Monday, Jul. 14, 2008
Besides making pasta’s curry tangy, the plump and red tomato has far more serious benefits – the humble fruit can be a suitable carrier for an oral vaccine against Alzheimer’s disease, says a group of researchers.
The study, conducted by HyunSoon Kim from the Korea Research Institute of Bioscience and Biotechnology (KRIBB) in Korea and colleagues from Digital Biotech Inc. and the Department of Biological Science at Wonkwang University, is currently in the early stages.
However, it is a promising first step towards finding an edible vaccine against the neurodegenerative disease.
Alzheimer’s disease is the most common cause of dementia and it progresses over a long period of time.
It is thought to be caused by the accumulation of human beta-amyloid, a toxic insoluble fibrous protein in the brain, which leads to the death of neurons.
Reducing the accumulation of beta-amyloid may inhibit the degeneration of the nervous system and therefore prevent or delay the onset of Alzheimer’s disease. One approach is to stimulate the immune system to reduce beta-amyloid in the brain.
In the study, the researchers’ aim was to develop a plant-derived vaccine against Alzheimer’s disease, since beta-amyloid is toxic to animal cells.
Tomatoes are an attractive candidate as a vaccine carrier because they can be eaten without heat treatment, which reduces the risk of destroying the immune stimulation potential of the foreign protein.
In the study, the scientists inserted the beta-amyloid gene into the tomato genome and measured the immune responses to the tomato-derived toxic protein in a group of 15-month-old mice. They immunized the mice orally with the transgenic tomato plants once a week for three weeks, and also gave the mice a booster seven weeks after the first tomato feed. Blood analyses showed a strong immune response after the booster, with the production of antibodies to the human foreign protein.
The authors conclude: “Although we did not reveal a reduction of existing plaques in the brain of mice challenged with tomato-derived beta-amyloid…this study represents a unique approach in which transgenic plants expressing beta-amyloid protein are used to produce a vaccine.”
Wednesday, Jun. 11, 2008
A breakthrough in research into Alzheimer’s Disease has been welcomed by those dealing with the condition.
Dr Calum Sutherland and colleagues at Dundee University’s Ninewells Medical School identified an enzyme which partially reverses the development of nerve clumps and tangles in the brains of those with Alzheimer’s.
The enzyme acts on a protein called CRMP2 which plays a key role in the formation of the clumps.
Drugs developed from the discovery could slow down their growth.
Dr Sutherland said: “One of the hardest tasks in Alz-heimer’s research is finding the abnormal biochemical pathways among the cascade of reactions taking place in the healthy brain, and working out how to repair them without causing unwanted side-effects.
“The new work highlights part of the natural process that could be harnessed to fully reverse the abnormal CRMP2 structure.”
Rebecca Wood, chief executive of the Alzheimer’s Research Trust which funded Dr Sutherland’s work, said such findings are crucial to understanding the condition.
“A better understanding of the changes that occur in the brain at the onset of Alzheim-er’s, and how the disease progresses, could enable scientists to develop effective treatments for slowing or stopp-ing the disease,” she said.
“With 700,000 people in the UK living with Alzheim-er’s and other dementias, we desperately need to find an effective treatment to help these people.”
The discovery has been welcomed by Alzheimer’s Scotland which supports sufferers and their families.
Gabrielle Colston-Taylor, service manager for the charity in Dundee, said there is some pride that the discovery has been made in the city.
“It’s really exciting that this has happened in Scotland and more so that it’s in Dundee,” she said.
“But with all these things it will take time for it to be turned into a usable medicine for treatment.”
Monday, Dec. 10, 2007
YORKSHIRE scientists are helping to develop the use of breakthrough technology that could transform the treatment of Alzheimer’s disease.
Leeds University is working with computer giant Microsoft on the system, which replicates artificially pictures that the healthy human brain captures and stores as memories.
The images are then viewed to stimulate the patient’s brain, improving their natural powers of recall.
Researchers describe the project as “potentially very exciting”. Early trials have produced dramatic results, with patients experiencing up to 90 per cent of their normal memory restored after only two weeks.
A small camera is worn by the patient to record details of their life by taking a photo every 30 seconds. The camera is later plugged into a computer and thousands of pictures viewed at high-speed as a memory aid.
Regular use of the system appears to stimulate patients’ memory even when not looking at pictures as a “trigger”, according to researchers.
Trials have been conducted with Alzheimer’s patients, the most common disease causing memory loss, and others with similarly debilitating illnesses or conditions, such as age-related dementia.
