Cure For Alzheimer's Disease - Stanford University

[rgray222]

Source

A drug which boosts the brain's immune response may prevent or cure Alzheimer's disease, scientists believe Alzheimer's could be prevented and even cured by boosting the brain's own immune response, scientists at Stanford University believe.

Researchers discovered that nerve cells die because cells which are supposed to clear the brain of bacteria, viruses and dangerous deposits, stop working.

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.
“Our experiments show that keeping them on the right track counters memory loss and preserves healthy brain physiology.”

By 2015 there will be 850,000 people with dementia in the UK, with Alzheimer's disease being the most common type. 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. They act as a frontline defence, looking for suspicious activities and materials. 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. 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. “If they lose their ability to function, things get out of control. 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. 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.

And for those mice who developed Alzheimer's, blocking EP2 reversed memory decline.

Now Stanford is hoping to produce a compound which only blocks EP2 to prevent unnecessary side effects.

The study was published in the Journal of Clinical Investigation.

Source

[WhiteFeather]

Hmm I wonder if Jim Humbles MMS would do justice for Alzheimers as well?
Just a thought, especially from what it stated concerning here in the post,,,, "Researchers discovered that nerve cells die because cells which are supposed to clear the brain of bacteria, viruses and dangerous deposits, stop working."

[Agape]

I found this little note once when researching medicine that is usually used as anti-emetic ( against nausea ) , in all possible indications ( allergy reactions , migraines , post-chemotherapy nausea and vomiting etc. )

Thiethylperazine activates the transport protein ABCC1 that clears beta-amyloid from brains of mice.

Accompanying article from Science Daily ( 2011 ) :

http://www.sciencedaily.com/releases...0901134628.htm

Alzheimer disease: Transport protein ABCC1 plays key role in clearing beta-amyloid from brains of mice


and maybe even more important entry on Beta Amyloid mechanism of action in brain :

http://en.wikipedia.org/wiki/Amyloid_beta

Circadian rhythm of amyloid beta[edit]
A 2009 report demonstrated that amyloid beta production follows a circadian rhythm, rising when an animal (mouse) or person is awake and falling during sleep.[64] The wakefulness-promoting neuroprotein orexin was shown to be necessary for the circadian rhythm of amyloid beta production.[64] The report suggested that excessive periods of wakefulness (i.e. due to sleep debt) could cause chronic build-up of amyloid beta, which could hypothetically lead to Alzheimer's disease.[64] This is consistent with recent findings that chronic sleep deprivation is associated with early onset Alzheimer's disease.[64]

Melatonin is also involved in circadian rhythm maintenance. Notably, melatonin has been connected with the "sundowning" phenomenon, in which Alzheimer's disease patients that have amyloid plaques in the hypothalamus exhibit exacerbation of Alzheimer's disease symptoms late in the day.[70] This "sundowning" phenomenon could be directly or indirectly related to the recently discovered continuous increase in amyloid beta throughout the day.

Where the above mentioned 'Torecan' ( thiethylperazine) medication is concerned , it's probably on-prescription medicine in most EU countries , not sure about the US ( http://www.healthdictionary.info/Torecan.htm )
but it's considered common anti-emetic and first-hand aid in emergencies . Something handy to have in your home pharmacy .

[Tesla_WTC_Solution]

It would be irony of ironies if Morgellons and Dementia came from the same root cause. Infections.

TY OP!

[Dennis Leahy]

I almost posted this article myself, a couple of weeks ago. 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.

This is not an attempt to "debunk" the article, but rather a call to investigate a bit before we get out the trumpets.

I looked up the scientific whitepaper at the "Journal of Clinical Investigation". 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. 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.

[Shadowself]

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.

Thank you for that comment Dennis. It is a bit overzealous. A good article yes and I've seen it as well.

Article quote:

“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. “If they lose their ability to function, things get out of control. A-beta builds up in the brain, inducing toxic inflammation.”

What do you suppose causes them to lose their ability to function?



REST/NRSF-interacting LIM domain protein

http://liweilab.genetics.ac.cn/tm/se...8&sot=nu&pg=38


http://en.wikipedia.org/wiki/RE1-sil...ription_factor

It is assumed that REST represses genes that promote cell death and Alzheimer’s disease pathology, and induces the expression of stress response genes. Moreover, REST potently protects neurons from oxidative stress and amyloid β-protein toxicity

https://projectavalon.net/forum4/show...l=1#post919566

REST is found to be down-regulated in elderly people with Alzheimer's disease.

[Agape]

Posted by Dennis Leahy (here)
This is not an attempt to "debunk" the article, but rather a call to investigate a bit before we get out the trumpets.

I looked up the scientific whitepaper at the "Journal of Clinical Investigation". Well, there is no paper using layman's terms, but I believe this is the article - from 2014 - that the conclusions were drawn from:[COLOR=blue][B] Prostaglandin signaling suppresses beneficial microglial function in Alzheimer’s disease models

Hello Dennis ,

I think you're right here . All it possibly means is that there's 'work in progress' ..in the research and something has ( finally !!! ) been observed on the metabolic level beyond the beta-amyloid plague accumulation that could lead to finding a way to reversing the process or maybe at least , determining the causality chain .

