Alzheimer's disease / Maladie d'Alzheimer

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Scientists at Cardiff University have developed a potential treatment for Alzheimer's disease.

Researchers say they have created an antibody which could block the production of brain chemicals linked to the debilitating disease.

Dr Emma Kidd, who led the research team, said the results of the tests were "highly encouraging".

There is no known cure for Alzheimer's, which causes irreversible loss of brain function and memory.

The disease affects one in 20 people aged over 65 and a fifth of all people over 80 in the UK.

The results of the study show that it is possible to decrease production of the protein amyloid, which is believed to be the main cause of the disease.

Deposits of amyloid build up in the brain, preventing it from functioning properly.

The antibody will reduce this build-up, improving the patient's memory and quality of life, say researchers.

Dr Kidd said: "Our results are highly encouraging at this stage.

"We believe that our approach could lead in time to a new therapy for this distressing and debilitating disease as it should prevent or reduce the irreversible deterioration of a patient's memory and other brain functions.

"This would also reduce the burden on carers, usually family members, who look after patients in the earlier stages of the disease."

Dr Kidd said it was possible the antibody could be used as a preventative treatment for people with a family history of Alzheimer's.

The work was carried out at the university's Welsh School of Pharmacy and was funded by the Alzheimer's Society.

A final treatment could take several years to develop and the team are now seeking more money for the next stage of the work.

Barbara Phillips, from Penarth, whose husband has Alzheimer's, said the "terrible disease" had robbed them of the future they had planned together.

Businessman Ed Phillips, 65, first showed signs of the disease six years ago.

Mrs Phillips said: "It means to me the loss of a lovely man whom I've known since I was 16 and I'm losing him slowly, quietly and insidiously.

"It's like a bereavement, but it's a living bereavement almost," she told the BBC.

"I would give my right arm if they could find a treatment for Alzheimer's. I dream about it."

Professor Clive Ballard, of the Alzheimer's Society, said: "We hope people will understand how important it is to invest more in research into all types of dementia, so that we eventually may have a selection of new treatments to change the lives of people with dementia and their carers."

The research is published in the Journal of Alzheimer's Disease.

Hopes for Alzheimer's treatment

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BEIJING, Dec. 22 (Xinhuanet) -- Until recently the only way to diagnose Alzheimer's disease has been to remove some brain tissue. Now a new study released Wednesday shows a chemical designed by doctors in Los Angeles could provide a new way to test for treatments.

The new study by doctors at the University of California, Los Angeles, is part of a larger challenge to find a better method to diagnose Alzheimer's using tracers that can be detected with a positron emission tomography (PET) scan.

The chemical, known as FDDNP, fixes to the abnormal clumps of proteins called amyloid plaques and tau tangles that develop in Alzheimer's sufferers and inhibit messages being processed by the brain.

In the study published in Thursday's New England Journal of Medicine, Gary Small and his colleagues found the chemical allowed doctors to determine which of 83 volunteers had Alzheimer's, which had mild memory problems, and which were functioning normally for their age.

It was 98 percent accurate in determining the difference between Alzheimer's and mild cognitive impairment.

That was much better than the 87 percent success rate for a PET scan test that measured sugar metabolism in the brain, and the 62 percent accuracy rate when doctors used a magnetic resonance imaging scan to gauge brain deterioration.

"You can see the (telltale FDDNP) signal in people years before they get Alzheimer's," Small said.

His team also found that the distribution of the FDDNP in the brain of Alzheimer's patients matched the pattern seen in people where the diagnosis is confirmed with an autopsy.

"If patients get worse clinically, we see a buildup of the FDDNP binding. That suggests we can track the disease over time," Small said.

Finding an easier way to track brain deterioration not only would help doctors diagnose the disease, it could become easier to assess experimental Alzheimer's treatments, as researchers try to prevent the accumulation of plaques and tangles, or to reduce them if they accumulate.

Small and four of the other 15 authors named in the research paper have a financial interest in FDDNP, which has been licensed to the German conglomerate Siemens AG. He said he hopes to see it on the market within three years.

Other researchers trying to track the progress of the disease are looking for telltale signs in spinal fluid or with a FDDNP-like chemical from the University of Pittsburgh known as PIB. But PIB can only find plaques and it disappears from the body 5.5 times faster than FDDNP.

One problem plaguing Alzheimer's tests is that the results are not always clear-cut. For example, some people who seem to have few memory problems can have a positive result on a test.