A team of researchers at Leeds University led by Professor Martin Conway and Dr Chris Moulin has received part of a £250,000 funding package from Microsoft because of their department’s global reputation for work on human memory.
The device, called a SenseCam, is a small camera worn on a cord around the neck. It takes continuous pictures, which are then viewed via a computer.
The technology has been engineered so a whole day’s images can be reviewed at high speed, with a day’s events condensed into a few minutes’ viewing time.
That helps users to remember events which would otherwise be lost from their minds, and also to re-experience the emotions attached to events and conversations.
Over time, using the equipment repeatedly appears to stimulate their memory to recall the events without the technology.
The camera’s design is deliberately simple, using a fish-eye lens and sensors which detect changes in light, body heat and activity. It can store up to 30,000 images, enough to cover a fortnight’s use in typical circumstances.
The Leeds team will use their expertise to try to refine the system, using data already gathered from initial trials.
Those tests included a 63-year-old woman with memory loss resulting from a brain infection, who used a SenseCam whenever she anticipated a significant event.
She spent about an hour every two days reviewing the images, for a two-week period.
Without any other memory aids she typically forgot everything within five days. But during the test her memory steadily increased, and after two weeks her recall was at around 90 per cent. She continued to remember events over time.
“It’s potentially very exciting,” said Dr Moulin, a neuropsychologist. “Once people in the
early stages of Alzheimer’s or other conditions involving memory loss realise they can’t remember events, people and places they stop doing things because of the frustration of not being able to remember later.
“A great use for such a camera would be for such events – things out of the normal routine. Having the camera could mean that they can revisit not only the facts of such events, but the essential feelings that are so much part of memory.”
Prof Conway added: “SenseCam images are one of the most potent cues to remembering I have ever encountered.”
Microsoft says wider research and development are needed before the company can make any decision to commercialise the camera.
Tuesday, Sep. 4, 2007
However far off a cure may be for Alzheimer’s disease, Baxter International Inc.’s announcement last week that a small-scale study showed progress in improving memory function in elderly patients.
Just as momentum built in the 1990s in the fight against AIDS, researchers have identified several potential avenues to follow in the search to slow the progression of Alzheimer’s.
There is neither a cure nor is there an approved treatment that will change the course of the disease; there are only some pills that slow the worsening of symptoms for about half of those who take them, experts say.
It is hoped the use of Baxter’s drug Gammagard and other drugs that work similarly to bolster immune systems would slow or even stop Alzheimer’s.
The 24-patient study represents a preliminary step forward, and a small one since hundreds of patients can be needed for some drugs to win approval. But researchers believe Baxter’s drug has an advantage in that it already is established as safe. It has been used for years to treat patients with immune disorders.
“This is really the beginning of a new era,” said Dr. David Bennett, professor of neurological sciences at Rush University Medical Center in Chicago.
The idea behind the Baxter drug is the body’s own immune system potentially can clear the brain of a protein fragment known as beta-amyloid is deemed a key player in the progression of Alzheimer’s disease.
Alzheimer’s disease affects nearly 5 million Americans, and the number is rapidly rising.
Specific results of Baxter’s 24-patient trial were not released. They are expected to be published in medical journals, perhaps by the end of the year.
Thursday, May. 24, 2007
In the continuing battle against Alzheimer’s one more breakthrough has been achieved. Scientists in New York promoted the growth of new neurons in the brains of mice using a magnetic stimulus in the region associated with memory.
The results were presented at the American Academy for Neuroscience conference. If proven, the technique is could help slow down the progression of the Alzheimer’s disease, if not a cure.
Experts said the work was encouraging but would need to be replicated in humans. Trans cranial magnetic stimulation (TMS) has been used to treat certain disorders, including depression and schizophrenia and to rehabilitate people after stroke.
To look at the effect of TMS on growth of neurons, Dr Fortunato Battaglia and Dr Hoau-Yan Wang at City University in New York, gave mice the therapy for five days and then examined their brains, New Scientist magazine reported.
They found large increases in the proliferation of stem cells – immature cells that go on to develop into nerves and other kinds of tissue – in a part of the brain called the dentate gyrus hippocampus.
These cells divide throughout life and are believed to play a crucial role in memory and mood regulation.
In particular they found one receptor in the cells was activated.
A subsequent study which is due to be published shortly showed that the activity of this receptor declines in mice and humans with Alzheimer’s disease.
