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posted by chromas on Wednesday August 01 2018, @01:28AM   Printer-friendly [Skip to comment(s)]
from the I-had-a-dept-for-this-but-I-forgot...what? dept.

Alzheimer's study sparks a new round of debate over the amyloid hypothesis

In the long-running debate over just what causes Alzheimer's disease, one side looks to have scored a victory with new results with an in-development drug. But there's enough variation in the data to ensure that the squabbling factions of Alzheimer's will have plenty to fight about.

At issue is the so-called amyloid hypothesis, a decades-old theory claiming that Alzheimer's gradual degradation of the brain is caused by the accumulation of sticky plaques. And the new drug is BAN2401, designed by Biogen and Eisai to prevent those amyloid plaques from clustering and attack the clumps that already have.

In data presented last week, one group of patients receiving BAN2401 saw their amyloid levels plummet, a result that was tied to a significant reduction in cognitive decline compared with placebo.

[...] But to skeptics, the trial was laden with confounding details that make it impossible to draw conclusions. "These results are a mess," wrote Baird biotech analyst Brian Skorney. "Not so much that they indicate an outright failure of the [amyloid] hypothesis, but they don't really say anything informative at all."

Related: Alzheimer's Disease: A "Whole Body" Problem?
Evidence That Alzheimer's Protein Spreads Like an Infection
Pfizer Halts Research Into Alzheimer's and Parkinson's; Axovant Sciences Abandons Intepirdine
Positive Result in Mice as Alzheimer's Drug Trials Fail and Regulatory Barriers Are Rolled Back

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Related Stories

Alzheimer's Disease: A "Whole Body" Problem? 21 comments

Alzheimer's disease, the leading cause of dementia, has long been assumed to originate in the brain but new research indicates that it could be triggered by breakdowns elsewhere in the body.

The findings, published today in Molecular Psychiatry [DOI: 10.1038/mp.2017.204] [DX], offer hope that future drug therapies might be able to stop or slow the disease without acting directly on the brain, which is a complex, sensitive and often hard-to-reach target. Instead, such drugs could target the kidney or liver, ridding the blood of a toxic protein [amyloid-β protein] before it ever reaches the brain.

"Alzheimer's disease is clearly a disease of the brain, but our research shows that we need to pay attention to the whole body to understand where it comes from, and how to stop it," said Dr. Weihong Song, UBC psychiatry professor.

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Evidence That Alzheimer's Protein Spreads Like an Infection 17 comments

Alzheimer's protein may spread like an infection, human brain scans suggest

For the first time, scientists have produced evidence in living humans that the protein tau, which mars the brain in Alzheimer's disease, spreads from neuron to neuron. Although such movement wasn't directly observed, the finding may illuminate how neurodegeneration occurs in the devastating illness, and it could provide new ideas for stemming the brain damage that robs so many of memory and cognition.

[...] Researchers at the University of Cambridge in the United Kingdom combined two brain imaging techniques, functional magnetic resonance imaging and positron emission tomography (PET) scanning, in 17 Alzheimer's patients to map both the buildup of tau and their brains' functional connectivity—that is, how spatially separated brain regions communicate with each other. Strikingly, they found the largest concentrations of the damaging tau protein in brain regions heavily wired to others, suggesting that tau may spread in a way analogous to influenza during an epidemic, when people with the most social contacts will be at greatest risk of catching the disease.

The research team says this pattern, described yesterday in Brain [open, DOI: 10.1093/brain/awx347] [DX], supports something known as the "transneuronal spread" hypothesis for Alzheimer's disease, which had previously been demonstrated in mice but not people. "We come down quite strongly in favor of the idea that tau is starting in one place and moving across neurons and synapses to other places," says clinical neurologist Thomas Cope, one of the study's authors. "That has never before been shown in humans. That's very exciting." Because the researchers looked at Alzheimer's patients with a range of disease severity, they were also able to demonstrate that, when tau accumulation was higher, brain regions were on the whole less connected. The strength of connections also decreased, and connections were increasingly random.

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Pfizer Halts Research Into Alzheimer's and Parkinson's; Axovant Sciences Abandons Intepirdine 11 comments

Pfizer has announced that it will halt efforts to find new treatments for Alzheimer's and Parkinson's diseases. Meanwhile, Axovant Sciences will halt its studies of intepirdine after it failed to show any improvement for dementia and Alzheimer's patients. The company's stock price has declined around 90% in 3 months:

Pfizer has announced plans to end its research efforts to discover new drugs for Alzheimer's and Parkinson's diseases. The pharmaceutical giant explained its decision, which will entail roughly 300 layoffs, as a move to better position itself "to bring new therapies to patients who need them."

"As a result of a recent comprehensive review, we have made the decision to end our neuroscience discovery and early development efforts and re-allocate [spending] to those areas where we have strong scientific leadership and that will allow us to provide the greatest impact for patients," Pfizer said in a statement emailed to NPR.

[...] Despite heavily funding research efforts into potential treatments in the past, Pfizer has faced high-profile disappointment in recent years, as Reuters notes: "In 2012, Pfizer and partner Johnson & Johnson (JNJ.N) called off additional work on the drug bapineuzumab after it failed to help patients with mild to moderate Alzheimer's in its second round of clinical trials."

Another potential treatment for neurodegenerative disorders — this one developed by Axovant, another pharmaceutical company — also found itself recently abandoned. The company dropped its experimental drug intepirdine after it failed to improve motor function in patients with a certain form of dementia — just three months after it also failed to show positive effects in Alzheimer's patients.

