Astrazeneca Share Discussion Threads

[buywell3] 02/5/2019 07:00

Alzheimer's can be caught .... It's a transmissible disease


Alzheimer's disease is a 'double-prion disorder'

Self-propagating amyloid and tau prions found in post-mortem brain samples, with highest levels in patients who died young

May 1, 2019


“I believe this shows beyond a shadow of a doubt that amyloid beta and tau are both prions, and that Alzheimer’s disease is a double-prion disorder in which these two rogue proteins together destroy the brain,” said Stanley Prusiner, MD, the study’s senior author and director of the UCSF Institute for Neurodegenerative Diseases, part of the UCSF Weill Institute for Neurosciences.

“The fact that prion levels also appear linked to patient longevity should change how we think about the way forward for developing treatments for the disease.


Over the past decade, laboratory studies at UCSF and elsewhere have begun to show that amyloid plaques and tau tangles from diseased brains can infect healthy brain tissue much like PrP, but considerably more slowly.

[buywell3] 02/5/2019 06:54

Alzheimer's can be caught .... It's a transmissible disease


Alzheimer's disease is a 'double-prion disorder'

Self-propagating amyloid and tau prions found in post-mortem brain samples, with highest levels in patients who died young

May 1, 2019


“I believe this shows beyond a shadow of a doubt that amyloid beta and tau are both prions, and that Alzheimer’s disease is a double-prion disorder in which these two rogue proteins together destroy the brain,” said Stanley Prusiner, MD, the study’s senior author and director of the UCSF Institute for Neurodegenerative Diseases, part of the UCSF Weill Institute for Neurosciences.

“The fact that prion levels also appear linked to patient longevity should change how we think about the way forward for developing treatments for the disease.


Over the past decade, laboratory studies at UCSF and elsewhere have begun to show that amyloid plaques and tau tangles from diseased brains can infect healthy brain tissue much like PrP, but considerably more slowly.

[badg] 01/5/2019 19:39

Just returning to the trend line

[nisbet] 01/5/2019 12:45

That should read one million pounds.

[nisbet] 01/5/2019 12:44

Interesting to see CEO buying £1m worth of shares.

[stewart64] 01/5/2019 09:13

A bit relentless this fall, now lost two thirds of the 5325 to 6540 calendar year ascent. Rode it up to near the top, but lost 20% of my gain on three stop outs on the way down. Possibly one to avoid until it settles a bit.

[buywell2] 01/5/2019 07:57

CWD a prion disease now in Oklahoma USA an Elk in a farm has tested positive

27 US states now affected over 50% of the USA




Alzheimer's is IMO a prion disease , no cure, fatal in every case

[smcni1968] 30/4/2019 21:14

Astra's issue doesn't seem to have been a popular move.

[jackdaw4243] 30/4/2019 16:20

Hard one to call.

[holts] 29/4/2019 21:33

With a roughly seventy per cent decline from this time last year I suppose there is a decent chance of picking them up at the bottom .

[bountyhunter] 26/4/2019 19:30

Exactly what I was thinking, and not even a sector thing as GSK ended up on the day!

[pilgrim] 26/4/2019 15:30

That is a rather strange response to what appeared to be decent results.

[spud] 26/4/2019 07:59

Nice set of results imo.spud

[crossing_the_rubicon] 24/4/2019 11:41

AstraZeneca chief claims vindication five years after Pfizer bid
Some investors and analysts still unconvinced UK company was right to resist approach




"Interesting article. Wish they;d have sold at £55 to pfizer all those years ago myself"

[stewart64] 18/4/2019 12:31

The chart's pretty awful. It got overbought with the enthusiasm on the results. I traded it from 5350 to 6200 and sold on results day. A few day trades around the lower 6000s. And decided on a long term trade yesterday at 5893. Could easily fall all the way back to lower 5000s though. I'm obviously betting the opposite.

[84stewart] 18/4/2019 11:46

Me thinks AZN should take some of its own medicine

[buywell3] 17/4/2019 07:09

..... CWD in the USA will make BSE in the UK look like getting a headache .....


BSE or Mad Cow Disease was caused by feeding prion contaminated MBM to cattle

MBM is Meat and Bone Meal.

In the USA the FDA still allow MBM to be fed to deer on deer farms , now Chronic Wasting Disease CWD , a prion disease in deer,moose and elk , is present in 26 states of the USA and 4 provinces in Canada, also now in Finland,Sweden and Norway.

Over 50% of the USA now has CWD infected deer present and people are still eating venison from deer they have shot.

Prion diseases mutate over time , it took over 10 years in the UK when BSE was first reported in Cattle before the first vCJD case was reported.