Taking the two studies together, Dr Battaglia said there were important implications for neuro-rehabilitation.
“When you have a stroke there is an area that is damaged and there are several ways your brain can recover.
“One is that the area which is not damaged will have to work more and it’s that we can promote with brain stimulation.”
He added that the hippocampus is much deeper in the brains of humans so it would be important to make sure the technique could produce the same effect as in mice.
“But it might improve symptoms or delay progression of things like Alzheimer’s disease,” he added.
Professor Vincent Walsh from the Institute of Cognitive Neuroscience at University College London said the findings were a good first step.
“There are lots of examples of TMS enhancing function in some way but we have never been able to explain the mechanics of how it might work.
“The work is particularly encouraging for the use of brain stimulation in chronic disease such as stroke and dementia.
“The challenge now is to find ways of combining stimulation with drug therapies.”
Professor Clive Ballard, director of research at the Alzheimer’s Society said: “This is a potentially interesting piece of work, but is a preliminary study in mice.
“Further research is now needed before we can find out if TMS is a useful treatment approach for Alzheimer’s disease in humans.”
Monday, May. 21, 2007
Australian researchers claim they have found the key to slowing dementia and even reversing the loss of memory, with a combination of diet, exercise, and brain activity designed to create a healthy mind and body.
Studies suggest nutrition, learning, socialising and drugs can prevent Alzheimer’s disease and other forms of dementia.
Scientists also say there is indication these practices could prolong the diseases progress and even delay its onset.
Human brains have the potential to create new cells at any age and researchers believe this enables the brain to create new connections, with the right stimulation such as diet and lifestyle.
It’s been found that a diet low in fat, high in Omega-3 fatty acids, antioxidants, Vitamin C, B12, and folic acid can benefit dementia sufferers.
Wednesday, Apr. 25, 2007
For those who struggle to remember birthdays and the location of car keys, hopes of a cure have arrived.
Scientists announced on Monday that the world’s first memory pill could be developed after they identified a gene mutation that affected the memory of mice.
The discovery was made when researchers suppressed the activity of the gene in mice before they swam around a water maze, noting that the altered mice performed better.
But when the gene’s activity was increased, the performance of the mice’s memory was worse.
The scientists hope to find molecules that target and inhibit the gene, which is also thought to exist in humans.
Ultimately this could lead to a memory-enhancing pill. Dr Mauro Costa-Mattioli, from McGill University, Montreal, said: “If such a pill could be generated, it might provide a new method for treating people with memory-related diseases such as Alzheimer’s.
“While a drug that worked in this way wouldn’t cure the disease itself, it might rescue the symptoms of memory loss.”
The identified gene makes a regulatory protein called eIF2a, which normally keeps a check on memory.
Mice that were genetically engineered to carry a defective version of the gene showed an improved talent for spatial learning.
In the maze, the mice were trained to swim to a hidden platform.
After several days the mutant mice were able to find the platform significantly faster than normal mice.
“If a person were reading a page of a textbook, it might take several times to memorise it,” said Dr Costa-Mattioli, who published his findings in the journal Cell.
“A human equivalent of these mice would get the information right away.”
Thursday, Mar. 29, 2007
Japanese scientists have developed an oral vaccine for Alzheimer’s disease that has proven effective and safe in mice, the research institute behind the project said today.
The team is preparing to move to small-scale clinical trials in humans, possibly this year, said Takeshi Tabira, director of the National Institute for Longevity Sciences in Aichi, central Japan.
“We hope the Phase I trials go well,” Tabira said. “Animals are able to recover their functions after developing symptoms, but humans are less able to do so. It may be that this only works in the early stages of the disease, when symptoms are light.”
When administered to mice suffering from the disease, which causes dementia and is currently incurable, the vaccine reduced the amount of amyloid plaques in the brain and improved mental function.
Amyloid plaques are believed to be at the root of Alzheimer’s – a growing problem for ageing populations around the world. The disease affects five million in the United States alone, the Alzheimer’s Association said in a report last week.
The treatment did not cause inflammation or bleeding in the brains of the mice, Mr Tabira said. The vaccine is made by inserting amyloid-producing genes into a non-harmful virus. When taken orally, the virus stimulates the immune system to attack and break down the amyloid proteins in the brain, he said.
The treatment was tested on 28 mice genetically modified to develop Alzheimer’s disease. Half the animals were given a dose of the vaccine at the age of 10 months, while the control group were not treated. Three months later, tests showed mental function in the treated mice had returned to levels close to those before they developed Alzheimer’s symptoms.
