Astrazeneca Share Discussion Threads

[buywell3] 14/1/2019 20:18

Why is Alzheimer's so prevalent ?

I think it is because you can catch it

Alzheimer’s in the United States

Alzheimer’s is the 6th leading cause of death in the United States.

Alzheimer’s is the only disease in the 10 leading causes of deaths in the United States that cannot be cured, prevented or slowed.

1 in 3 seniors dies with some form of dementia.

1 in 10 Americans over the age of 65 has Alzheimer’s.

One-third of Americans over age 85 are afflicted with the illness.

Between 2017 and 2025 every state is expected to see at least a 14% rise in the prevalence of Alzheimer’s.

There has been an 89% increase in deaths due to Alzheimer’s between 2000 and 2014.

More than 5 million Americans are living with Alzheimer’s.

By 2050, it’s estimated there will be as many as 16 million Americans living with Alzheimer’s.

Every 66 seconds someone in the United States develops Alzheimer’s.

When the first wave of baby boomers reaches age 85 (in 2031), it is projected that more than 3 million people age 85 and older will have Alzheimer’s.

Typical life expectancy after an Alzheimer’s diagnosis is 4-to-8 years.

By 2050, there could be as many as 7 million people age 85 and older with Alzheimer’s disease, accounting for half (51%) of all people 65 and older with Alzheimer’s.


Proportion of People With Alzheimer’s Disease in the United States by Age:
85+ years, 38%, 75-84 years, 44%, 65-74 years, 15%, <65 years, 4%

Projected Number of People Age 65 and Older in the U.S. Population With Alzheimer’s Disease, 2010 to 2050:

2010

Ages 65+: 4.7 Million

2020

Ages 65+: 5.8 Million

2030

Ages 65+: 8.4 Million

2040

Ages 65+: 11.6 Million

2050

Ages 65+: 13.8 Million




74% of caregivers of people with Alzheimer’s disease and other dementias reported that they were “somewhat concerned” to “very concerned” about maintaining their own health since becoming a caregiver.

[buywell3] 14/1/2019 18:19

beta-Amyloid Prions and the Pathobiogy of Alzheimer's Disease

2018

Author(s): Watts, JCPrusiner, SB

Running title: Aβ prions and AD pathobiology




'It is becoming increasingly clear that Aβ aggregates exhibit many similarities to prions composed of PrP (Table 2), making it more difficult to refute the notion that Aβ can become a prion during AD.'

[bili1946] 14/1/2019 16:38

Yes but AZN down around 3.5%?

[bountyhunter] 14/1/2019 12:15

The general market is down 1%+

[jackdaw4243] 14/1/2019 11:55

Any reason for the fall when AZN has been tipped as a potential star for 2019 by Accendo

[buywell3] 14/1/2019 01:29

Alzheimer’s Protein May Be Transmissible, in Rare Cases

When Injected, Amyloid-β from Contaminated Vials of Human Growth Hormone Built up in Mice Brains

December 18, 2018

[buywell3] 09/1/2019 15:47

.......... A surprising development I have just come across ............

CBD oil comes from the cannabis plant it is just gaining traction in the manufacture of cosmetics products , it is also being used in medicine for pain relief and other treatments.

CBD has been linked with the reduction of Amyloid Beta protein in the lab ... this protein is present in the brains of many Alzheimer's sufferers. NO CURE or drug exists for Alzheimer's.

In the USA 1 in 3 people over the age of 65 now have Alzheimer's ( how many people knew that one ) It is increasing and costs the USA over $250 BILLION a year.


Thus it is becoming a burden on the USA economy and will cost the USA OVER $1 TRILLION dollars within just over 10 years time ie it has the potential to BANKRUPT the USA ... it is only getting worse and the cost and numbers of carers keeps growing.


Cannabis has had and still gets bad press ... smoking it does seem to affect the smokers brain . We all know that ... it makes you feel good as the doctor said.

