause debilitating damage. These microbes may include herpes simplex virus 1 (HSV-1), the ubiquitous virus that causes cold sores as well as Chlamydophila pneumoniae and Borrelia burgdorferi, the bacteria that cause pneumonia and Lyme disease, respectively.Helderberg Memory Centre Somerset West

The controversial idea butts heads with the long-standing theory that amyloid-beta proteins and tau tangles, both of which build up inside the brains of those with Alzheimer’s, are the main drivers of disease-induced cell death. Instead, supporters of the pathogen hypothesis, as it is called, posit that either pathogens induce brain cells to produce the amyloid proteins and tau tangles or that nerve cells that have been damaged by infection produce them as part of an immune response. “We think the amyloid story does come into play, but it’s secondary to the initial inflammation,” says editorial co-author Brian Balin, who directs the Center for Chronic Disorders of Aging at the Philadelphia College of Osteopathic Medicine.

Critics of the pathogen theory point out that much of the supportive human research does not establish cause and effect. In a study published in The Lancet in 1997, a team led by Ruth Itzhaki, one of the editorial’s co-authors and a molecular neurobiologist at the University of Manchester in England, reported that people whose brains were infected with HSV-1 and who also had the APOE ε4 gene variant were 12 times more likely to develop Alzheimer’s than those with either the gene variant or the infection alone. One hypothesis is that the APOE ε4 variant makes it easier for HSV-1 to infect brain cells—but, critics say, it could also be that the gene variant and the infection are associated with Alzheimer’s in ways that are not causal.

Scientists have tried to nail down the mechanics of the relationship using animals. Researchers in Spain have found, for instance, that mice whose brains have been infected with HSV-1 produce nearly 14 times as much viral DNA when they have the APOE ε4 variant compared with when they do not. And after infecting the brains of mice with HSV-1, Itzhaki’s group showed that their brains accumulated amyloid plaques. But these studies are criticized, too—after all, what happens in a mouse’s brain may not happen in a human’s.

The burden of proof is formidable for this theory, in part because it is impossible to detect infections like HSV-1 in the brains of living people—they can only be seen postmortem. “‘Proof of causation is a major, critical and very complex issue,” says David Relman, an infectious disease specialist at Stanford University. Itzhaki agrees, noting that one cannot just inject people with the virus and wait to see if they develop Alzheimer’s. (That said, Australian microbiologist Barry Marshall finally convinced skeptics that Heliobactor pylori bacteria cause gastric ulcers by infecting himself.) Itzhaki says that one potential solution would be to conduct a pilot clinical trial that evaluates whether HSV-1-infected individuals with mild Alzheimer’s and the APOE ε4 variant improve if they are treated with antiviral drugs. They have already shown in the lab that these drugs inhibit amyloid plaque production in HSV-1 infected cells. But she has applied for funding for a human study multiple times and has so far has been unsuccessful.

Rudolph Tanzi, a neurologist at Harvard University who directs the Genetics and Aging Research Unit at Massachusetts General Hospital, agrees that microbes likely play a role in Alzheimer’s—but his work suggests that the brain’s response to the infection is more dangerous than the infection itself. “We do need to take the role of microbes in the brain seriously, but it’s going to be a lot more involved than simply saying ‘infection causes Alzheimer’s disease,’” he notes. (He was not involved in the editorial.) In a 2010 study Tanzi and his colleagues reported that the amyloid protein strongly inhibits microbial growth in the brain, which suggests that it accumulates as a protective response to infection. “Over the last five years, following up from that 2010 paper, we’ve showed that in every Alzheimer’s model tested—from cells to flies to dirt worms to mice—beta amyloid potently protects from infection,” he explains. The presence of even just a few microbes in the brain, he says, triggers its accumulation.

Infections induce potent immune responses, too, and they likely worsen the problem. Normally, brain immune cells called microglia clear amyloid proteins from the brain. But when these cells get fired up in response to infection, they stop, causing the proteins to build up even faster. As Tanzi’s team showed in a 2014 Nature paper, the amyloid proteins that fill up the brain then spark the creation of tau tangles, which cause more brain cell death. “And now, you have the full-blown disease,” he says. (Scientific American is part of Springer Nature.)

As for which pathogens might be triggers, HSV-1 is a contender, Tanzi says, but it is too soon to know for sure. “I think we have to take a couple of steps back and say, ‘What types of bacteria, viruses and fungus accumulate in the brain as we age?’ and study this systematically in an unbiased, agnostic way,” he says. He is leading a consortium funded by the nonprofit Cure Alzheimer’s Fund to map the microbiome of the human brain; once potentially important microbes are identified, it might be possible to develop neuroimaging techniques to track them in the brains of living individuals, he says.

Other Alzheimer’s scientists still are not convinced, however. David Holtzman, chair of the department of neurology at Washington University School of Medicine in St. Louis and associate director of its Knight Alzheimer’s Disease Research Center, told Scientific American that although more research on the idea is warranted, “there is not clear or conclusive evidence of whether or how different infections influence risk for Alzheimer’s disease.” Tanzi says that when he presents his findings and ideas at scientific meetings, reactions are indeed mixed. One comment Itzhaki often hears is that HSV-1 cannot cause Alzheimer’s if it is also found, as it is, in the brains of elderly healthy people. But she points out that other pathogens, including tuberculosis, only cause symptoms in subset of vulnerable individuals, too.

If microbes do turn out to be a potential trigger for Alzheimer’s—and to most in the field, this is still a big “if”—the implications would be huge: It might be possible to vaccinate against the debilitating disease simply by inoculating against offending infections. At the very least, doctors might be able to treat infections with antimicrobial drugs before they harm the brain. But building enough evidence to prove the theory could take decades. Among other challenges, researchers working in the area complain of funding woes. “Over the 50-plus years that I’ve been doing the work, our group has had extreme difficulties nearly all the time—we’ve been working on a shoestring,” Itzhaki says.

