Cure for alzheimer’s disease – stanford university

These cells, called ‘microglia’ function well when people are young, but when they age, a single protein called EP2 stops them operating efficiently.

Now scientists have shown that blocking the protein allows the microglia to function normally again so they can hoover up the dangerous sticky amyloid-beta plaques which damage nerve cells in Alzheimer’s disease.

The researchers found that, in mice, blocking EP2 with a drug reversed memory loss and myriad other Alzheimer’s-like features in the animals.

“Microglia are the brain’s beat cops,” said Dr Katrin Andreasson, Professor of neurology and neurological sciences at Stanford University School of Medicine.


By 2015 there will be 850,000 people with dementia in the UK, with Alzheimer’s disease being the most common type. Cause of alzheimer’s disease The disease kills at least 60,000 people each year.

Microglial cells make up around 10 to 15 per cent of cells in the brain. What are the treatment of alzheimer disease They act as a frontline defence, looking for suspicious activities and materials. Familial alzheimer’s disease When they spot trouble, they release substances that recruit other microglia to the scene which then destroy and get rid of any foreign invaders.

They also work as garbage collectors, chewing up dead cells and molecular debris strewn among living cells including clusters of amyloid-beta which aggregate as gummy deposits and break the connections between neurons, causing loss of memory and spatial awareness. Alzheimer’s disease treatment options These clusters are believed to play a substantial role in causing Alzheimer’s.

“The microglia are supposed to be, from the get-go, constantly clearing amyloid-beta, as well as keeping a lid on inflammation,” added Dr Andreasson. Alzheimer’s disease pdf “If they lose their ability to function, things get out of control. About alzheimer’s disease A-beta builds up in the brain, inducing toxic inflammation.”

The scientists discovered that in young mice, the microglia kept the sticky plaques under control. Alzheimer disease test peanut butter But when experiments were done on older mice, the protein EP2 swung into action and stopped the microglia producing enzymes which digested the plaques.

Similarly mice which were genetically engineered not to have EP2 did not develop Alzheimer’s disease, even when injected with a solution of amyloid-beta, suggesting that their cells were getting rid of the protein naturally.

I almost posted this article myself, a couple of weeks ago. Pathophysiology of alzheimer disease pdf When I dove deeper into it, it appeared that (just as was indicated by the original provocative article title, “Did Stanford researchers just find a cure for Alzheimer’s?”), that there is research being conducted that is somewhat promising (just how promising depends on who you talk to), but the layman’s conclusion may be overstated.

I looked up the scientific whitepaper at the ” Journal of Clinical Investigation”. How early can you get alzheimer’s disease Well, there is no paper using layman’s terms, but I believe this is the article – from 2014 – that the conclusions were drawn from: Prostaglandin signaling suppresses beneficial microglial function in Alzheimer’s disease models

My searches at that site included the terms: “microglia”, “microglia AND amyloid-beta plaque”, “microglia AND alzheimer’s”, and finally (when I could not find an article newer than 2007 and none citing Stanford University), I searched for one of the authors mentioned, “Andreasson”, which led to the article linked above. Signs and symptoms of alzheimer’s disease I can read some of it, but don’t have the physiology, neuroanatomy, and biochemistry background to really understand it.

Though I usually avoid reading the comment section beneath articles in mainstream publications (expecting the mean-spirited anonymous trolls like many YouTube commenters), there were several comments that appeared to be from scientifically literate people who appeared to me to be either neurochemical researchers themselves or family members of Alzheimer’s patients, and cautioned that this article was an overzealous interpretation of the study.

Again, I do not pretend to know, but would ask if we have some scientifically literate members, perhaps even in one of these related fields of study, that could offer their interpretation of the whitepaper.

Insulin-like growth factor 1 (IGF1) is upregulated in vivo in microglia derived from Cd11b-Cre Ep2fl/fl brains. Alzheimer’s disease test In addition, we found an unexpected increase in Igf1 mRNA levels in microglia derived from i.c.v. Can you die from alzheimer’s disease Aβ–treated Cd11b-Cre Ep2fl/fl mice (Figure 4E). What are the causes and symptoms of alzheimer disease Whereas at the organismal level, reduced IGF1 signaling increases longevity (43), at the cellular level, IGF1 promotes cell survival through the PI3K/AKT pathway and RasGTPase/RAF-1/MEK pathways, and in brain, IGF1 signaling promotes synaptogenesis, neurogenesis, angiogenesis, and neuroprotection (44). Types of alzheimer’s disease Although IGF1 receptors are expressed on all cell types in the CNS, in general, IGF1 is synthesized in the liver and is transported to the brain bound to IGF1 binding proteins. Alzheimer’s disease meaning Exceptions include postnatal brain development, where microglia transiently express IGF1 that supports developing layer V neurons (45), and following brain injury, where microglia express IGF1 and astrocytes and neurons increase IGF receptor expression (44). Is there treatment for alzheimer’s disease Validation of the EP2-dependent regulation of IGF1 was carried out in aged primary macrophages, where Igf1 mRNA expression was found to be suppressed by the EP2 agonist butaprost (Figure 4F). Stages of dementia alzheimer’s disease Taken together, our unbiased analyses indicated the activation of multiple beneficial pathways in Ep2-deficient microglia in vivo, including antiinflammatory nuclear hormone, Aβ clearing, and trophic pathways. Alzheimer’s disease history Moreover, these pathways were activated in parallel with suppression of the proinflammatory response (see below).

There seems to be a correlation between the prostaglandin metabolism – for example – and the Igf1 – insulin-like growth factor : http://en.wikipedia.org/wiki/Insulin…rowth_factor_1

The Igf1 is related to growth hormone , so one of the most important hormonal bonds in the body – though in fact , they’re all somehow related and depend one upon another .

It is now widely accepted that signaling through the insulin/IGF-1-like receptor pathway is a significant contributor to the biological aging process in many organisms. Facts about alzheimer’s disease This avenue of research first achieved prominence with the work of Cynthia Kenyon, who showed that mutations in the daf-2 gene double the lifespan of the roundworm, C. Test for alzheimer’s disease elegans.[10][11] Daf-2 encodes the worm’s unified insulin/IGF-1-like receptor. What causes alzheimer disease yahoo Despite the impact of IGF1-like on C. Signs and symptoms of alzheimer disease pdf elegans longevity, direct application to mammalian aging is not as clear as mammals do not form dauer-like developmental stages.

Insulin/IGF-1-like signaling is conserved from worms to humans. Alzheimer disease caused by virus In vitro experiments show that mutations that reduce insulin/IGF-1 signaling have been shown, in laboratory conditions, to decelerate the degenerative aging process and extend lifespan in a wide range of organisms, including Drosophila melanogaster, mice,.[12] Reduced IGF-1 signaling is also thought to contribute to the “anti-aging” effects of Calorie restriction

It’s fairly possible – there would be a correlation between failed insulin metabolism – such as in all types of diabetes – or , wrong diets , fasting , obesity etc. How can you die from alzheimer’s disease ,

So I suppose there’s a whole chain of causes and consequences with too many factors in play, from hereditary predispositions to life style and diet, number of infections and quality or absence of treatment .