June 27, 2016

Cannabinoids remove plaque-forming Alzheimer’s proteins from brain cells
Preliminary lab studies at the Salk Institute find THC reduces beta amyloid proteins in human neurons.
hxxps://www.salk.edu/news-release/cannabinoids-remove-plaque-forming-alzheimers-proteins-from-brain-cells/


Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids

[buywell3] 07/1/2019 04:01

CWD a prion disease is now affecting 26 USA states over 50% of the USA

Tennessee is the latest state to find it in deer, the other being

Colorado, Wyoming, South Dakota, Nebraska, Montana,Wisconsin, New Mexico, Minnesota, Oklahoma, Illinois, Utah,New York, West Virginia, Kansas, Michigan, Virginia,Missouri,
North Dakota, Maryland, Iowa, Pennsylvania, Ohio, Mississippi, Texas, Arkansas


It is now looking very likely that Alabama will be added to the list within the next few months

Many meat processing companies are not taking in any more deer meat for human consumption/processing





Problem is that eating CWD infected deer meat might not show up in humans for a decade or longer

[buywell3] 06/1/2019 22:04

STRAINS OF Aβ PRIONS

In the PrP prion diseases, distinct strains of prions can be classified according to their incubation periods upon inoculation into rodents, the resultant clinical signs of disease and neuropathological features, and their biochemical characteristics, such as their relative resistance to protease digestion and their stability upon exposure to chemical denaturants (Collinge et al. 2007).

A myriad of evidence argues that prion strain-specificproperties are encoded within unique conformations of PrP aggregates (Bessen et al. 1994; Telling et al. 1996). AD is a clinically and pathologically heterogeneous disorder, with variability present in the age of onset, the rate of cognitive decline, and the morphology and neuroanatomical location of Aβ pathology (i.e.,parenchymal versus vascular). It is conceivable that some of this heterogeneity may arise due to the presence of distinct “strains&rdquo; of Aβ prions in the brain.



beta-Amyloid Prions and the Pathobiogy of Alzheimer's Disease

2018

CONCLUDING REMARKS


Sterilization methods for surgical tools may need to be reconsidered, especially since Aβ seeds remain active once bound to stainless steel (Eisele et al. 2009).

Although AD is unlikely to be transmissible under physiological circumstances, the realization that Aβ aggregates can become prions during disease has many potential implications.

First, the existence of self-propagating Aβ aggregates may provide a molecular explanation for why AD is a progressive disorder. Spreading of Aβ prions along neuroanatomical pathways in conjunction with a potential stimulation of tau prion formation may cause a progressive worsening of disease symptoms.




buywell says

Re strains of prions

My take on this is that now there is an explosion of differing prion mutations due to the many different animals that have acquired the disease by eating contaminated food /pellets eg Bone meal some containing infected human bone waste from India which was identified pre the BSE outbreak in the UK and also new animals both in captivity eg sheep/goats/cattle/mink/camels/deer /elk/moose/caribou and in the wild that have acquired the disease via grazing on land contaminated by infected human biosolids.

Humans then eat the above animals / drink the milk / not always sterilized ( although those temps would not kill prions anyway ) and then the human processes a new strain via the animal product/modified strain of prion being ingested

Thus it can only be a matter of time whilst the use of human bio-solids continues that humans will acquire a very aggressive mutant form of prion which will kill in less than 12 months and is transmissible.

[buywell3] 05/1/2019 02:14

U.S. death rate from Alzheimer’s rose dramatically over 15 years. Why?




Why is easy

Because it is a Prion Disease is why

Death rates from Alzheimer’s climbed 55 percent from 1999 to 2014, CDC found, and the number of Americans afflicted is likely to rise rapidly in the coming years. About 5.5 million people 65 years and older have the disease — a wretched and fatal form of dementia that erases memories and ultimately can destroy mental and physical capacity. By 2050, that’s expected to more than double to 13.8 million people.

[buywell3] 03/1/2019 23:01

buywell says

The spread and indeed the creation of many new animal prion diseases is being caused by using human sewage waste in the form of biosolids.


