Quatre cuillères à soupe de cet « aliment pour le cerveau » pourraient prévenir la maladie d'Alzheimer. Visionnez cette vidéo où le Dr Mary Newport présente une découverte étonnante qui pourrait « soigner » la maladie d’Alzheimer et les pertes de mémoire. Les cétones de la noix de coco – 22 juillet 2008 Commentaires du Dr Mercola: Dans la vidéo ci-dessus, le Dr Mary Newport présente les corps cétonés, un carburant alternatif pour votre cerveau que votre organisme produit pendant la digestion de l’huile de noix de coco, et le grand intérêt de cette huile pour lutter contre la maladie d’Alzheimer.
Cette information est vraiment remarquable, et je vous encourage à visionner la vidéo du Dr Newport dans son intégralité pour comprendre toute l’histoire. Gardez toutefois à l’esprit qu’à contrario du Dr Newport, je ne soutiens pas l’usage de médicaments pour soigner l’Alzheimer, et, étant donné l’état de santé de son mari, l’enrôler dans une cohorte de tests d’un vaccin est totalement contre-indiqué et mal avisé. « La famine du cerveau » est une des caractéristiques de la maladie d’Alzheimer 1. 2. 3.
The Role of Tau in Brain Function and Dementia. Recent research into the causes of Alzheimer’s has become increasingly complex. For a long time it was assumed that buildup of amyloid-β causes destruction of neurons and, therefore, the degenerative brain disease. Most current drug trials are trying to eliminate the toxic form of amyloid. However, very recent research has shown that many (possibly 30%) of Alzheimer patients have no such buildup and many normal elders do have amyloid in the brain (See post on Amyloid and Alzheimer’s). Therefore, amyloid as a cause of Alzheimer’s is not at all certain.
Tau is a critical protein that holds together the very active microtubules that build and rebuild structures in the axon and dendrite (see post on axon transport). It is not known whether the travelling destructive toxic tau consists of aggregates (probably not), small oligomers (several stuck together), or other tau molecules that are soluble in water. Tau Protein in the Neuron From Zwarck Normal Tau Functions Structure of Tau From Splette. Resveratrol Stabilizes Alzheimer’s Biomarker that Decreases with Progression of disease | Science, Astronomy, Medical News & Updates. The largest nationwide clinical trial to study high-dose resveratrol long-term in people with mild to moderate Alzheimer’s disease found that a biomarker that declines when the disease progresses was stabilized in people who took the purified form of resveratrol.
Resveratrol is a naturally occurring compound found in foods such as red grapes, raspberries, dark chocolate and some red wines. The resveratrol clinical trial was a randomized, phase II, placebo-controlled, double blind study in 119 patients with mild to moderate dementia due to Alzheimer’s disease. An “investigational new drug” application was required by FDA to test the pure synthetic (pharmaceutical-grade) resveratrol in the study.
It is not available commercially in this form.The highest dose of resveratrol tested was 1g by mouth twice daily = to amount in 1,000 bottles of red wine. The researchers studied resveratrol because it activates proteins sirtuins, the same proteins activated by caloric restriction. La maladie d’Alzheimer serait-elle transmissible ? Une équipe londonienne a identifié l’une des anomalies de cette démence dans six cerveaux de victimes de l’hormone de croissance contaminée. LE MONDE | • Mis à jour le | Par Paul Benkimoun Quelques cas de transmission d’une anomalie d’une protéine, qui fait partie des caractéristiques de la maladie d’Alzheimer, semblent avoir été découverts pour la première fois dans le cerveau de personnes mortes, rapporte une équipe médicale londonienne sur le site de la revue Nature, mercredi 9 septembre.
Ces malades avaient été victimes d’une forme de la maladie de Creutzfeldt-Jakob provoquée par un traitement, plusieurs décennies auparavant, avec l’hormone de croissance contaminée. Ces constatations ponctuelles doivent encore être confirmées par d’autres équipes. Plusieurs maladies neurodégénératives partageraient des mécanismes analogues : l’accumulation dans le système nerveux central de protéines anormales.
Autopsie de victimes de Creutzfeldt-Jacob Un petit nombre de malades étudiés. Cet aliment fait des merveilles contre Alzheimer. L’histoire suivante, nous a été communiquée par le Dr Whitaker. Elle nous prouvera une fois de plus qu’il peut-être payant de sortir des sentiers battus et suivre les solutions que nous offre la nature. Steve Newport un comptable américain de 59 ans a été diagnostiqué de la maladie d’Alzheimer. Il n’était plus en mesure de faire de simples opérations mathématiques, ni d’utiliser une calculatrice.
