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Alzheimer's disease / Maladie d'Alzheimer

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  • #46

    September 6, 2009 -- Scientists have discovered a trio of genetic mutations that account for nearly 100,000 cases of Alzheimer's disease in Britain today. Three genes that protect the brain from damage and ensure neurons work properly were found to be impaired in many patients with the disease, in the largest genetic study of the condition yet. The work has been hailed as a "huge step" towards earlier testing and better treatment for Alzheimer's and is the first in 15 years to find new genes associated with the disease. Previously, scientists knew of only one gene, called APOE4, which increases the risk of developing the most common form of the disease.

    "If we were able to remove the detrimental effects of these genes, we could reduce the proportion of people suffering Alzheimer's disease by approximately 20%," said Julie Williams, an Alzheimer's researcher at Cardiff University. "In the UK alone this would prevent just under 100,000 people developing the disease." About 417,000 people have Alzheimer's disease in Britain, the vast majority of whom have the late-onset form that develops after the age of 65. A very rare form of Alzheimer's disease that runs in families can affect much younger people.

    Scientists believe that genes account for 80% of our chance of developing late-onset Alzheimer's, the rest coming from lifestyle and environmental factors. The newly discovered genes have challenged scientists' thinking on how Alzheimer's disease develops in older people. Patients often suffer inflammation of the brain, an effect that was thought to be a symptom of the disease. But the latest findings suggest that unchecked inflammation may actually play a role in causing the condition.

    Scientists believe they will find more genes linked to Alzheimer's that in future could help in assessing a person's risk of developing the disorder. "This study is a huge step towards achieving an earlier diagnosis of Alzheimer's and improving the lives of the many people affected by the disease," said Sir Leszek Borysiewicz, chief executive of the Medical Research Council, which partly funded the work.

    Williams's team conducted a "genome wide association study", in which the genetic codes of nearly 4,000 Alzheimer's patients were compared with the genomes of almost 8,000 healthy individuals. The researchers found variants of three genes that were risk factors for developing Alzheimer's. One of the genes was APOE4, but the other two had not previously been linked to the disease.

    One gene, called clusterin, helps to protect the brain from exessive inflammation caused by infections and other illnesses. The gene is also involved in removing clumps of rogue protein known as amyloid plaques, which are commonly seen in the brains of Alzheimer's patients. Defects in the gene hamper its ability to do these jobs and increase the risk of Alzheimer's. The second new gene, called Picalm, is crucial for maintaining the health of connections between brain cells. Mutations in the Picalm gene are thought to disrupt the ability of brain neurons to talk to each other and form memories.

    A related study of more than 7,000 Alzheimer's patients and healthy volunteers, led by Philippe Amouyel at the National Institute of Health and Medical Research in Lille, also identified a variant of the clusterin gene as a risk factor for the disease. When the two groups combined their data, they discovered a third new gene called CR1 that was also linked to Alzheimer's disease. The CR1 gene is involved in protecting the brain by clearing out amyloid plaques that can build up in Alzheimer's patients.

    The work will enable scientists to start work on drugs that mimic the effects of the healthy genes and so help to prevent Alzheimer's developing in patients who carry mutated variants. Rebecca Wood, of the Alzheimer's Research Trust, which part-funded the study, said the work was "a leap forward for dementia research".

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    • #47

      September 21, 2009 -- The number of people with dementia and Alzheimer's disease is soaring around the world and will nearly double in the next 20 years, according to a report published today. The report, by a team of researchers led by Professor Martin Prince of the Institute of Psychiatry at King's College London, says that by next year there will be 35 million people globally with dementia. By 2030, that will have risen to 65.7 million and the steep rise will continue to more than 115 million by 2050. The burden on those with the disease, on their carers and on society is immense, according to the report, which is published by Alzheimer's Disease International (ADI). It calls on the World Health Organisation to make dementia a world health priority in the hope that this will spur countries to produce national plans for coping with the disease and encourage research into treatments.