The title of the article should better read : ''Increased prostaglandin signalling in impaired microglial function ( in Alzheimers disease research )''

I've tried to read some of the article you're referring to .. and all it seems is that they could observe increased signalling of EP2 ( Prostaglandin E2 , also called PGE2 ) in these poorly functioning microglial cells showing very low clearance ability of any 'toxic residue' including the beta-amyloid
and when an EP2 antagonist was introduced to those cells ( in living mice ) the clearance ability was vertically improved .

It's a symptomatic approach to medicine ( very common and widespread in todays pharmacology , the chemical one as we know it in the west especially ) that can occasionally lead to great improvements , other times they produce an agent that can bring on some improvement in some people but it does not target the main or real cause of the disease ,
whereas here we may presume there is more than one or two such causes .

Brain chemistry is perhaps the most complicated biological process available on this planet to this day .

If I was to implicate something 'simple' from the research paper quoted above it'd probably read 'stress reaction' and 'reducing stress signalling' .

The prostaglandin metabolism seems to be essential for brain on cellular level , sort of survival mechanism that will keep brain alive till the 'last breath' .
It may fix cells that are impaired even if not always well , 'it' does not care . If there's inflammation - it maybe even any common inflammation accompanying virosis or else - that can break through the 'brain blood barrier' - and it does happen with or without peoples full knowledge in many cases ,
and in case that these cells fail to clear the 'waste' of various chemicals and broken cells after the inflammation is over , this sort of 'plague' is being formed without our noticing it , perhaps for long time .
In course of time , again, this may slow down or impair some brain functions unless we happen upon healthy way of cleaning this out n away . Now when when these cells - microglia - responsible for brain immunity start to 'suffocate' under the load of work they think they can't perform they start sending distress signals to each other ,
trying to fix each other . That's what the prostaglandin metabolism can be ( at least partially about ) .
In almost-healthy functioning brain cells it would mean repairing those who are weaker so that the all-over clean-up could be performed well .

In brain where most of these cell function deteriorated to a degree very little happens and in response to it , they send more 'distress signals' and send more EP2 ,
a typical biological stress reaction ..
while 'successfully' blocking all the rest of healthy communication of the cell .

So according to the above research team above , if EP2 antagonist is applied , this 'stress communication' ceases and those remaining healthy microglia are capable of better clearance ability .

In reality , I think the mechanism is indefinitely more complicated , see here for example ...

Insulin-like growth factor 1 (IGF1) is upregulated in vivo in microglia derived from Cd11b-Cre Ep2fl/fl brains. In addition, we found an unexpected increase in Igf1 mRNA levels in microglia derived from i.c.v. Aβ–treated Cd11b-Cre Ep2fl/fl mice (Figure 4E). 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). 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. 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). 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). 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. Moreover, these pathways were activated in parallel with suppression of the proinflammatory response (see below).

http://www.jci.org/articles/view/77487

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. 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. elegans.[10][11] Daf-2 encodes the worm's unified insulin/IGF-1-like receptor. Despite the impact of IGF1-like on C. 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. 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. ,
and increase of the Igf1 metabolism instead - they can replace each other in certain situations since they're molecularly very similar .

Whether and how this exactly affects brain cell function needs to be determined yet .

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 .

[Dennis Leahy]

Excellent, thanks Agape!

I'm thrilled that university researchers and even the (evil) Big Pharma corporations are working on Alzheimer's cures, but I'll be ecstatic when we figure out cause(s) and natural (non pharmacological) prevention. Since not everyone gets Alzheimer's as they age (and it certainly appears that Alzheimer's is rising exponentially), there may be predispositions (and environmental causal factors) that have markers, and that group of people inentified would (in this herbal fantasy) simply take megadosage of some natural nutrient that is required to keep the microglia in tip top shape so that no plaques form.

Dennis

[Omni]

Posted by Dennis Leahy (here)
Excellent, thanks Agape!

I'm thrilled that university researchers and even the (evil) Big Pharma corporations are working on Alzheimer's cures, but I'll be ecstatic when we figure out cause(s) and natural (non pharmacological) prevention. Since not everyone gets Alzheimer's as they age (and it certainly appears that Alzheimer's is rising exponentially), there may be predispositions (and environmental causal factors) that have markers, and that group of people inentified would (in this herbal fantasy) simply take megadosage of some natural nutrient that is required to keep the microglia in tip top shape so that no plaques form.

Dennis

You might already be aware of this, but I believe aluminum has been linked to alzhiemers. Chemtrails are full of aluminum. That could be the biggest cause. I do know the cabal likes the condition in people. They like old people being 'senial' instead of sources of wisdom from all their years.

There is an old saying: "When an old person dies a library burns down" Same could be said with alzhiemers....