En fait, on devait même lui rappeler de prendre ses repas et de prendre ses médicaments prescrits pour la maladie. L’épouse de Steve, Mary Newport M.D. est médecin, et tout en étant consciente de l’état avancé de la maladie de Steve, elle ne perdait pas espoir et recherchait sans cesse de nouvelles avenues de traitement pour son mari. Un jour de printemps elle découvrit une offre d’étude clinique pour évaluer un nouveau médicament pour traiter l’Alzheimer. Des progrès stupéfiants L’explication du Dr Whitaker M.D. Le Dr Julian Whitaker M.D. est un médecin très célèbre aux États-Unis. Eating away at cognitive decline: MIND diet may slow brain from aging by 7.5 years. While cognitive abilities naturally diminish as part of the normal aging process, it may be possible to take a bite out of this expected decline.
Eating a group of specific foods known as the MIND diet may slow cognitive decline among aging adults, even when the person is not at risk of developing Alzheimer's disease, according to researchers at Rush University Medical Center. This finding is in addition to a previous study by the research team that found that the MIND diet may reduce a person's risk in developing Alzheimer's disease. Mediterranean, with a DASH of other ingredients The National Institute of Aging funded study evaluated cognitive change over a period of 4.7 years among 960 older adults who were free of dementia on enrollment. Averaging 81.4 years in age, the study participants also were part of the Rush Memory and Aging Project, a study of residents of more than 40 retirement communities and senior public housing units in the Chicago area. A wine and no cheese party. Chemical treatment transforms skin cells into neurons. Two teams of researchers have found different ways to perform the same biological identity swap: turning skin cells into neurons.
Both approaches, which involve merely adding a few chemicals to cells, could lead to new ways to treat a person’s disease using cells from their own body. Most of the ways scientists turn one type of cell into another, or into more basic stem cells, depend on adding genes to the original cells. But this gene insertion approach has drawbacks. Its intricate steps are time-consuming, and there’s always a chance the added gene could land somewhere on a chromosome that activates a cancer-causing gene. The new approaches—both published online today in Cell Stem Cell—take a less invasive route. The key, explains Gang Pei, a biochemist at the Shanghai Institutes for Biological Sciences in China, and a co-author on one of the studies, are so-called small molecule chemicals that can slip into a cell, enter the DNA-containing nucleus, and alter the activity of a gene.
Scientists have turned the skin cells of Alzheimer's patients into new brain cells. Using a purely chemical method, two independent teams of Chinese researchers have successfully transformed skin cells into functional neurons, one working with Alzheimer's patients, and the other with cells extracted from mice. The secret is a complex formulation of small molecules that alter the gene expression of the skin cells, and it’s hoped that the technique could be used to grow new neurons to replace the defective ones in the brains of Alzheimer’s patients.
For example, scientists could extract skin cells, turn them into neurons, and transplant them into a patient’s brain with a low risk of rejection. The process of converting one type of cell into another is about as complicated as it sounds. One of the main challenges is that you might end up with cells that look like they have successfully been transformed, but they won’t quite act the same as their natural counterparts. Long-term memories are maintained by prion-like proteins. Research from Eric Kandel's lab at Columbia University Medical Center (CUMC) has uncovered further evidence of a system in the brain that persistently maintains memories for long periods of time. And paradoxically, it works in the same way as mechanisms that cause mad cow disease, kuru, and other degenerative brain diseases. In four papers published in Neuron and Cell Reports, Dr. Kandel's laboratory show how prion-like proteins - similar to the prions behind mad cow disease in cattle and Creutzfeld-Jakob disease in humans - are critical for maintaining long-term memories in mice, and probably in other mammals.
The lead authors of the four papers are Luana Fioriti, Joseph Stephan, Luca Colnaghi and Bettina Drisaldi. When long-term memories are created in the brain, new connections are made between neurons to store the memory. But those physical connections must be maintained for a memory to persist, or else they will disintegrate and the memory will disappear within days. Small loop in human prion protein prevents chronic wasting disease.
Chronic wasting disease (CWD)—an infectious disease caused by prions—affects North American elk and deer, but has not been observed in humans. Using a mouse model that expresses an altered form of the normal human prion protein, researchers at University of California, San Diego School of Medicine have determined why the human proteins aren't corrupted when exposed to the elk prions. Their study, published Feb. 23 in the Journal of Clinical Investigation, identifies a small loop in the human prion protein that confers resistance to chronic wasting disease. "Since the loop has been found to be a key segment in prion protein aggregation, this site could be targeted for the development of new therapeutics designed to block prion conversion," said Christina Sigurdson, DVM, PhD, associate professor at UC San Diego and UC Davis and senior author of the study.
Prions aren't microorganisms like bacteria or viruses; they're simply protein aggregates.