      The true scale of dementia around the world is hard to establish because many low- and middle-income countries do not keep good statistics. The figure of 35 million is a revised estimate, and 10% higher than that stated in a review in the Lancet medical journal in 2005. The proportion of older people affected has risen in three regions of the world – in south Asia (up to 5.7% from 3.4%), Latin America (up to 8.5% from 7.3%) and western Europe (up to 7.3% from 5.9%). The biggest increase in future years is expected to be in low- and middle-income countries, as people start to live longer.

      Prince emphasised the enormous indirect toll dementia can take on carers, who are often unpaid family members. "Caring is a full-time job – an average of around eight hours per day for a relative with moderate to severe dementia," he said. "In all parts of the world, carers – who are most commonly female and the spouses or children of the persons with dementia – often experience high levels of strain. Studies reviewed in the new report suggest that half to three-quarters of carers have significant psychological illness, while up to a third have clinical depression." He said that given these statistics, "current investment in research, treatment and care is actually quite disproportionate to the overall impact of the disease".

      Marc Wortmann, ADI's executive director, said much more could be done by governments to alleviate the burden of the disease on patients and their families. "The crisis of dementia and Alzheimer's can no longer be ignored. Unchecked Alzheimer's will impose enormous burdens on individuals, families, healthcare infrastructures and the global economy," he said. "There is hope yet, if action is taken now to fund improvements in dementia care services, and to increase investment in research."

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      • #48

        September 24, 2009 -- Chronic lack of sleep may promote the development of Alzheimer's disease, two new studies suggest. The findings may have implications for people suffering from insomnia and other sleep disorders. Researchers monitored levels of amyloid beta, a protein fragment known to be linked to Alzheimer's, in the brains of sleep-deprived mice with symptoms of the disease. They found that preventing the mice from sleeping caused a 25% increase in amyloid beta levels. The peptide builds up in the brains of Alzheimer's sufferers to form damaging plaques. Amyloid beta levels were generally higher when mice were active than when they were sleeping, and animals that stayed awake longer had higher amounts of the peptide in their brains. The research will be published tomorrow in the journal Science. Another study, also published in Science, links the finding to humans, showing that amyloid beta levels in the spinal fluid of volunteers increased when they were awake and fell during sleep.

        Professor David Holtzman from the Barnes-Jewish Hospital in St Louis, U.S., where both studies were carried out, said: "The results suggest that we may need to prioritise treating sleep disorders not only for their many acute effects, but also for potential long-term impacts on brain health." The scientists also found a link with orexin, a protein involved in regulating the sleep cycle. When orexin was injected into the brains of mice, the animals stayed awake longer and levels of amyloid beta in their brains increased. A drug that blocked the action of orexin led to a significant reduction in levels and increased the amount of sleep. Three weeks of chronic sleep deprivation was enough to accelerate the deposition of amyloid plaque in the brains of the mice. But after two months of treatment with the orexin blocker, the deposits had shrunk by more than 80% in some cases. "This suggests the possibility that a treatment like this could be tested to see if it could delay the onset of Alzheimer's disease," said Prof Holtzman. He pointed out that as people age and their risk of Alzheimer's increases, they usually sleep for shorter periods. Further studies are being considered to see whether chronic sleep loss in young and middle-aged adults increases the risk of Alzheimer's in later life. Alzheimer's is the most common form of dementia, affecting an estimated 700,000 people in the UK. The figure is expected to double within a generation.

        Rebecca Wood, chief executive of the Alzheimer's Research Trust, said: "This study appears to indicate for the first time that sleep disorders could have a connection to the development of dementia, though the study is only in mice. People who experience sleep disturbance should not be unduly worried about these preliminary findings. "We urgently need more research into the causes of dementia to provide hope of a treatment to the 35 million people worldwide with the condition." Professor Clive Ballard, director of research at the Alzheimer's Society, said: "It is interesting that there may be a link between sleep and the build-up of the protein associated with the development of Alzheimer's disease. However, there are many other biological factors that may have an impact on the protein's production, so further research in this area would be needed."

