Posts tagged ‘Alzheimer’
Changes to specific cells in the retina could help diagnose and track the progression of Alzheimer’s disease, scientists say.
A team found genetically engineered mice with Alzheimer’s lost thickness in this layer of eye cells.
As the retina is a direct extension of the brain, they say the loss of retinal neurons could be related to the loss of brain cells in Alzheimer’s.
The findings were revealed at the US Society for Neuroscience conference.
The team believes this work could one day lead to opticians being able to detect Alzheimer’s in a regular eye check, if they had the right tools.
[This] could lead to new ways to diagnose or predict Alzheimer’s that could be as simple as looking into the eyes”
Dr Scott TurnerGeorgetown University Medical Center
Alterations in the same retinal cells could also help detect glaucoma – which causes blindness – and is now also viewed as a neurodegenerative disease similar to Alzheimer’s, the researchers report.
Scott Turner, director of the memory disorders programme at Georgetown University Medical Center, said: “The retina is an extension of the brain so it makes sense to see if the same pathologic processes found in an Alzheimer’s brain are also found in the eye.”
Dr Turner and colleagues looked at the thickness of the retina in an area that had not previously been investigated. This included the inner nuclear layer and the retinal ganglion cell layer.
They found that a loss of thickness occurred only in mice with Alzheimer’s. The retinal ganglion cell layer had almost halved in size and the inner nuclear layer had decreased by more than a third.
“This suggests a new path forward in understanding the disease process in humans and could lead to new ways to diagnose or predict Alzheimer’s that could be as simple as looking into the eyes,” said Dr Turner.
- Symptoms include loss of memory, mood changes, and problems with communication and reasoning
- No one single factor has been identified as a cause for Alzheimer’s disease – a combination of factors, including age, genes, environment, lifestyle and general health are implicated
- One of the leading theories involves the formation of clumps of a protein called beta-amyloid, which damage and kill brain cells
Treatments developed for Alzheimer’s could therefore also be useful for treating glaucoma, he added.
But he also said that so far it was still speculation to say that retinal thinning may predict impending Alzheimer’s disease.
“We’re hoping that this translates to human patients and we suspect that retinal thinning, just like cortical thinning, happens long before anyone gets dementia,” Dr Scott told BBC News.
“Human studies are needed to test this idea as a diagnostic [test]. Current leading biomarkers of Alzheimer’s disease are either very costly or invasive. A retinal thickness scan – as measured by optical coherence tomography – would be both inexpensive and non-invasive.”
Alzheimer’s is a neurodegenerative disease and is the most common type of dementia. The cause is still unknown and there is currently no cure. It often goes undetected for years until so many cells die that symptoms become increasingly prevalent.
But treating the disease early is believed to be vital to prevent memory loss.
Laura Phipps, at Alzheimer’s Research UK, said there was increasing evidence linking retinal cell loss to Alzheimer’s disease, and that it was “positive to see this line of research being followed up”.
“This early-stage study, which is yet to be published in full, was carried out in mice, and further research will be necessary to determine whether changes in the retina found here are also found in people with Alzheimer’s.
“Diagnosing Alzheimer’s with accuracy can be a difficult task, which is why it’s vital to continue investing in research to improve diagnosis methods,” Dr Phipps added.
It could lead to new ways of diagnosing the condition and of testing the effectiveness of new drugs.
The technology, reported in the journal Neuron, can identify inside a living brain clumps of a protein called tau that is closely linked to the disease.
Alzheimer’s Research UK said it was promising work.
Alzheimer’s disease is a problem for researchers trying to come up with a cure. The brain starts to die years before any symptoms are detected, which means drugs are probably given too late.
A diagnosis of Alzheimer’s cannot be made with absolute certainty until a patient has died and their brain is examined. It is also not 100% clear what is the cause of the dementia and what are just symptoms.
One protein, called tau, is very closely linked to the disease, with tangles of tau thought to be one way in which brain cells are killed.
The team, lead by the National Institute of Radiological Sciences in Chiba, used positron emission tomography to build a 3D picture of tau in the brain.
They developed a chemical that could bind to tau and then be detected during a brain scan.
Finding tau in the brain
Tests on mice and people with suspected Alzheimer’s showed the technology could detect tau.
Dr Makoto Higuchi, from the National Institute of Radiological Sciences in Japan, said: “Positron emission tomography images of tau accumulation… provide robust information on brain regions developing or at risk for tau-induced neuronal death.”