But given that hundreds of clinical trials for Alzheimer’s drugs have failed based on the prevailing dogma, those working on the various versions of the pathogen theory believe it is worth pushing forward. More than anything, they hope their editorial will encourage skeptics to at least consider the possibility that microbes could play a role in Alzheimer’s disease and support their desire to study it more. “We’re saying ‘wait a minute, folks—we have a body of evidence here from decades of work that we have to stop ignoring,’” Balin says.


Brain scan to diagnose Alzheimer’s Disease developed by scientists

Brain scan to diagnose Alzheimer’s Disease developed by scientists

Alzheimer’s disease could be definitively diagnosed for the first time after scientists proved brain scans can pick up the condition in its earliest stages.

Currently the only way to determine whether Alzheimer’s is present is to look at the brain of a patient after death.

For patients who are still alive, doctors usually use special cognitive tests which monitor memory and everyday skills such as washing and dressing.

But now researchers at the University of California have proven that it is possible to spot the sticky amyloid plaques and tau protein tangles which cause the disease and pinpoint the moment that they trigger Alzheimer’s disease.

The US scientists were able to track the progressive stages of Alzheimer’s disease, even in adults who showed no symptoms. It means that people at risk from the condition – such as one in five of the population who carry the APOE gene variant– could be regularly screened.

And it could reassure people who are suffering mild memory problems that they do not have the disease.

The distribution of tau and amyloid plaques in the brain is known as ‘Braak staging’ because it was discovered by Heiko and Eva Braak who studied the brains of Alzheimer’s patients after death.

“Our study is the first to show the staging in people who are not only alive, but who have no signs of cognitive impairment,” said study principal investigator Dr William Jagust, a professor at UC Berkeley’s School of Public Health.

“This opens the door to the use of scans as a diagnostic and staging tool.”

Brain Pet Scan Alzheimer's Disease

There are currently 850,000 people living with dementia in Britain which is due to rise to one million by 2025 and two million by 2050. Although there are currently no drugs to treat the disease it is hoped that within as little as five years treatments may be available which can delay the onset. It is therefore crucial to be able to pick up the disease early enough for drugs to be effective.

The new brain imaging is carried out using positron emission tomography scanners which look at cellular-level changes in organs and tissue.

Current scans only look for a decrease in brain cells or check that symptoms are not caused by another condition, such as a brain tumour.

The new technology was tested on 53 adults, five of whom were young adults, 33 pensioners without any neurodegeneration and 15 who had suspected Alzheimer’s disease. The scientists were able to prove definitively which were clear, at risk and those who had the condition.

The findings also shed new light on how tau protein and amyloid plaques build up as the brain ages.

For many years, the accumulation of amyloid plaques was considered the main culprit in Alzheimer’s disease. But tau is now also known to be responsible. When tau protein gets tangled and twisted, its ability to support connections between brain cells becomes impaired.

Through the PET scans, the researchers confirmed that with advancing age, tau protein accumulates in the medial temporal lobe – home to the hippocampus and the memory center of the brain. However when the tau went beyond that area Alzheimer’s begins.

The scientists believe that both tau and amyloid work together to cause the disease.

“Amyloid may somehow facilitate the spread of tau, or tau may initiate the deposition of amyloid. We don’t know. We can’t answer that at this point,” added Dr Jagust.

“All I can say is that when amyloid starts to show up, we start to see tau in other parts of the brain, and that is when real problems begin. We think that may be the beginning of symptomatic Alzheimer’s disease.”

Dr Samuel Lockhart, of UC Berkeley’s Helen Wills Neuroscience Institute added: “It’s not that one is more important than the other. Our study suggests that they may work together in the progression of Alzheimer’s.”

“Tau is basically present in almost every aging brain,” said visiting scholar Dr Michael Schöll, of Sweden’s University of Gothenburg.

“Very few old people have no tau. In our case, it seems like the accumulation of tau in the medial temporal lobe was independent of amyloid and driven by age.”

Dr James Pickett, Head of Research at Alzheimer’s Society said: “We know it can take months, and sometimes years, for some people to get diagnosed with Alzheimer’s and so a definitive way to diagnose the disease would be a big leap forward. Currently, the only way to know for sure whether someone’s memory impairment is due to Alzheimer’s disease is to examine their brain tissue after death and look for damaged proteins.

“This new scan allows us to see tangles of a protein called tau – one of the hallmarks of Alzheimer’s disease – inside the brain,but so far it has only been tested in a small number of people. Only 15 people with Alzheimer’s disease were included in this study, some of whom were not typical of the majority of cases. This makes it difficult to determine how useful the scan could be to support diagnosis.

“This technology is in the early stages of development and while it is beginning to provide researchers with important data about how Alzheimer’s disease develops, it is still many years before we could expect to see the scan being used in the clinic.”

Dr Simon Ridley, Director of Research at Alzheimer’s Research UK, said that the new brain scan looked ‘promising.’

“One challenge for diagnosing and researching diseases like Alzheimer’s is that it’s hard to know exactly what’s happening inside the brain over time.

“One important question that still remains in Alzheimer’s research is exactly where and when amyloid and tau proteins start to build in the brain and how this leads to the symptoms that people experience. It’s promising to see brain scan research now looking at both amyloid and tau in the brain in living people.

“Further research using PET scans to study tau will provide greater insight into how it interacts with amyloid and contributes to the disease, and whether this information could translate to meaningful improvements in diagnosis or treatments in the clinic.”

Source: The research was published in the journal Neuron.