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        • #49

          Samedi 16 Janvier 2010 -- Une méthode détectant la mort des neurones via un ophtalmoscope permettrait de diagnostiquer à l’avance certaines maladies neurodégénératives, comme Alzheimer. La maladie d’Alzheimer est une maladie neurodégénérative, elle affecte le cerveau par la mort des neurones. Elle entraîne une diminution progressive et irréversible des facultés mentales, notamment de la mémoire. Une équipe de chercheurs a trouvé un moyen de déterminer chez les souris, celles qui étaient les plus inclines à développer cette maladie. Pour cela, il faut pouvoir détecter le nombre de neurones mourants ce qui, hélas, n’est pas chose facile. La maladie d’Alzheimer est la plupart du temps diagnostiquée trop tard, quand ses symptômes sont apparents et que les dommages sont déjà importants. Les scientifiques ont donc pensé à se référer aux cellules des yeux via un simple ophtalmoscope car la mort des cellules s’élargit au niveau de la partie arrière des yeux. Les cellules meurent soit par apoptose, mort programmée par l’organisme, soit par nécrose, c'est-à-dire par cassure de la membrane plasmique de la cellule qui, perdant son contenu cytoplasmique, meure. Au début de la maladie, les cellules meurent par apoptose, puis progressivement, la nécrose la remplace.

          Durant leurs expérimentations, les scientifiques ont injecté dans les yeux de souris un colorant vert pour détecter les cellules mourant d’apoptose, ainsi qu’un colorant rouge pour les cellules arrachées par une nécrose. Ils ont ensuite observé à l’ophtalmoscope la partie arrière des yeux des rongeurs, là où les cellules mourantes peuvent être détectées. Grâce à différents filtres, ils ont pu aisément détecter les cellules fluorescentes reconnues comme nécrosées ou apoptotiques selon leur couleur. Il s’est avéré que beaucoup plus de cellules malades étaient présentes chez les souris victimes d’Alzheimer que chez les souris saines. Plus la maladie en était à un stade évolué, plus les cellules nécrosées étaient présentes par opposition aux cellules apoptotiques dont le nombre diminuait.

          Chez les souris, il a été possible d’arrêter le processus lorsque les cellules n’étaient encore victimes que d’apoptose en leur administrant le médicament contre Alzheimer, la mémantine. Ces conclusions pourraient être utiles pour diagnostiquer Alzheimer chez l’être humain bien avant les symptômes apparents tels la perte de mémoire et donc, ralentir fortement voir stopper la maladie. De plus, l’évolution de la maladie serait visible via les cellules et un traitement plus adapté pourrait être prescrit selon le stade de la maladie. Cependant, les coûts de cette technique seraient très élevés.

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          • #50

            January 16, 2010 -- Alzheimer's and other neurological disorders are often diagnosed after a disease has progressed. Using a special ophthalmoscope that detects fluorescent markers signaling early neurological disease is being explored by researchers that could allow clinicians to detect and track Alzheimer's disease with a simple eye exam. Professors Francesca Cordeiro and Stephen Moss have identified a process that directly measures retinal (therefore brain cell) death in real time. According to Dr. Cordeiro, "Few people realize that the retina is a direct, albeit thin, extension of the brain.” Cordeiro adds, “The death of nerve cells is the key event in all neurodegenerative disorders – but until now it has not been possible to study cell death in real time. This technique means we should be able to directly observe retinal nerve cell death in patients, which has a number of advantages in terms of effective diagnosis. This could be critically important since identification of the early stages could lead to successful reversal of the disease progression with treatment.” The study is the first to be observed in animal models, and could lead the way to new and earlier treatments for neurological disorders such as Alzheimer’s disease. It also opens the door to research by allowing scientists a means to measure the effects of new treatments. "Currently, the biggest obstacle to research into new treatments for neurodegenerative diseases is the lack of a technique where the brain's response to new treatments can be directly assessed – this technique could potentially help overcome that”, explains Dr. Cordeiro. The equipment used by the scientists on animals is the same that would be used in humans. The researchers will begin studying humans later this year using the simple, non-invasive, and inexpensive eye exam that measures retinal cell death that could detect Alzheimer’s disease early.

