Slashdot Mirror
New Alzheimer's Drug Shows Promise
An anonymous reader writes "The Herald Sun is reporting that researchers may have some progress to report on the Alzheimer's front. A new drug, called PBT2, was developed by a Melbourne-based biotech firm that has been showing some promising results. From the article: 'Early clinical testing has confirmed the drug is fast-acting. Levels of amyloid dropped by 60 per cent within 24 hours of a single dose. It found also that PBT2 suppresses the impairment of memory function. More human studies begin in Sweden next month and Australians will join a major international trial of the drug next year.'"
Now I can have photographic memory.
"The Herald Sun is reporting that researchers may have some progress to report on the Alzheimer's front. Maybe. They can't exactly remember one way or the other..."
The Herald Sun is reporting that researchers may have some progress to report on the Alzheimer's front. A new drug, called PBT2, was developed by a Melbourne-based biotech firm that has been showing some promising results.
Fantastic. Now they just have to remember to take it.
Push Button, Receive Bacon
From the article: 'Early clinical testing has confirmed the drug is fast-acting. Levels of amyloid dropped by 60 per cent within 24 hours of a single dose. It found also that PBT2 suppresses the impairment of memory function.
;-)
The article seems to be wrong - press releases on the Prana Biotechnology website indicate these results are from studies in mice.
More human studies begin in Sweden next month and Australians will join a major international trial of the drug next year.
If the data is from mice, then the above clinical trial is presumably a phase I clinical trial, which is designed to show safety and not efficacy. It could be a while before human data is available.
Of course, none of this will stop investors believing the article
"Because it's there." - George Mallory, when asked why he wanted to climb Mt Everest, March 18, 1923 (New York Times)
If this drug is found to actually work, and proceeds to be available for general use within the next five years, it would be a major reversal of the trends we're seeing at the moment. I work in a nursing home designed and built in the 70's, when nursing homes tended to be the place you stayed briefly before dying. Now with our medical advances, together with the high level of day to day care, individually tailored diets etc, we're dealing with people who are living longer. This means we're now running into problems with alzheimers, excarberated by the cocktail of drugs administered. Effectively we're now running into trouble trying to keep people with high level dementia in unsuited facillities. The possibility of an effective treatment for alzheimers makes me wonder if we might be going to move back to the older situation, with lives limited by health again.
[clever sig]
It's interesting but not (yet) as significant as TFA makes out.
e wsid=47696
These are studies on transgenic mice, so it's more a proof-of-concept rather than clinical trials which will be some way off - mostly due to bureaucracy.
For those who want a quick *scientific-ish* summary:
It is widely believed that a protein called Beta-Amyloid is reponsible synaptic dysfunction in Altzheimer's disease. Another variant (Alpha-Amyloid) also does horrible things to the body such as renal failure and constrictive pericarditis. This often happens as a result of certain auto-immune diseases (which is my speciality).
These tests are based on the accidental discovery that a dysentry drug (PBT-1) has some effects on restoring some cognitive function in patients. The company pursuing this has created a drug which is more specifically targeted towards reducing levels of A-A. And... so far, so good. The mice show greatly reduced A-A levels and they perform better in mazes. I wish them all the best - Altzheimers is a horrible and frightening disease.
For those who would like a fuller summary in non newspaper-speak, try http://www.medicalnewstoday.com/medicalnews.php?n
Living through your parent's early onset (at 50 years) Alzheimer's really takes egde off any humour of this story. Personally, I welcome these news, there are too few of them. Unfortunately, this drug would come too late for my father, who has now been living with this for 15 years (he really takes his time to do things properly, even dying). New drugs would also offer some hope for relatives, since A is also hereditary to at least some extent.
Brothers, our time has come. This is the secret weapon that will allow our final victory over The Old People! With this technology in our hands, they will be our slaves. They will mine our ore and harvest our lumber to have access to our precious Alzheimers medicine. The Groundor has become the Groundee. He who controls the spice, er, meds, controls the universe!
AFAIK BSE/The mad cow disease is only connected to the Creutzfeldt Jakob Disease.
Or is CJD related to Alzheimer?
Is it just me or does it seem like every few months, the healthcare media pops up an article about some newfangled treatment that shows "promise" for some disease that everyone knows about? And is it me again, or do we almost never hear about these promising treatments years later? The cynic in me would say that it smells like someone trying to drum up some investment money. What's that? Prana Biotechnologies is listed on the Nasdaq as "PRAN"? And the announcement hit the media before the Monday opening bell? I'm shocked.