The sheer numbers of wild deer with CWD , first case found late 1960's, that are now roaming the USA means that many mutated CWD forms must be present that now have the potential to infect humans.

When this happens if it has not already done so, there will be a spread of another strain of vCJD across the USA.

The feeding of MBM continues in the USA like never before

[buywell3] 14/4/2019 11:29

!YOUTUBEVIDEO:AkN16QDCClg:

[buywell3] 10/4/2019 08:24

Read the header ... then read the last post and this one

In the post above TDP-43 protein is identified ... it is a prion protein


htTtp://perspectivesinmedicine.cshlp.org/content/8/3/a024463


TDP-43 Prions and Alzheimer's

The most common neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, and amyotrophic lateral sclerosis, are all protein-misfolding diseases and are characterized by the presence of disease-specific protein aggregates in affected neuronal cells. Recent studies have shown that, like tau and α-synuclein, TAR-DNA binding protein of 43 kDa (TDP-43) can form aggregates in vitro in a seed-dependent, self-templating, prion-like manner. Insoluble TDP-43 prepared from the brains of patients has been classified into several strains, which can be transferred from cell to cell in vitro, suggesting the involvement of mechanisms reminiscent of those by which prions spread through the nervous system. The idea that aberrant TDP-43 aggregates propagate in a prion-like manner between cells presents the possibility of novel therapeutic strategies to block spreading of these aggregates throughout the brain.

[buywell3] 10/4/2019 08:09

Soon to be called human prion dementia



April 8, 2019

The Diagnosis Is Alzheimer’s. But That’s Probably Not the Only Problem.
Most people with dementia have a number of brain abnormalities, not just Alzheimer’s disease. The finding is forcing scientists to rethink the search for treatments.



Allan Gallup, a retired lawyer and businessman, grew increasingly forgetful in his last few years. Eventually, he could no longer remember how to use a computer or the television. Although he needed a catheter, he kept forgetting and pulling it out.

It was Alzheimer’s disease, the doctors said. So after Mr. Gallup died in 2017 at age 87, his brain was sent to Washington University in St. Louis to be examined as part of a national study of the disease.

But it wasn’t just Alzheimer’s disease, the researchers found. Although Mr. Gallup’s brain had all the hallmarks — plaques made of one abnormal protein and tangled strings of another — the tissue also contained clumps of proteins called Lewy bodies, as well as signs of silent strokes. Each of these, too, is a cause of dementia.

Mr. Gallup’s brain was typical for an elderly patient with dementia. Although almost all of these patients are given a diagnosis of Alzheimer’s disease, nearly every one of them has a mixture of brain abnormalities.

For researchers trying to find treatments, these so-called mixed pathologies have become a huge scientific problem. Researchers can’t tell which of these conditions is the culprit in memory loss in a particular patient, or whether all of them together are to blame.

Another real possibility, noted Roderick A. Corriveau, who directs dementia research programs at the National Institute of Neurological Disorders and Stroke, is that these abnormalities are themselves the effects of a yet-to-be-discovered cause of dementia.

These questions strike at the very definition of Alzheimer’s disease. And if you can’t define the condition, how can you find a treatment?

In addition to plaques and tangles, other potential villains found in the brains of people with a diagnosis of Alzheimer’s include silent strokes and other blood vessel diseases, as well as a poorly understood condition called hippocampal sclerosis.

Potential culprits also include an accumulation of Alpha-synuclein, the abnormal protein that makes up Lewy bodies. And some patients have yet another abnormal protein in their brains, TDP-43.



No one knows how to begin approaching the multitude of other potential problems found in the brains of Alzheimer’s patients. So, until recently, they were mostly ignored.

“I wouldn’t say it’s a dirty little secret,” said Dr. John Hardy, an Alzheimer’s researcher at University College London. “Everybody knows about it. But we don’t know what to do about it.”

In interviews, some experts said they had been reluctant to talk much about mixed pathologies for fear of sounding too negative. But “at a certain point we have to be somewhat more realistic and rethink what we are doing,” said Dr. Albert Hofman, chairman of the epidemiology department at Harvard’s T.H. Chan School of Public Health.

The problem began with the very discovery of Alzheimer’s disease. In 1906, Dr. Alois Alzheimer, a German psychiatrist and neuroanatomist, described a 50-year-old woman with dementia.

On autopsy, he found peculiar plaques and twisted, spaghetti-like proteins known as tangles in her brain. Ever since, they have been considered the defining features of Alzheimer’s disease.

But scientists now believe this woman must have had a very rare genetic mutation that guarantees a person will get a pure form of Alzheimer’s by middle age.

Patients with the mutation appeared to develop only plaques and tangles, and no other pathologies. So for decades, plaques and tangles were the focus of research into dementia.