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            • #51

              January 16, 2010 -- A new study on mice shows that in the next five years Alzheimer’s disease could be detected via a simple eye test, wherein a harmless fluorescent dye placed on the retina of the eye will make it possible for the optician to identify dying nerve cells, an early sign of the condition, and diagnose Alzheimer’s and other neurological diseases before symptoms develop. Research testing the newly developed technique indicates dead cells in the retina of rodents and other animals with rodent versions of human diseases like glaucoma and Alzheimer’s can be detected using it.

              Using fluorescent markers that attach themselves to cells that are dying, including indicating the stage of cell death, the technique using a laser ophthalmoscope to look at the dying cells in the retina, an indication of dying cells in the brain can diagnose and prevent neuro-generative disorders in the early stages, including successful reversal of the disease progression with treatment early on. When injected into the retina, attaching itself to only cells that are dying, the fluorescent dye makes them glow when exposed to certain wavelengths of light, and is also able to distinguish the different ways cell death can occur, including identifying whether a cell is in the early or late stages of dying. However, whether the technique is able to effectively distinguish between different diseases or if the results can tell us about the health of nerve cells in the brain remains to be tested. Diagnosing Alzheimer’s is complicated and additional tests that help identify the condition will help though it cannot be said, yet, whether the test will prove successful in humans, as it has in the study on animals.

              Published in the open-access peer-reviewed journal Cell Death and Disease, Professor Francesca Cordeiro and colleagues from University College London and other research centres in USA and Italy conducted the study, funded by the Wellcome Trust and The Foundation Fighting Blindness. It is not possible to detect nerve cell death, a key feature of diseases like Alzheimer’s disease and glaucoma, while it is occurring in the brain. Due to similarities between nerve cell death in the eye and in the brain, researchers tested a system that could detect nerve-cell death in the retina of the eye, hoping this technique could give insight into brain nerve cell death. Human trials will be conducted to test whether this new technique has the potential to diagnose Alzheimer’s disease, the occurrence of nerve-cell death in various neurological and eye diseases, including Parkinson’s and glaucoma. In the future, it is possible a visit to a high-street optician for getting your eyesight tested will also include checking the brain.

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              • #52

                PHOENIX, January 20, 2010 (UPI) -- U.S. researchers say three proteins may contribute to Alzheimer's disease. Researchers from the Translational Genomics Research Institute in Phoenix have identified three kinases - or proteins - that dismantle connections within brain cells. The study, published in BMC Genomics, found the kinases - EIF2AK2, DYRK1A and AKAP13 - cause a malfunction in tau, a protein critical to the brain cell. "The ultimate result of tau dysfunction is that neurons lose their connections to other neurons, and when neurons are no longer communicating, that has profound effects on cognition - the ability to think and reason," Dr. Travis Dunckley, the senior author, said in a statement. Dunckley and colleagues created tests to look at all 572 known and theoretical kinases within human cells and identified 26 associated with the formation of tau and the three found to cause tau dysfunction.

