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Alzheimer's disease / Maladie d'Alzheimer

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  • Alzheimer's disease / Maladie d'Alzheimer

    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

  • #2
    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


    • #3
      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


      • #4


        • #5


          • #6
            Originally posted by Al-khiyal View Post
            Gene discovery offers new hope of Alzheimer's therapy


            • #7
              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


              • #8


                • #9
                  Scientists in Japan have developed an oral vaccine for Alzheimer's disease that has proved effective in mice, raising hopes that an effective treatment for humans can be found for the fatal condition, which affects millions.

                  Scientists at the National Institute for Longevity Sciences in central Japan said today that they hope to begin small-scale clinical trials of the oral vaccine later this year.

                  "We hope the phase one trials go well," Reuters news agency quoted Takeshi Tabira, the institute's director, as saying.

                  "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."

                  The vaccine reduced the amount of amyloid plaques - believed to be the cause of Alzheimer's - and improved brain function when administered to mice that had been genetically modified to develop the disease, Mr Tabira said.

                  The vaccine works by stimulating the immune system to attack and destroy amyloid proteins in the brain, and the mice suffered no side-effects, such as inflammation or bleeding in the brain.

                  Tests showed that mental function in the mice returned to near-normal levels three months after they were administered the treatment.

                  Successful trial on humans would boost attempts to prevent Alzheimer's from becoming a medical emergency in countries with rapidly ageing populations.

                  The disease affects 5 million Americans, according to the Alzheimer's Association, and a recent report by the London School of Economics and the Institute of Psychiatry warned that 1.7 million people in the UK will have dementia by 2051.

                  One in 20 people aged over 65 and one in five people over 80 have a form of dementia, with around two-thirds of the total suffering from Alzheimer's.


                  • #10
                    · Sedatives blamed for thousands of deaths

                    A class of drugs widely prescribed for people suffering from dementia is leading to the premature deaths of thousands of patients every year, according to research published today. Campaigners branded the continued use of the sedatives, called neuroleptics, a national scandal after a five-year study revealed that people with Alzheimer's disease and other forms of dementia are twice as likely to die if they are prescribed them.

                    Neuroleptics are widely prescribed to help control symptoms of Alzheimer's and dementia including agitation, hallucinations and erratic behaviour, despite only being licensed for use in people suffering from schizophrenia. The research suggests they are of little benefit to patients with milder symptoms, greatly increase their risk of dying prematurely, and that 45% of Alzheimer's patients in care homes are prescribed a neuroleptic drug.

                    A group of 165 Alzheimer's patients were randomly assigned to take one of three types of neuroleptic drugs, or a placebo. After two years 45% of those who took the real drugs had died compared with 22% who were given the placebo.

                    The King's College London researchers who undertook the project, funded by the Alzheimer's Research Trust, found that after three years 65% of those on the drugs had died compared with 38% of those on placebos. After 42 months 75% of those on the drugs had died compared with 60% on the placebo. On average patients who were on the drugs died six months earlier.

                    Clive Ballard, professor of age-related disorders at King's and the lead researcher, said that not only were people more likely to die but they also suffered severe side-effects including stroke, chest infections and falls.

                    "If this was a massive increase in mortality in children there would be an outcry. Older people aren't seen as a priority. These sedatives are being used because the services can't cope with people who are in a distressed state. There are ways to avoid them but it would involve training of staff, which is costly."

                    In 2004 the medicines watchdog issued a warning that two types of neuroleptics, olanzapine and risperidone, should not be given to Alzheimer's patients because of an increased risk of stroke and death.

                    Despite this, in 2005 the Alzheimer's Society presented evidence that 100,000 people suffering from dementia were being prescribed a neuroleptic drug.

                    Neil Hunt, chief executive of the society, said: "Neuroleptics have been used as a dangerous fix for 'challenging behaviour' in people with dementia for too long. They are not licensed for use among people with dementia, but continue to be hugely over-prescribed. It is a national scandal that people are being sedated in this way ... These drugs must be a last resort, only used when all other methods have failed to alleviate the most distressing symptoms of dementia."

                    Rebecca Wood, chief executive of the Alzheimer's Research Trust, said: "These results are deeply troubling and highlight the urgent need to develop better treatments."

                    The Medicines and Healthcare products Regulatory Agency (MHRA), which is responsible for the safety of medications, said neuroleptics were not licensed for use to treat dementia. "The MHRA continues to monitor the unlicensed use of neuroleptics in the treatment of patients with Alzheimer's disease and will carefully review this new study to see what further action may be necessary."

                    Professor Mayur Lakhani, chairman of the Royal College of General Practitioners, said: "We would like to reassure patients, relatives and carers that neuroleptic drugs are not routinely prescribed to patients with dementia, and are used only as a last resort when patients suffer from severe episodes."


                    • #11
                      now that is alarming, my GODDD!


                      • #12
                        The Good things with Alzheimer`s is that they meet evey time a NEW PEOPLE...
                        A government that robs Peter to pay Paul can always depend on the support of Paul.
                        By: George Bernard Shaw


                        • #13
                          NEW YORK, June 6, 2007 (Reuters Health) - People with high levels of inflammatory markers are more likely to develop Alzheimer's disease than those who do not, according to a report in the journal Neurology.

                          "Physicians should take our research findings as further evidence of the involvement of inflammation in the pathogenesis of Alzheimer's disease," Dr. Zaldy S. Tan from Harvard Medical School, Boston, told Reuters Health. The findings can be used to develop strategies to "advance research in Alzheimer's disease diagnosis and treatment."

                          Tan and associates compared the relationship between proteins produced by the immune system to generate an inflammation response and the risk of developing Alzheimer's disease in 691 men and women without dementia who were living in the community.