The research is at an early stage, but it could eventually lead to an actual test for Alzheimer’s disease.
It might also allow researchers to closely follow the impact drugs that affect tau have on the brain.
Another protein – beta amyloid – is also linked to Alzheimer’s and can be detected in similar tests.
Dr Eric Karran, director of research at Alzheimer’s Research UK, said: “This promising early study highlights a potential new method for detecting tau – a key player in both Alzheimer’s and frontotemporal dementia – in the living brain.
“With new drugs in development designed to target tau, scans capable of visualising the protein inside the brain could be important for assessing whether treatments in clinical trials are hitting their target.
“If this method is shown to be effective, such a scan could also be a useful aid for providing people with an accurate diagnosis, as well as for monitoring disease progression.”
File photo: A woman suffering from Alzheimer’s disease walks along a corridor in a retirement home in France. (AFP/Sebastien Bozon)
Scientists have reported new evidence that copper can lead to the plaque buildup in the brain that causes Alzheimer’s disease, fuelling debate over whether copper — found in red meat, vegetables as well as drinking water pipes — causes or prevents the disease.
WASHINGTON: Scientists on Monday reported new evidence that copper can lead to the plaque buildup in the brain that causes Alzheimer’s disease, fuelling fresh debate over the mineral’s role in dementia.
The scientific community is divided on the question of whether copper — found in red meat, vegetables, dairy products as well as pipes that carry drinking water in much of the developed world — causes or prevents Alzheimer’s disease.
For the latest study in the Proceedings of the National Academy of Sciences, researchers looked at how copper in the capillaries may cause a breakdown in the blood-brain barrier, leading to a buildup of the protein amyloid beta, or plaques that are a hallmark of Alzheimer’s.
According to lead author Rashid Deane, a research professor at the University of Rochester Medical Center, experiments using mice and human cells showed that low levels of copper delivered via drinking water accumulated in the capillary walls that feed blood to the brain.
“These are very low levels of copper, equivalent to what people would consume in a normal diet,” said Deane.
The copper caused oxidation which interfered with another protein, called lipoprotein receptor-related protein 1 (LRP1), that would normally clear amyloid beta from the brain, his study said.
Not only did copper appear to prevent the clearance of plaque that is believed to be a prime culprit in Alzheimer’s, it also stimulated neurons to produce more amyloid beta.
Researchers described their findings in a press release as a “one-two punch” that “provides strong evidence that copper is a key player in Alzheimer’s disease.”
“Copper is an essential metal and it is clear that these effects are due to exposure over a long period of time,” said Deane in a statement.
“The key will be striking the right balance between too little and too much copper consumption. Right now we cannot say what the right level will be, but diet may ultimately play an important role in regulating this process.”
However, other experts who have studied copper and Alzheimer’s questioned the paper’s findings.
“Research including our own shows the opposite, that copper prevents amyloid from forming the type of structures seen in the plaques,” said Christopher Exley, professor in Bioinorganic Chemistry at Keele University in Staffordshire.
Exley and colleagues recently published their latest paper on the topic in the British journal Nature in February.
“As a group we would be thinking, based on everything that we know — and our research has been done with human brains and brain tissues — that if anything, copper would be protective against Alzheimer’s.”
Exley said a “number of things” in the PNAS paper raised red flags, such as the way they measured the copper amounts and the fact that they used animal models which do not always translate directly to humans.
“You do need a significant amount of tissue to produce results that you have a high level of confidence in. A mouse capillary — these are very, very, very small things,” Exley told AFP.
“The amount of copper which they are talking about as being possibly proactive is normal,” he added.
“If you took this paper at absolute face value, it is telling everybody that we are all suffering from the effects that this paper is documenting right now because we are all exposed to this amount of copper.”
Another outside researcher, George Brewer, emeritus professor of internal medicine at the University of Michigan medical school, said the “authors miss an important point about copper toxicity to the brain.”
“They don’t differentiate copper delivered in drinking water, as they delivered it in their study, from copper in food,” Brewer said in an email to AFP.
“We have always had copper in food, so it couldn’t possibly be the cause of this new AD epidemic,” he said.
“If they had added this trace amount of copper to food, rather than putting it in drinking water, it would have had no effect.”
Alzheimer’s is a growing problem as people live longer
Researchers believe they are closer to developing a blood test that could diagnose Alzheimer’s.