US drugmaker Wyeth and its Irish partner, Elan, have an Alzheimer’s vaccine called ACC-001 in early stage human trials.
Tuesday, Feb. 27, 2007
Brain diseases such as Alzheimer’s and Parkinson’s could be cured with drugs in as little as five years’ time, according to scientists.
A study published today proves for the first time that a region of the brain contains stem cells, which have the ability to act as a repair system for the body.
As diseases such as Alzheimer’s speed up the process by which brain cells die, scientists say that drugs could be developed which would stimulate stem cells to replace them.
This would mean that the body could be ‘tricked’ into repairing itself – reversing the damage caused to cells by a degenerative disease.
Professor Peter Eriksson, a neurobiologist at Sweden’s University of Gothenburg, said: ‘I think this discovery will open up totally new avenues of treatments for Alzheimer’s and Parkinson’s.
‘It may be possible to develop a drug to trick the brain into replacing cells.
‘It could also help patients who have suffered a stroke, as well as people with Huntingdon’s Disease and schizophrenia.’
He added that the drugs could be developed
A spokesman for the Alzheimer’s Society echoed his enthusiasm, saying: ‘This study raises the potential to treat damaged tissues and repair brain damage from neurological conditions, such as Alzheimer’s disease.
‘For the first time, this study demonstrates that stem cells are routinely involved in replenishing nerve cells in at least one part of the adult human brain.
‘This process raises exciting new questions for the treatment of Alzheimer’s disease, such as whether stem cells could be stimulated into action when the brain has been injured.
‘These findings are the first step to unlocking potentially exciting new treatments.’
The study, published in Science magazine, was also welcomed yesterday by British scientists.
Dr Mark Baxter, Wellcome Trust senior research fellow at Oxford University, said: ‘This study is exciting because it reveals a group of brain cells in the adult human brain that are continuously regenerating.
‘Animal studies have pointed to the existence of such groups of cells, but it has been difficult to determine whether they exist in the human brain as well.
‘This opens another direction by which we may discover ways to repair human brains that are damaged from injury or diseases.’
Scientists used to believe that the brain stopped producing new cells after the teenage years, when the body stopped growing.
It had been known for some years that some other mammals retained the ability to generate certain nerve cells well into adulthood.
Evidence that the phenomenon occurred in humans has been elusive but scientists in New Zealand and Sweden have now demonstrated it for the first time.
They used brain scanners on corpses to pinpoint the path that new cells take as they emerge from the centre of the brain to the region linked to the sense of smell.
Professor Eriksson said: ‘There has been a long controversy about whether this structure exists in the human brain.
‘It has been shown in rats and mice that these stem cells are essential for repair mechanisms to take place after a stroke.’
One of the main features of diseases such as Alzheimer’s is that brain cells begin to die more quickly.
The finding raises the possibility that scientists could isolate a chemical compound to prompt stem cells in the brain to produce more of these cells.
However, some scientists warned that progress in this direction could be slow.
Jim Cohen, professor of cellular neurobiology at King’s College London, said: ‘We could be decades down the line of using this to come up with therapeutic treatments.
‘There are many unknowns. For example we know these stem cells are present in one part of the brain – but how easy would it be to replicate them in a different part?’
Another option scientists could look at would be to transplant healthy regenerating cells into the brain of an Alzheimer’s or Parkinson’s disease sufferer.
The discovery could also help in the fight against brain cancer.
Friday, Oct. 27, 2006
SCIENTISTS in Merseyside may have discovered the first drug ever to tackle the causes of Alzheimer’s disease.
Experts at the University of Liverpool said they are ready to test what could be a breakthrough treatment for Alzheimer’s – on mice bred with a rodent form of the disease.
They have created a new compound, called engineered heparans, made out of a type of sugar which naturally occurs in the body and is normally used to stop blood clots.
Initial findings show it is between 50% and 100% effective at preventing clumps of protein forming in the brain, which disrupt normal brain functions and cause gradual memory loss.
Professor Jerry Turnbull and Dr Ed Yates have led the research at the university’s School of Biological Sciences for the past four years.
They hope their new method could be developed into a drug treatment sufferers can take either in pills, or through an intravenous drip or inhaler, within the next three to 10 years.
Alzheimer’s is the most common form of dementia. There are around 412,500 people living with the disease in the UK. That is 55% of all 750,000 dementia cases in this country.