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                • #53

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                  • #54

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                    • #55

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                      • #56

                        Mercredi 14 Juillet 2010 -- La maladie d'Alzheimer est un sujet qui préoccupe les scientifiques du monde entier. Des chercheurs anglo-saxons se sont penchés sur l'efficacité de divers régimes et pratiques censés prévenir l'apparition de la maladie. La Conférence internationale sur la maladie d'Alzheimer qui s'est tenue à Hawaï fut l'occasion pour les chercheurs des quatre coins de la planète de partager leurs découvertes. Les Anglo-Saxons proposent des comportements à adopter au quotidien afin de freiner l'apparition ou l'évolution de cette dégénérescence mentale. L'université de Californie conseille ainsi une consommation quotidienne de thé ou de café. Les personnes suivant ces préconisation verraient en effet, à partir de 65 ans, les signes de démence diminuer de 37% pour les buveurs de thé et de 20% pour les buveurs de café. À New York, on s'est intéressé à la consommation de noix. Elles amélioreraient considérablement les aptitudes du cerveau. L'université de médecine de Boston a, elle, mis en évidence les bienfaits du golf ou encore du jogging. De façon plus générale, l'exercice et l'exposition au soleil seraient de bons moyens de lutte contre la maladie d'Alzheimer. Enfin, au Royaume-Uni, des chercheurs de l'université d'Exeter pointent du doigt les carences en vitamine D. Il faut donc faire le plein avant 65 ans.

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                        • #57

                          ''أصبح من الضروري جدا فتح وإنجاز مؤسسات مختصة ومراكز استقبال نهارية للمصابين بمرض الزهايمر في الجزائر، أو ما يسمى بدور حضانة نهارية للكبار، لأجل التكفل بهم ورعايتهم لتخفيف العبء على عائلات المرضى، خاصة وأن عددهم فاق 100 ألف حالة مرضية''.

                          قال البروفيسور أرزقي رئيس مصلحة طب الأعصاب والمجلس العلمي والطبي لدى المركز الاستشفائي الجامعي في البليدة، فرانتز فانون سابقا في تصريح لـ''الخبر'' على هامش اليوم الدراسي العالمي لزرع الأعضاء، إن على الجهات المعنية والمسؤولة في الجزائر التعجيل بإنجاز وتجهيز هياكل استقبال المصابين بداء الزهايمر أو مرض فقدان الذاكرة والنسيان، تكون على شاكلة دور الحضانة ولكنها موجهة للكبار، مع التفكير المزدوج بمسألة التكوين الطبي والبحث العلمي، لأن عدد المصابين بهذا المرض ارتفع وقفز إلى ما يفوق 100 ألف مصاب.

                          وقال المتحدث إن الأرقام لا تزال غير مضبوطة وغير دقيقة، ويمكن أن يكون العدد الحقيقي للمصابين أكثـر بكثير من الرقم المصرح به، مشيرا إلى أن عائلات المرضى أصبحت عاجزة عن التكفل ورعاية مرضاهم لمدة تكاد تكون مطلقة بمعنى 24 على 24 ساعة، وأن المراكز يجب أن تكون في تكفلها نهارية مثلها مثل الخدمة التي تقدمها دور حضانة الأطفال، بحيث ينزل المريض نهارا ثم يعود رفقة أهله إلى بيته في المساء.

                          ونوه البروفيسور بتجربة تونس الرائدة في الوطن العربي، والتي عرفت إنجاز ما يشبه المستشفى لاستقبال مرضى الزهايمر نهارا، مذكرا في معرض حديثه بتجربة ثانية في الجزائر بإنجاز مؤسسة شبيهة ستكون عملية العام 2011 وأن غلافا ماليا تم تخصيصه لأجل ذلك.

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                          • #58

                            ALGIERS, May 17, 2011 (KUNA) -- Up to 100,000 people are infected with Alzheimer's disease in Algeria, a disease which mainly affects the elderly, a neurologist said Tuesday. Dr. Suheila Amalo, of the CHU Frantz Fanon in Blida, said a large proportion of infectees were diagnozed with Alzheimer's disease late in time which is why it was difficult to treat. She made the remarks during a national conference about Geriatrics. The neurologist noted that at the national level these numbers were less than official figures because many families do not use any treatment due to ignorance regarding the disease and lack of awareness.

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