Sadly, the less cynical part of me wonders why we only ever read articles about drugs that show "promise"? When was the last time we saw an article titled "Cure for Disease Found!"? And no, I don't have Alzheimers. I honestly can't recall.
The problem with this drug is that its promise is based on 2 assumptions:
1) that amyloid has a causal role in Alzheimers
2) lowering amyloid will halt or reverse Alzheimers
Given that we don't actually know that either is true, we really have no idea how good the promise of this drug is. What we DO know is that promises have made a lot of pharmaceutical companies and their management very very very rich. Not that I would begrudge them that if they actually come through with a halfway effective drug. But I also think there should be penalties for putting out media announcements and raising false hopes without even having tested it out on a single human being yet.
"The only normal people are the ones you don't know very well."
I think this may be a dupe, but I can't remember. Perhaps I really suffer from attention defi Let's go ride BICYCLES!
Do not mock my vision of impractical footwear
I wonder (and perhaps someone with more education than I can speculate), if amyloid concetrations in the brain are reduced, will the patients be able to remember things that they have forgotten, or will they "just" be capable of remembering new information again?
They're not linked per se, but they have a lot of symptom similarities, which makes scientists think that the molecular mechanism underlying both of them could be the same.
This means that a treatment for one, *might* give insights into treatments for the other, not that a drug will treat both. nvCJD (what BSE is in humans) and alzheimers are thought to be caused by buildups of different proteins, though they do have very similar structures.
Remember kids, it's all fun and games until someone commits wholesale galactic genocide.
There are many non-Alzheimer's dementias. It will be great if they can cure, or even treat Alzheimer's; but if that's the case, I hope it doesn't cause people to lose interest (and funding) to find treatments/cures for all the other types.
For all intensive purposes, "whom" is no longer a word. That begs the question, "who cares"?
In two related stories from the UK, the National Institute for Clinical Excellence explained that this was not a cost effective treatment for early stage Alzheimers, but was endorsed for use by the National Health Service for extreme late stage cases with a life expectancy not exceeding 6 months. The news was applauded by the Ministry of Health, who released a statement yesterday in which they said that just as it was inappropriate to treat macular degeneration until it has caused the loss of sight in at least one eye, so it could not be a national priority to treat Alzheimers patients until they were well and truly demented.
The second story followed a day later, and consisted of a chorus of local health authorities explaining that they were not proposing to prescribe the drug in cases endorsed by NICE because it was too expensive and they were running out of budget, and of course, they would find it impossible to prescribe for cases where NICE had not endorsed it.
However, they encouraged the British public who felt that they would benefit from this and other treatments which they chose not to provide, or not to provide in a timely manner, to remortgage their houses, and pay for the treatments themselves. This after all was the general practice in the UK for other rare and exotic treatments for uncommon conditions, such as hip replacements, tamoxifen for breat cancer, diagnostic scans following accidents and so on.
Members of the British public, interviewed on the BBC, said they were delighted to be living in the UK and looked after by the NHS. It was after all the envy of the world, and free at the point of use. Many of them volunteered that they had been looked after in a most caring fashion by the staff of their local hospital, who had cured them of difficult cases of MRSA, doubtless contracted by their relatives not washing their hands before visiting the ward.
"Professor Bush also presented mechanistic findings showing that PBT2 blocks the copper-dependent formation of amyloid oligomers, considered by many to be the toxic chemical entity leading to brain damage in Alzheimer's disease."
So, at 76 should I stop taking 1 mg of copper supplementation daily?
Man, if drug companies are evil, this is where they are: hyping up compounds that have only begun to be tested in humans, just to pump up share prices (literally only begun, the announcement of the plan to test this drug in humans was made in May 2006). Although the preclinical, rodent data is good, drugs which have treated the transgenic models of Alzhiemer's have fallen flat many times before. It's worth noting that this same company had the drug PBT1 already being trialed in human Alzhimer's patients in 2003, but for some reason (*cough* probably toxic as hell *cough*) the trials were canceled, and this new drugs was rolled out. Again, skepticism is the order of the day for pharmaceutical company press releases.
-BilZ0r www.ilikethings.net