• Log in with Facebook Log in with Twitter Log In with Google      Sign In    
  • Create Account
  LongeCity
              Advocacy & Research for Unlimited Lifespans

Photo

Massive scandal in Alzheimer's research just uncovered! The plaque theory was based on fraud

alzheimers fraud

  • Please log in to reply
7 replies to this topic

#1 Phoebus

  • Guest
  • 851 posts
  • 238
  • Location:Upper Midwest, US

Posted 24 July 2022 - 02:15 PM


More at link, this is huge 

 

 

 

 

  Sylvain Lesné, Who Found Aβ*56, Accused of Image Manipulation 22 Jul 2022

The Alzheimer’s field was rocked this week by allegations against Sylvain Lesné at the University of Minnesota, Minneapolis. Lesné stands accused of manipulating data images in multiple papers, including his 2006 Nature paper identifying Aβ*56 as a toxic oligomer associated with cognitive decline. The potentially altered images were found by neuroscientist Matthew Schrag at Vanderbilt University. Earlier this year, Schrag alerted the National Institutes of Health and UMN, as well as the journals that published the papers. Multiple investigations are ongoing.

A July 21 Science article by investigative journalist Charles Piller broke the news to the field at large. Science magazine conducted its own six-month investigation, in which independent analysts agreed the images showed signs of tampering.

Alzheimer's researchers expressed dismay. Most thought that even if the allegations are confirmed, the impact on oligomer research would be much smaller than the general effect of bringing disrepute to the field. “The refutation of Aβ*56 would have no impact on the huge weight of evidence that supports a role for soluble aggregates (aka oligomers) in AD,” Dominic Walsh at Brigham and Women’s Hospital, Boston, wrote to Alzforum. Mathias Jucker at the University of Tübingen, Germany, concurred. “The Aβ*56 work was just one paper among many others claiming that Aβ oligomers are key toxic species in AD pathogenesis. I do not think the field would have developed differently without the Lesné work,” he wrote.

“I am speechless about these allegations. This damages the reputation of the oligomer research field, where much good work is being done,” Christian Haass of DZNE Munich wrote to Alzforum (full comments below).

https://www.alzforum...ge-manipulation


  • Informative x 4

#2 Turnbuckle

  • Location:USA
  • NO

Posted 26 July 2022 - 12:27 AM

Another case like that of Haruko Obokata's stem cell breakthrough that wasn't. Disgraced, she wrote a book blaming everyone else.



Click HERE to rent this BIOSCIENCE adspot to support LongeCity (this will replace the google ad above).

#3 Danail Bulgaria

  • Guest
  • 2,217 posts
  • 421
  • Location:Bulgaria

Posted 26 July 2022 - 01:17 PM

Hm... amyloid plaques have been found not only from her, but from many clinicians and researchers in many patients with Alzheimer's disease. They are definately there in patients with Alzheimer's disease.

 

Is 'identifying Aβ*56 as a toxic oligomer associated with cognitive decline' enough to be dismissed the plaque theory? What exactly that theory postulates?

 


  • Good Point x 1

sponsored ad

  • Advert

#4 kurt9

  • Guest
  • 271 posts
  • 29

Posted 26 July 2022 - 06:59 PM

The failure of many drug trials based on the plaque hypothesis should have been sufficient evidence the theory was bogus from the get-go.



#5 Turnbuckle

  • Location:USA
  • NO

Posted 27 July 2022 - 10:19 AM

The failure of many drug trials based on the plaque hypothesis should have been sufficient evidence the theory was bogus from the get-go.

 

 

I think it has to do more with profits. Have you seen any trial of HEPPS (EPPS, 4-(2-Hydroxyethyl)-1-piperazinepropanesulphonic acid), other than the trial in rodents in which HEPPS cleared plaques?

 

The oral administration of EPPS substantially reduces hippocampus-dependent behavioural deficits, brain Aβ oligomer and plaque deposits, glial γ-aminobutyric acid (GABA) release and brain inflammation in an Aβ-overexpressing, APP/PS1 transgenic mouse model when initiated after the development of severe AD-like phenotypes. The ability of EPPS to rescue Aβ aggregation and behavioural deficits provides strong support for the view that the accumulation of Aβ is an important mechanism underlying AD.

https://www.ncbi.nlm...les/PMC4686862/

 

 

The problem, of course, is that HEPPS is old stuff and not patentable.


Edited by Turnbuckle, 27 July 2022 - 10:28 AM.

  • Good Point x 1

#6 kurt9

  • Guest
  • 271 posts
  • 29

Posted 27 July 2022 - 05:25 PM

We all know that 90% of what the medical establishment and big pharma does is bogus.

 

That's why we're all here on the :Longecity forums rather than talking to doctors. :)


  • Needs references x 1
  • like x 1
  • Agree x 1

Click HERE to rent this BIOSCIENCE adspot to support LongeCity (this will replace the google ad above).

#7 Mind

  • Life Member, Director, Moderator, Treasurer
  • 19,386 posts
  • 2,000
  • Location:Wausau, WI

Posted 27 July 2022 - 05:36 PM

It is still a fact, as far as I am aware, that A-beta builds up in the brain as we age. I would rather have a "clean" brain if A-beta does not provide any benefit, even if it is only tangentially related to Alzheimer's.



Click HERE to rent this BIOSCIENCE adspot to support LongeCity (this will replace the google ad above).

#8 Nate-2004

  • Guest
  • 2,375 posts
  • 357
  • Location:Heredia, Costa Rica
  • NO

Posted 19 November 2022 - 05:53 PM

I'm with Mind on this, supposedly this kind of thing gets cleaned out by CSF which loses functionality as we age. Improving sleep can help a lot because that's when it happens but I think they're looking at how addressing loss of function in CSF can be used to treat and prevent Alzheimers.  One thing I know of is that based on recent looks into PDE5 inhibitors such as cialis and viagra, they say the improved blood flow to the brain can help so I've been taking those regularly like 3 times a week (cialis has a long half life) but not every day. It's cheap here in CR. There's also GLA which is in evening primrose, I take as much of that as possible as it's directly related to loss of CMA (chaperone mediated autophagy) which may be partly why experiments with young blood and blood dilution improves certain biomarkers. 

 

Just as with cancer, they should start addressing root causes of dysfunction within our own natural cleanup and defense systems, not the symptoms way down the line.


Edited by Nate-2004, 19 November 2022 - 05:57 PM.





4 user(s) are reading this topic

0 members, 4 guests, 0 anonymous users