Hence CWD (compulsive wasting disease , a prion disease, occurring in Deer/Elk/Moose/Caribou and Camels in USA, Canada Algeria Norway South Korea Finland ( Algeria for camels)

CWD is now in 24 states of the USA this year over 50% of the USA Deer population will be affected by CWD ie 25 states plus.

These geographically separated countries in different continents are all like the UK did ... spread human sewage waste on fields ... and still do


Dr David Lewis got the push from the EPA for blowing the whistle , the EPA is a USA Government Agency charged with protecting the Environment.






EPA’s fake data destroying America’s health

THE OCONEE ENTERPRISE, JUNE 1, 2017:
DR. DAVID LEWIS


When Congress passed the Clean Water and Clean Air Acts in the late 60s and early 70s, President Nixon established EPA to develop regulations aimed at protecting public health and the environment. President Carter followed by having wastewater treatment plants built throughout America to remove traces of pollutants before discharging wastewater into rivers and other water bodies. Wastewater treatment plants remove trace amounts of water insoluble pollutants by concentrating them in the animal fats contained in sewage sludges, which collect in settling tanks.

EPA deregulated virtually all pollutants in sewage sludge, and promoted their application to land as biosolids. Its only challenge was to explain how trace amounts of petrochemicals and other industrial wastes it strictly regulates in air and water become harmless when mixed with sewage sludge at far higher concentrations, and spread on land where animals graze and children play. According to an internal memo, EPA decided to fund research at land grant universities to “support the science and substance” of its sludge rule, and “overcome misinformation spread by opponents.”

In April 2000, EPA Administrator Carol Browner presented me with the agency’s Science Achievement Award for Biology and Ecology for a study I published in Nature, which raised concerns about EPA’s sludge rule. Ironically, EPA had just recently transferred me to the University of Georgia’s Department of Marine Sciences pending termination for publishing a Nature commentary that was critical of the way EPA handles science in this and other areas.


My UGA appointment ended in 2008 when Nature published an editorial and news article supporting my research on sewage sludge at UGA. It criticized EPA and UGA for publishing data that a federal judge determined were fudged to cover up links between cattle deaths and sewage sludges.

In the wake of this negative publicity, UGA terminated my Visiting Scientist status. My former department head testified under oath in my whistleblower case against EPA. He stated that UGA administrators warned him that the university is “dependent on this money … grant and contract money … money either from possible future EPA grants or [from] connections there might be between the waste-disposal community [and] members of faculty at the university.”

The tragedy is that sewage sludges could be converted into valuable soil amendments and cheap fertilizers using pyrolysis to destroy toxic chemicals, bind heavy metals to activated charcoal, and return carbon to the soil instead of adding it to the atmosphere.

Even doing nothing would have been better than diverting chemical wastes to wastewater treatment plants for land application. At least most toxic chemicals that entered rivers were carried away from human populations and ended up in trace amounts in sediments at the bottoms of oceans. Now, thanks to EPA and its body of fake science, they’re spread all around us on land at millions of times higher concentrations.

The opinions expressed are those of David Lewis, Research Director for the Focus for Health Foundation in Watchung, NJ (www.focusforhealth.org/davidlewis), author of Science for Sale (Skyhorse Publishing, NY) and CEO of Saxon Road Church Inc. in Watkinsville, Georgia.

[buywell3] 03/1/2019 21:44

The protein that prions are made of (PrP) is found throughout the body, even in healthy people and animals.

PRNP (PRioN Protein) is the human gene encoding for the major prion protein PrP (for prion protein), also known as CD230 (cluster of differentiation 230).

Expression of the protein is most predominant in the nervous system but occurs in many other tissues throughout the body.

It is a 100% natural occurring protein ... however ... what nature has provided it for is very interesting indeed.


It serves no useful purpose whatsoever


What is is there for is to make sure we do not live too long and overpopulate the planet thus destroying it faster than we are already doing.


What I have found out by reading many medical articles over the last 3 years is quite worrying which is why the cat is being kept in the bag regarding Alzheimer's and Parkinson's the two biggest named diseases within the group named ''Dementia''

I am now 99% convinced that all most named diseases in the '' Dementia '' group are in fact various forms of Prion Disease and need reclassifying as such if a brave Government somewhere has the balls to do so.