There is no definitive test for the brain-wasting disease. Doctors rely on cognition tests and brain scans.
A technique published in the journal Genome Biology showed differences in the tiny fragments of genetic material floating in the blood could be used to identify patients.
The test was accurate 93% of the time in trials on 202 people.
One of the main goals of Alzheimer’s research is to find ways of detecting the disease earlier.
It starts years before symptoms appear and it is thought that future treatments will need to be given before large parts of the brain are destroyed. This will require new ways of testing for the condition.
The team at the Saarland University, in Germany, analysed 140 microRNAs (fragments of genetic code) in patients with Alzheimer’s disease and in healthy people.
They found 12 microRNAs in the blood which were present in markedly different levels in people with Alzheimer’s. These became the basis of their test.
Early trials showed it was successful and was “able to distinguish with high diagnostic accuracies between Alzheimer’s disease patients and healthy” people.
However, more research to improve accuracy and to see whether it would work in the clinic is still needed before the test would be considered as a way of diagnosing patients.
Dr Eric Karran, from the charity Alzheimer’s Research UK, said: “This is an interesting approach to studying changes in blood in Alzheimer’s and suggests that microRNAs could be playing a role in the disease.
“The findings highlight the importance of continuing research efforts to understand the contribution of microRNAs to Alzheimer’s, but the translation of this into a blood test for Alzheimer’s in the clinic is still some way off.
“A blood test to help detect Alzheimer’s could be a useful addition to a doctor’s diagnostic armoury, but such a test must be well validated before it’s considered for use. We need to see these findings confirmed in larger samples and more work is needed to improve the test’s ability to distinguish Alzheimer’s from other neurological conditions.”
October 8, 2012 (WLS) — Two large studies show patients with mild Alzheimer’s disease taking an experimental drug had 34 percent less decline in memory over 18 months compared with those taking placebos.
The drug is called solanezumab. The analysis of data from two large studies were presented Monday at a medical meeting in Boston. But this closely watched drug did not significantly protect against loss of physical functions.
Scientists say the latest data lend further credence to the theory that Alzheimer’s must be attacked early in the disease for drugs to have a clinically meaningful impact.
The drug works by blocking a protein called beta amyloid that forms plaque deposits on the brain.
Problems sleeping may be an early sign of Alzheimer’s if a study in mice also applies to people, say researchers.
Clumps of protein, called plaques, in the brain are thought to be a key component of the illness.
A study, published in the journal Science Translational Medicine, showed that when plaques first developed, the mice started having disrupted sleep.
Alzheimer’s Research UK argued that if the link was proven it could become a useful tool for doctors.
The hunt for early hints that someone is developing Alzheimer’s is thought to be crucial for treating the disease.
People do not show problems with their memory or clarity of thought until very late on in the disease. At this point, parts of the brain will have been destroyed, meaning treatment will be very difficult or maybe even impossible.
‘Detectable sign’It is why researchers want to start early, years before the first symptoms.
If sleep abnormalities begin this early in the course of human Alzheimer’s disease, those changes could provide us with an easily detectable sign of [the disease]”
Prof David Holtzman
One large area of research is in plaques of beta amyloid which form on the brain.
Levels of the beta amyloid protein naturally rise and fall over 24 hours in both mice and people. However, the protein forms permanent plaques in Alzheimer’s disease.
Experiments at Washington University showed that nocturnal mice slept for 40 minutes during every hour of daylight. However, as soon brain plaques started to form the mice were sleeping for only 30 minutes.
One of the researchers, Prof David Holtzman, said: “If sleep abnormalities begin this early in the course of human Alzheimer’s disease, those changes could provide us with an easily detectable sign of [the disease].”
“If these sleep problems exist, we don’t yet know exactly what form they take, reduced sleep overall or trouble staying asleep or something else entirely.”
However, findings in mice do not always apply to people as there are many reasons for disrupted sleep.
Dr Marie Janson, from the charity Alzheimer’s Research UK, called for more studies in people to see if there was a link between sleeping patterns and Alzheimer’s.
She added: “There has already been research linking changes in sleep patterns to a decline in thinking skills, but these results suggest that disrupted sleep may also be a warning sign of Alzheimer’s.
“If research confirms specific sleep changes as a possible early marker of Alzheimer’s, it could prove a useful strategy for doctors to identify patients at risk of the disease.”