Looks like GlaxoSmithKline got a good deal when they sold the rights to intepirdine to Axovant Sciences in 2014.

Also at Bloomberg.

Related: Can we Turn Back the Clock on Alzheimer's?
Possible Cure for Alzheimer's to be Tested Within the Next Three Years
Mefenamic Acid Might Cure Alzheimers - Generic Cost in US is Crazy
New Alzheimer's Treatment Fully Restores Memory Function in Mice
Power Outage in the Brain may be Source of Alzheimer's
Another Failed Alzheimer's Disease Therapy
The FDA Saved Taxpayers from Paying Billions for Ineffective Alzheimer's Therapy
Alzheimer's Disease: A "Whole Body" Problem?
Bill Gates Commits $100 Million to Alzheimer's Research
Evidence That Alzheimer's Protein Spreads Like an Infection

Original Submission

Positive Result in Mice as Alzheimer's Drug Trials Fail and Regulatory Barriers Are Rolled Back 7 comments

Merck has ended a trial for the experimental Alzheimer's treatment verubecestat, a BACE1 inhibitor, after it was found to be ineffective. Biogen has increased the sample size of a trial for aducanumab, worrying some investors. The news comes after the failure of drugs such as solanezumab and intepirdine to treat Alzheimer's and dementia.

The FDA has proposed new guidelines that would make it easier to treat Alzheimer's by lowering the bar for clinical success:

In proposed new guidelines released on Thursday, the FDA appears open to trial goals that better match early patient populations, including people who have yet to display memory loss or functional impairment, such as the ability to wash or dress themselves or cook meals.

The draft guidelines suggest that improvement in biomarkers, such as amount of beta amyloid in the brain, a protein linked to the disease, may be an acceptable goal for deeming a drug successful in patients with no symptoms. FDA guidelines used in prior studies demanded that a drug demonstrate both cognitive and functional improvements.

A bipartisan group of Senators and Congressman have introduced the Concentrating on High-Value Alzheimer's Needs to Get to an End (CHANGE) Act, which would also reduce regulatory barriers faced by clinical trials. The annual cost of Alzheimer's and dementia care in the U.S. is projected to rise to $1.1 trillion by 2050.

Meanwhile, a group of researchers has found that targeting BACE1 enzymes could remove existing amyloid plaques (in mice):

Knocking back an enzyme swept mouse brains clean of protein globs that are a sign of Alzheimer's disease. Reducing the enzyme is known to keep these nerve-damaging plaques from forming. But the disappearance of existing plaques was unexpected [open, DOI: 10.1084/jem.20171831] [DX], researchers report online February 14 in the Journal of Experimental Medicine.

The brains of mice engineered to develop Alzheimer's disease were riddled with these plaques, clumps of amyloid-beta protein fragments, by the time the animals were 10 months old. But the brains of 10-month-old Alzheimer's mice that had a severely reduced amount of an enzyme called BACE1 were essentially clear of new and old plaques.

An Alzheimer's treatment, donepezil, has been used to treat alcohol-related brain damage in mice.

FDA Approves New Treatment for Alzheimer's Disease 20 comments

The FDA has approved a new drug for Alzheimer's disease, while not a cure it is supposed to slow the decline. Even though data is not entirely positive or straight forward in its interpretation or that it will actually even work as thought.

But if you have it then you are probably desperate enough to try almost anything that claims to work, until you get to the price tag of $56,000 per year. That will probably make it out of reach for most people, it's doubtful if any insurance will cover something like this. Perhaps you can just forget to pay the bill, they might understand due to your condition.

Biogen CEO Michel Vounatsos [...][said] he thought the drug's price was "fair" but also vowed that the company would not hike its price for four years.

In Surprise Turnaround, Biogen to Submit Previously Failed Alzheimer Drug for Approval
Disputed Alzheimer's Study Links Decrease in Amyloid Levels to Reduction in Cognitive Decline
Positive Result in Mice as Alzheimer's Drug Trials Fail and Regulatory Barriers Are Rolled Back

Original Submission

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  • (Score: 2) by Snotnose on Wednesday August 01 2018, @02:43AM (3 children)

    by Snotnose (1623) on Wednesday August 01 2018, @02:43AM (#715496)

    Mom died at 76 after losing her mind 4-5 years earlier. Dad died at 89 after 11 years. I think dad hung on for mom to pass before he really went downhill.

    I'm 60. The thought of being like mom her last 2-3 years is bad, but damn. Dad his last 5-7 years, *shudder*.

    At least come up with a diagnostic, so I know when I can lock myself into the bathroom with an hibachi so I leave as little mess as possible.

    The 3 symptoms of laziness: 1) think of something tomorrow 2)
    • (Score: 0) by Anonymous Coward on Wednesday August 01 2018, @02:47AM (2 children)

      by Anonymous Coward on Wednesday August 01 2018, @02:47AM (#715499)

      A pressurized nitrogen bottle will result in lesser mess. Just set aside enough in your retirement fund for one.

      • (Score: 2) by Snotnose on Wednesday August 01 2018, @02:52AM (1 child)

        by Snotnose (1623) on Wednesday August 01 2018, @02:52AM (#715500)

        I plan to cook a steak and potato on that hibachi.....

        The 3 symptoms of laziness: 1) think of something tomorrow 2)
        • (Score: 0) by Anonymous Coward on Wednesday August 01 2018, @08:40AM

          by Anonymous Coward on Wednesday August 01 2018, @08:40AM (#715565)

          Uh-oh. You think you'll remember how to?