[rgray222]

A lot of news stories are proclaiming a cure has been found but it is way to premature to express such a sentiment. That said, this is a huge step in finding a viable treatment or actually curing this horrific disease.

University of Cincinnati study: Decreased proteins, not amyloid plaques, tied to Alzheimer’s disease

Research on patients with mutations published in Journal of Alzheimer’s Disease

New research from the University of Cincinnati bolsters a hypothesis that Alzheimer’s disease is caused by a decline in levels of a specific protein, contrary to a prevailing theory that has been recently called into question.

UC researchers led by Alberto Espay, MD, and Andrea Sturchio, MD, in collaboration with the Karolinska Institute in Sweden, published the research on Oct. 4 in the Journal of Alzheimer’s Disease.

Questioning the dominant hypothesis

The research is focused on a protein called amyloid-beta. The protein normally carries out its functions in the brain in a form that is soluble, meaning dissolvable in water, but it sometimes hardens into clumps, known as amyloid plaques.

The conventional wisdom in the field of Alzheimer’s research for more than 100 years stated that Alzheimer’s was caused by the buildup of amyloid plaques in the brain. But Espay and his colleagues hypothesized that plaques are simply a consequence of the levels of soluble amyloid-beta in the brain decreasing. These levels decrease because the normal protein, under situations of biological, metabolic or infectious stress, transform into the abnormal amyloid plaques.

“The paradox is that so many of us accrue plaques in our brains as we age, and yet so few of us with plaques go on to develop dementia,” said Espay, professor of neurology in the UC College of Medicine, director and endowed chair of the James J. and Joan A. Gardner Family Center for Parkinson’s Disease and Movement Disorders at the UC Gardner Neuroscience Institute and a UC Health physician. “Yet the plaques remain the center of our attention as it relates to biomarker development and therapeutic strategies.”

Sturchio noted that many research studies and clinical trials over the years have aimed at reducing amyloid plaques in the brain, and some have lessened plaques. But until the Sept. 27 announcement of a positive trial by Biogen and Eisai (with drug lecanemab), none slowed the progression of Alzheimer’s disease.

More importantly, in support of their hypothesis, in some clinical trials that reduced the levels of soluble amyloid-beta, patients showed worsening in clinical outcomes.

“I think this is probably the best proof that reducing the level of the soluble form of the protein can be toxic,” said Sturchio, first author of the report and adjunct research instructor at UC’s College of Medicine. “When done, patients have gotten worse.”

Research results

Previous research from the team found that regardless of the buildup of plaques in the brain, people with high levels of soluble amyloid-beta were cognitively normal, while those with low levels of the protein were more likely to have cognitive impairment.

In the current study, the team analyzed the levels of amyloid-beta in a subset of patients with mutations that predict an overexpression of amyloid plaques in the brain, which is thought to make them more likely to develop Alzheimer’s disease.
“One of the strongest supports to the hypothesis of amyloid toxicity was based on these mutations,” Sturchio said. “We studied that population because it offers the most important data.”

Even in this group of patients thought to have the highest risk of Alzheimer’s disease, the researchers found similar results as the study of the general population.

Sturchio noted that many research studies and clinical trials over the years have aimed at reducing amyloid plaques in the brain, and some have lessened plaques. But until the Sept. 27 announcement of a positive trial by Biogen and Eisai (with drug lecanemab), none slowed the progression of Alzheimer’s disease.

More importantly, in support of their hypothesis, in some clinical trials that reduced the levels of soluble amyloid-beta, patients showed worsening in clinical outcomes.

“I think this is probably the best proof that reducing the level of the soluble form of the protein can be toxic,” said Sturchio, first author of the report and adjunct research instructor at UC’s College of Medicine. “When done, patients have gotten worse.”

Source and to read full article: https://www.uc.edu/news/articles/202...lzheimers.html

[Casey Claar]

A drug will never address the root issue and is never a "cure". ( full stop )

[Bill Ryan]

Please also see this thread — which is extremely moving, full of personal accounts (many from Avalon members), and contains a number of excellent suggestions for treatment and care.

• Caring for relatives with Alzheimer's : the modern curse of the elderly
  
  

[onawah]

I thought I was developing Alzheimer's when I was in my 50s, when the cell phone towers first started going up.
At home, I would perform a task, then a little later go to do it again.
When I realized I had already done it, I often had a panic attack.
But because this was a totally new developmen, and when I drove by the towers and felt a very unpleasant vibe coming from them, I suspected the towers were the cause.
I moved to a place deep in the country where there were no towers, and the problem disappeared.
Nowadays, I live in a small town and there are towers here, but using my Spooky 2 device helps with my EMF sensitivity.
Keeping lots of house plants, crystals and other healing stones in my home seems to help too.
When I go out and about though, I get very spacey, so I don't go out much anymore.
I've become a night owl, up until three am because it's easier to focus when most are asleep and not on their cell phones, and less electrical devices are being used.
The price we pay for our modern conveniences is much steeper than most suspect...