Des scientifiques de l'Université de Dundee, Ecosse, ont obtenu une subvention de plus de 1 M£ pour un projet visant à tester si l'observation des vaisseaux sanguins de la rétine (veineux et artériels) pourrait révéler des signes précoces de la maladie d'Alzheimer. Cette hypothèse repose sur d'autres travaux de recherche suggérant que des changements morphologiques de ces vaisseaux pourraient être liés à certaines maladies telles que les accidents cérébraux vasculaires ou les maladies cardiovasculaires.
Muses Labs (http://museslabs.com), which creates software-based systems to enable personalized therapy for the treatment of complex diseases, announces the development of its first offering for addressing Alzheimer’s disease.
Giant pharmaceutical companies have spent billions of dollars trying to crack Alzheimer’s disease, only to come up empty time after time. For small, cash-strapped biotechs, the challenge is even harder. Tufts University professor Philip Haydon is trying to make the improbable journey anyway.
Haydon has created GliaCure, a tiny startup run out of his Boston condominium, to go after a target often overlooked in drug development: microglial cells, one of the family of cells that provide the “glue” to hold together the brain’s hard-working neurons. And he’s about to find out if he’s on to something.
Une équipe internationale de scientifiques, comprenant une équipe de l'Inserm et menée par King's College London, a publié des résultats encourageant dans la lutte contre la maladie d'Alzheimer. Selon cette étude analysant des études précédentes, un cocktail de 10 protéines, retrouvées dans le sang d'individus présentant un déclin cognitif modeste, prédit à 87% quels individus sont à risque de développer la maladie.
Une équipe de recherche du département Sciences de la vie de la Faculté des Sciences de la Hong Kong University of Science and Technology [1] a découvert une nouvelle cible moléculaire impliquée dans la maladie d'Alzheimer, ainsi qu'une molécule issue de la pharmacopée traditionnelle chinoise capable d'interagir avec cette cible. Ces découvertes successives majeures, ouvrant de nouvelles perspectives de traitement de cette maladie, ont été publiées dans la revue prestigieuse Proceedings of the National Academy of Sciences of the United States of America (PNAS) [2].
In a groundbreaking study that looked at how diet, exercise and other non-drug interventions affect cognitive decline, researchers see some hope for relatively easy dementia-fighting strategies
No one believes that a disease as complicated as Alzheimer’s can be warded off by an apple a day or by faithfully hitting the weight room.
Cytox, a leading developer of assays for risk assessment and prediction of dementia, announced the timing of a presentation discussing the development of a novel proprietary blood-based assay for the assessment of risk of cognitive decline.
The talk, entitled “The evaluation of mTOR pathway dysregulation as a novel blood-based phenotypic risk biomarker for the assessment of Alzheimer’s Disease and dementia” will be given on Thursday 17 July, between 08.30 and 10.00am, during the AAIC Symposia and Featured Research Sessions at the Bella Centre, A/S Convention Center, Copenhagen, by Professor Harald Hampel of Université Pierre et Marie Curie (Sorbonne), Paris, France.
Research by a Tel Aviv University team may point the way to protecting cells from the damage wrought by Alzheimer’s disease, and even reverse damage that the disease caused before treatment. The method involves a protein similar to one which protects the brain from damage, but which is lacking in Alzheimer’s patients.
What causes Alzheimer’s is still a mystery, but the direct physical conditions leading to the dementia associated with the disease are very clear to scientists. Plaque accumulations and tangles in neurons kill brain cells in Alzheimer’s sufferers, leading to the degeneration of cognitive function and the loss of memory associated with the disease.
La maladie d'Alzheimer est une affection neuro-dégénérative qui entraine une détérioration progressive et définitive des cellules nerveuses au niveau du système nerveux central [1]. Les neurones situés dans la région de l'hippocampe, qui est le siège de notre mémoire, sont les premiers touchés par la maladie, provocant, dès les premiers stades d'évolution de la maladie, des pertes de mémoire chez le patient. "Où me suis-je marié ? Où sont mes clés ? Où est la boulangerie, déjà ?"...
Research by a Tel Aviv University team may point the way to protecting cells from the damage wrought by Alzheimer’s disease, and even reverse damage that the disease caused before treatment. The method involves a protein similar to one which protects the brain from damage, but which is lacking in Alzheimer’s patients.
What causes Alzheimer’s is still a mystery, but the direct physical conditions leading to the dementia associated with the disease are very clear to scientists. Plaque accumulations and tangles in neurons kill brain cells in Alzheimer’s sufferers, leading to the degeneration of cognitive function and the loss of memory associated with the disease.