                          The participants were 79 years old on average. During an average follow-up of 7 years, 44 subjects developed Alzheimer's disease and 262 died.

                          Higher levels of interleukin-1 were associated with more than a twice the risk of developing Alzheimer's disease, the authors report, and individuals with the highest production of tumor necrosis factor-alpha were 30 percent more likely to develop Alzheimer's disease than those with the lowest production of tumor necrosis factor-alpha.

                          Subjects with highest levels of both interleukin-1 and tumor necrosis factor-alpha had a 61 percent greater risk of developing Alzheimer's disease than did individuals with the lowest levels, the investigators found.

                          However, neither C-reactive protein nor interleukin-6 levels were related to the risk of Alzheimer's disease.

                          Higher production of a blocker of interleukin-1, call interleukin-1 receptor antagonist, was not associated with a significantly lower risk of developing Alzheimer's disease, the results indicate.

                          "These data strengthen the evidence for a pathophysiologic role of inflammation in the development of clinical Alzheimer's disease," the researchers conclude.

                          "There are still many unanswered questions in Alzheimer's disease research, and information such as this can help get us closer to finding the answers," Tan said.

                          SOURCE: Neurology May 29, 2007


                          • #14
                            PHOENIX, June 7, 2007 - A team of Arizona researchers think they've found a gene that could help better predict a person's risk of developing Alzheimer's disease.

                            The gene — called GAB2 — seems to affect the odds that some people will get the progressive neurological disease that afflicts about 5 million Americans, according to the research team led by the Translational Genomics Research Institute and Banner Alzheimer's Institute.

                            "This is a major breakthrough in Alzheimer's genetic research that will have an impact on the clinical treatment of the disease," said Dr. Dietrich Stephan, director of TGen's neurogenomics division.

                            Researchers here believe the study marks a new milestone for genetic research of Alzheimer's disease because it used a high-powered computer chip to measure more than a half-million genetic variations, the most robust such study to date.

                            Alzheimer's triggers memory lapses, clouds the thought process and leads to confusion and death in older adults.

                            About 78,000 Arizonans suffered from Alzheimer's in 2000, a number expected to jump to 130,000 by 2025, according to Banner Alzheimer's Institute.

                            Researchers worldwide are not sure what causes the disease. They do know that sufferers' brains are harmed by plaques and tangles that block signals and ultimately cause cells to shrink and die.

                            TGen's Stephan began investigating the possibility of conducting an ambitious study of the disease three years ago.

                            He sought funding from the Kronos Science Laboratory in Phoenix, which provided most of the money for the $5 million project.

                            In turn, Kronos secured the intellectual property rights from the Arizona study and is seeking patent protection for the GAB2 gene and its role in the onset of Alzheimer's.

                            The study is the latest to draw national attention for the gene investigators at TGen, which launched here five years ago as part of a push to build Arizona's research prowess.

                            Other significant studies conducted by TGen and collaborators in Arizona include genetic tests relating to pancreatic cancer and amyotrophic lateral sclerosis, also known as Lou Gehrig's disease.


                            • #15
                              June 29, 2007 -- Britain's obesity explosion could trigger a second even more serious epidemic - of dementia. Experts warned yesterday that our fondness for fast food and resistance to exercise was not only causing waistlines to bulge - it is also damaging our brains.

                              An estimated 700,000 people have dementia in the UK and the number is forecast to rise to as many as 1.5 million over the next 50 years, according to the Alzheimer's Society.

                              But if the population goes on getting fatter, the total could rise to 2.5 million, said Clive Ballard, director of research at the society. "Obesity is a huge risk factor," he said. "People who are overweight at 60 are twice as likely to get dementia at 75. We have a public health epidemic of dementia given the ageing of the population, and it is essential to reduce the risks. If these factors are not controlled, it may not be 1.5 million but 2 or 2.5 million people affected."

                              Currently one in 20 people aged over 65 has signs of dementia, rising to one in five over 80. Increasing obesity could double the incidence among over-65s to one in 10, said Mr Ballard.

                              The mechanism of how obesity affects the brain was unclear but it encompassed diet, exercise and physiological effects. Research has shown that people who eat a diet rich in fruit and vegetables have an up to 40 per cent reduced risk of developing dementia. Exercise has a similar effect.

                              Studies also suggested that amyloid protein which can build up in the brain, causing damage to nerve cells, is cleared from the blood more efficiently when cholesterol levels are low. High cholesterol could increase build-up of the protein and hasten the onset of Alzheimer's. Neil Hunt, chief executive of the Alzheimer's Society, said: "I remain genuinely mystified why this is still such a low priority. The cost of dementia to individuals, families and the state is £17bn a year. Now there is research suggesting dementia is not as inevitable as we thought. There is no cure but evidence is building that lifestyle choices make a difference to risk."

                              Launching a booklet, Be Headstrong, he said that five steps were necessary to reduce the risks - do not smoke, eat less saturated fat, exercise regularly, lead an active social life and have blood pressure and cholesterol checked regularly. "If we could delay the incidence of dementia by five years we could reduce its incidence by 50 per cent," he said.

                              Professor Jeremy Pearson, associate medical director of the British Heart Foundation, said risk factors for heart disease were also risk factors for dementia. "We now know that protecting the heart will also protect the brain," he said. "Treatments that reduce heart disease also reduce dementia. There are very similar pathological processes underlying both."

                              Tony Rudd, consultant stroke physician at Guy's and St Thomas NHS Trust, said up to one-third of the over-65s who had a stroke would develop dementia within three months. "Public health initiatives to prevent stroke and related risks are essential," he said.


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