Existing treatments only target the symptoms, which include the gradual decline of a person’s ability to remember, understand, communicate and reason.
Prof Turnbull said: “Our initial research in test tubes showed the treatment was between 90% and 100% effective at inhibiting the growth of these proteins, which are also called plaques.
“Then we did further research on brain cells, mostly from mice, but also some from humans, and we found they are usually at least 50% effective.”
“At the very least, it could slow the disease process down, and therefore prolong survival of normal brain processes, so the person doesn’t lose the ability to think so quickly.
“It could give them five to 10 years more of quality life.”
“At best, it’s possible that it could offer a long-term cure.
“We don’t know yet, but it may give 10-15 years of normal life before the person eventually dies of some other disease or of natural old age.”
Prof Turnbull said because the sugar used, called Heparan Sulphates (HS), is found on nearly every cell of the body, he did not expect any risk of toxic side-effects.
He said the team was ready to test the compound on mice that have been bred with a rodent form of Alzheimer’s, in Leicestershire.
The university has already commissioned a company, IntelliHep Ltd, to research the commercial opportunities for developing the drug.
But clinical trials on humans would have to be carried out before the drug could be marketed, and the whole process could take anywhere from three to 10 years.
He said the sugar is normally used to stop blood clots in patients with deep-vein thrombosis. But researchers have modified it to remove its anti-coagulent qualities.
Clive Ballard, director of research for the Alzheimer’s Society, said: “This study is one of several projects examining new ways of targeting Alzheimer’s disease.
“The new approach hopes to treat Alzheimer’s by preventing a build-up of amyloid, the chemical at the core of plaques which scientists suspect cause the disease.
“There is no known cure for Alzheimer’s disease, but it is an exciting possibility a new treatment for the disease will be developed in the next five years.”
The research, funded by the Medical Research Council and the Biotechnology and Biological Sciences Research Council, is published in the Journal of Medicinal Chemistry.
Thursday, Jul. 27, 2006
Scientists have developed a once-a-day pill that they hope could potentially cure Alzheimer’s disease.
Tests in mice have shown the drug, PBT2, prevents build up of the amyloid protein linked to the disease.
Protein levels dropped by 60% within 24 hours of a single dose, and memory performance improved within five days.
A team from Australia’s Mental Health Research Institute of Victoria, who are behind the research, hope the drug could be on the market in four years.
Human tests are due to start next month, followed by a major international trial next year.
Already preliminary tests in humans have showed the drug does not cause any major side-effects.
The researchers believe the drug has the potential to delay the onset of disease, or slow down its progression.
Alzheimer’s is a progressive and fatal brain disease. It is the most common cause of dementia and affects around 450,000 people in Britain.
It is linked to the build up of deposits of amyloid protein – called Abeta – in the brain, which form plaques often seen in the brains of Alzheimer’s patients at post mortem.
The Australian researchers showed that PBT2 therapy quickly and significantly improved spatial memory in mice.
They used a water-maze test which involved the mice remembering the location of a submerged platform in order to navigate the maze.
Lead researcher Professor Ashley Bush said: “This data is compelling and very exciting because it shows that PBT2 not only may facilitate the clearance of Abeta from the brain or prevent its production, but more importantly may improve cognition.”
His colleague Professor George Fink, head of the Mental Health Research Institute, described the research as a major breakthrough.
“Though much depends on the next phase of human clinical trials, early results indicate this drug offers hope to people with Alzheimer’s disease.”
Dr Susanne Sorenson, head of research at the Alzheimer’s Society, said: “Initial tests have shown that the drug improves cognition and memory in mice, and we hope the same results can be recreated in humans.”
However she added: “These findings are still relatively new and many more tests and studies are now needed to prove the concept will work in people with Alzheimer’s disease and ensure the best treatments for this condition are made available as quickly as possible.”
Dr Sorenson said the results of the PBT2 study were one of many encouraging discoveries presented at last week’s International Convention for Alzheimer’s Disease which showed positive steps were being made towards finding new and better treatments.
Rebecca Wood, chief executive of the Alzheimer’s Research Trust, said PBT2 was related to Clioquinol, an ointment used to treat skin infections such as athlete’s foot.
She said “Scientists still have a lot of work to do before a drug could be available for patients.
“Much more research is needed even to see whether preventing the amyloid build-up is really a true benefit for patients.
“It would also be necessary to develop a drug that reduced the amyloid without removing it entirely, since a healthy brain still needs amyloid.”