Elucidate yourself

2017 Feb 19




Cellular prion protein as a receptor for amyloid-β oligomers in Alzheimer's disease.

Salazar SV1, Strittmatter SM2.
Author information

Abstract

Soluble oligomers of amyloid-beta (Aβo) are implicated by biochemical and genetic evidence as a trigger for Alzheimer's disease (AD) pathophysiology. A key step is Aβo interaction with the neuronal surface to initiate a cascade of altered signal transduction leading to synaptic dysfunction and damage. This review discusses neuronal cell surface molecules with high affinity selectively for oligomeric disease-associated states of Aβ, with a particular focus on the role of cellular prion protein (PrPC) in this process. Additional receptors may contribute to mediation of Aβo action, but PrPC appears to play a primary role in a number of systems. The specificity of binding, the genetic necessity in mouse models of disease and downstream signaling pathways are considered.

Signal transduction downstream of Aβo complexes with PrPC involves metabotropic glutamate receptor 5 (mGluR5), Fyn kinase and Pyk2 kinase, with deleterious effects on synaptic transmission and maintenance. Current data support the hypothesis that a substantial portion of Aβo toxicity in AD is mediated after initial interaction with PrPC on the neuronal surface. As such, the interaction of Aβo with PrPC is a potential therapeutic intervention site for AD.

[buywell3] 02/1/2019 19:28

Our proposal that human transmission of Aβ pathology had occurred as a result of intramuscular injection of c-hGH is now firmly supported by experimental evidence. While the individuals we described in our earlier report did not meet the full neuropathological criteria for Alzheimer’s disease, they might have done so if they had not died of iCJD at a relatively young age.

Coupled with the news that amyloid pathology has been spread through surgical procedures and with other experiments on spreading amyloid deposits, it seems past time to start being careful about this business.

Although we reiterate that there is no suggestion that Alzheimer’s disease is contagious, and no supportive evidence from epidemiological studies that it is transmissible (notably by blood transfusion), we consider it important to evaluate the risks of iatrogenic transmission of CAA, and potentially of Alzheimer’s disease. Given the lack of disease-modifying therapeutics for Alzheimer’s disease and other distressing and fatal neurodegenerative conditions, it will be important to consider introducing improved methods for removing proteopathic seeds from surgical instruments on a precautionary basis.


Prions can survive 200 degrees centigrade

Water boils at 100 degrees centigrade ... which is why NHS washers are no good for prion removal

[buywell3] 02/1/2019 18:20

December 17, 2018

Mouse Study Backs Idea That Alzheimer's May Be Transmitted

Certain archived human growth hormone samples can "seed" amyloid-β deposits in the brains of genetically engineered mice

[buywell3] 31/12/2018 21:19

Exploring the link between Amyloid Beta plaques; CJD (a Prion Disease) and Alzheimer's ( as yet not classified as a prion disease)

March 2016 a report stated

228 cases of CJD were caused by transplantation of prion-contaminated dura mater—the membrane surrounding the brain and spinal cord—prepared from cadavers around the world.

Dura-mater preparations were regularly used in brain surgery as repair patches until the late 1990s.

For the study published in January, Herbert Budka at the National Prion Diseases Reference Center at University Hospital Zurich and his colleagues examined the brains of seven such patients from Switzerland and Austria, and found that five had amyloid deposits in grey matter and blood vessels.

In Japan, dementia researcher Masahito Yamada at Kanazawa University is making his way through a large number of such autopsy specimens and says that the 16 brains he has examined so far show signs of unusually high levels of amyloid deposition in cerebral blood vessels.



In 2015 a team of pathologists were examining the autopsied brains of four people who had once received injections of growth hormone derived from human cadavers. It turned out that some of the preparations were contaminated with a misfolded protein—a prion—that causes a rare and deadly condition called Creutzfeldt–Jakob disease (CJD), and all four had died in their 40s or 50s as a result.