Study finds more accurate test for Alzheimer's disease

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WASHINGTON (Reuters) - Scientists said on Sunday they have pinpointed a new gene linked to Alzheimer's disease, the incurable brain disorder that is the top cause of dementia in the elderly.

Abnormalities in a gene called SORL1 increased the risk for the disease, and this finding could help scientists develop new treatments, the researchers reported in the journal Nature Genetics.

The researchers looked at DNA samples from 6,000 people from four ethnic groups: Caribbean-Hispanics, North Europeans, black Americans and Israeli-Arabs. They found certain variations of SORL1 more often in people with late-onset Alzheimer's disease than in healthy people.

The late-onset form, affecting people age 65 and up, represents about 90 percent of Alzheimer's cases. The rarer early-onset form affects people from about age 30 to 65.

Only one other gene, called ApoE4, has been identified as a risk factor for late-onset Alzheimer's. It was identified in 1993.

Several genes are linked with early Alzheimer's, and study of both types might lead to better understanding of how the disease begins and how to tackle it.

Many scientists think Alzheimer's begins with the buildup in the brain of a gooey material called amyloid that clumps together to form plaques. That material stems from a protein called amyloid precursor protein, or APP.

SORL1 controls the distribution of APP inside nerve cells of the brain. When working normally, the gene prevents APP from being degraded into a toxic byproduct called amyloid beta peptide. When SORL1 is deficient, it allows more of the bad amyloid beta peptide to accumulate, fostering amyloid plaques.

Alzheimer's is a complex disease that gradually destroys a person's memory and ability to learn, reason, make judgements, communicate and carry out daily activities. Scientists have struggled to understand the biology of the disease and its genetic and environmental causes.

"It's another clue to the way in which this disease comes about, another piece of the puzzle," Dr. Peter St. George-Hyslop, director of the Centre for Research in Neurodegenerative Diseases at the University of Toronto and one of the key researchers, said in a telephone interview.

"Every time you get a piece of the puzzle and you can relate it to something else in the puzzle, you're that much closer to knowing what the picture on the puzzle is," he added.

St. George-Hyslop said it is premature to say what percentage of cases of late-onset Alzheimer's disease can be attributed to SORL1. ApoE4, which also may be involved in the production of amyloid plaques, has been linked to about 20 percent of late-onset Alzheimer's cases.

"This appears to be the fifth Alzheimer's disease gene, and there are likely to be other important genetic variants that need to be identified before the entire picture is complete," Dr. Richard Mayeux of Columbia University Medical Centre in New York, also involved in the research, said in a statement.

The disease first affects parts of the brain controlling memory and thinking, but as it advances it kills cells elsewhere in the brain. Eventually, if the patient has no other serious illness, the loss of brain function will prove fatal.

Researchers from Boston University and the Mayo Clinic College of Medicine in Jacksonville, Florida, also took part in the five-year study.

New gene linked to Alzheimer's identified

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Nature Genetics

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Journal of Alzheimer's Disease

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New gene linked to Alzheimer's identified

Gene discovery offers new hope of Alzheimer's therapy

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WASHINGTON, Jan 23 (KUNA) -- Learning appears to slow the development of two brain lesions that are the hallmarks of Alzheimer's disease, scientists at the University of California-Irvine have discovered. The finding suggests that the elderly, by keeping their minds active, can help delay the onset of this degenerative disease.

This study, with genetically modified mice, is the first to show that short but repeated learning sessions can slow a process known for causing the protein beta amyloid to clump in the brain and form plaques, which disrupt communication between cells and lead to symptoms of Alzheimer's disease. Learning also was found to slow the buildup of hyperphosphorylated-tau, a protein in the brain that can lead to the development of tangles, the other signature lesion of the disease.

Scientists say these findings have large implications for the understanding and treatment of Alzheimer's disease, as it is already known that highly educated individuals are less likely to develop the disease than people with less education.

"This study shows learning can delay the progression of Alzheimer's neuropathology in mice genetically engineered to develop this insidious disorder, and learning also delays the cognitive decline," said Frank LaFerla, professor of neurobiology and behavior and co-author of the study. "These remarkable findings suggest stimulating the mind with activities such as reading books or completing crossword puzzles may help delay and-or prevent Alzheimer's disease in senior citizens".

The study appears in the January 24 issue of the Journal of Neuroscience.

Learning appears to slow physical progression of Alzheimer's disease