The reason that these brains looked extraordinary was not the damage wrought by prion disease; the team stated ''it was that they were scarred in another way. It was very clear that something was there beyond what you'd expect

The brains were spotted with the whitish plaques typical of people with Alzheimer's disease. They looked, in other words, like young people with an old person's disease.''

This led to a worrying conclusion:

that the plaques might have been transmitted, alongside the prions, in the injections of growth hormone —

ie The first evidence that Alzheimer's could be transmitted from one person to another. If true, that could have far-reaching implications: the possibility that 'seeds' of the amyloid-β protein involved in Alzheimer's could be transferred during other procedures in which fluid or tissues from one person are introduced into another, such as blood transfusions, organ transplants and other common medical procedures.

f the transmissibility hypothesis proves true, the implications could be severe.

Amyloids stick like glue to metal surgical instruments, and normal sterilization does not remove them, so amyloid seeds might possibly be transferred during surgery.

The seeds might sit in the body for years or decades before spreading into plaques, and perhaps enabling the other pathological changes needed to induce Alzheimer's disease.

Having amyloid plaques in cerebral blood vessels could be dangerous in another way, because they increase the risk that the vessel walls might break, leading to small strokes.

A previous study in 1989 links up to 13% of all "Alzheimer's" victims as really having Creutzfeldt-Jakob disease


Mad cow disease has been of great concern since 1986, when it was first reported among cattle in the U.K. At its peak in January 1993, almost 1,000 new cases per week were identified. Concern about this disease grew significantly in 1996 when an association between mad cow disease and vCJD in humans was discovered.

[buywell3] 31/12/2018 16:20

Amyloid plaques are associated with Alzheimer's referred to as Aβ plaques ( Amyloid Beta plaques in medical studies)



Dec 21, 2017 - Amyloid Plaques. One of the hallmarks of Alzheimer's disease is the accumulation of amyloid plaques between nerve cells (neurons) in the brain. Amyloid is a general term for protein fragments that the body produces normally. Beta amyloid is a protein fragment snipped from an amyloid precursor protein (APP).




In 2016 a study was published that reported four patients who received donor grafts of dura mater, the tough membrane that covers the brain, developed fatal brain hemorrhages due to disseminated amyloid decades after receiving their transplant.



The study ended with:

We conclude that congophilic amyloid angiopathy and brain parenchymal Aβ plaques are frequent in iCJD after dural grafting.

The presence of Aβ pathology in young individuals is highly unusual and suggests a causal relationship to the dural grafts.

Further studies will be needed to elucidate whether such pathology resulted from the seeding of Aβ aggregates from the grafts to host tissues.




Or put in simple english ... the use of transplanted Amyloid Beta protein contaminated Dura Mater killed all 4 many years later


And We conclude that congophilic amyloid angiopathy and brain parenchymal Aβ plaques are frequent in iCJD after dural grafting

In plain english this is a form of angiopathy in which amyloid deposits form in the walls of the blood vessels of the central nervous system.

Angiopathy is the generic term for a disease of the blood vessels (arteries, veins, and capillaries)


the essential and distinctive tissue of an organ or an abnormal growth as distinguished from its supportive framework


brain parenchymal Aβ plaques are frequent in iCJD after dural grafting


in plain english is the abnormal growth , as distinguished from its supportive framework of the brain of a patient of Amyloid Beta , Aβ plaques are frequent in Iatrogenic Creutzfeldt-Jakob Disease (iCJD after dural grafting

iatronic Creutzfeldt-Jakob Disease (iCJD) is a rare, progressive degenerative disease of the brain that occurs following infection with certain protein types, called prions

These prions may be acquired from an individual, who has or has had any type of CJD, by coming into contact with certain bodily fluids or tissues, either through direct contact or via contaminated medical supplies ie dural grafting in this case

Creutzfeldt-Jakob Disease is also known as subacute or transmissible spongiform encephalopathy. Several types of CJD exist.

All types involve an abnormal form of a naturally-occurring protein in the central nervous system.

[buywell3] 31/12/2018 01:09

Children may have been infected with Alzheimer's protein during brain surgery, suggests study

Thursday 15 February 2018