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posted by martyb on Friday November 03 2017, @02:22PM   Printer-friendly
from the progress-against-a-nasty-disease dept.

https://news.ubc.ca/2017/10/31/alzheimers-disease-might-be-a-whole-body-problem/

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.


Original Submission

Related Stories

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

Disputed Alzheimer's Study Links Decrease in Amyloid Levels to Reduction in Cognitive Decline 4 comments

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


Original Submission

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  • (Score: 3, Interesting) by DannyB on Friday November 03 2017, @02:55PM (6 children)

    by DannyB (5839) Subscriber Badge on Friday November 03 2017, @02:55PM (#591690) Journal

    Would a drug that targets amyloid-β in the body be helpful in preventing the onset of Alzheimer's? Could the potential onset even be detected by screening for amyloid-β which TFA says is a precursor? The presence of amyloid-β and other factors could indicate to treat with drugs targeting amyloid-β. (Not mentioned is how many drugs treat this.)

    Millions of people could benefit from such treatment if it enabled politicians to remember what they said, promised or tweeted just yesterday. It might also be helpful for press secretaries and even people running for office.

    --
    To transfer files: right-click on file, pick Copy. Unplug mouse, plug mouse into other computer. Right-click, paste.
    • (Score: 2, Insightful) by Anonymous Coward on Friday November 03 2017, @03:03PM (5 children)

      by Anonymous Coward on Friday November 03 2017, @03:03PM (#591694)

      How many hundreds of billions (trillions) of $ will be spent on targeting a-beta before this is over? No data or reasoning seems to put a dent in the enthusiasm for this idea.

      • (Score: 0) by Anonymous Coward on Friday November 03 2017, @03:49PM (4 children)

        by Anonymous Coward on Friday November 03 2017, @03:49PM (#591706)

        To whoever downvoted, can you find one disease state where someone has looked for a link to amyloids and not found it? Amyloids are like the generic cold symptoms of diseases because it requires constant vigilance to prevent their formation (they are the lowest energy state for any peptide).

        • (Score: 3, Informative) by maxwell demon on Friday November 03 2017, @05:22PM (3 children)

          by maxwell demon (1608) on Friday November 03 2017, @05:22PM (#591753) Journal

          To whoever downvoted,

          Which would be: No one. The only moderation that post got up to now is a single Disagree, which doesn't reduce the post's score, therefore is not a downvote.

          --
          The Tao of math: The numbers you can count are not the real numbers.
          • (Score: 0) by Anonymous Coward on Friday November 03 2017, @05:52PM (2 children)

            by Anonymous Coward on Friday November 03 2017, @05:52PM (#591772)

            It sure feels like a downvote.

            • (Score: 1, Touché) by Anonymous Coward on Friday November 03 2017, @07:14PM

              by Anonymous Coward on Friday November 03 2017, @07:14PM (#591822)
            • (Score: 0) by Anonymous Coward on Friday November 03 2017, @08:59PM

              by Anonymous Coward on Friday November 03 2017, @08:59PM (#591881)

              Get off Reddit, fake internet points shouldn't be affecting your mental health. Don't you know what kind of invertebrates inhabit the net??

  • (Score: 1) by Sulla on Friday November 03 2017, @03:32PM (6 children)

    by Sulla (5173) on Friday November 03 2017, @03:32PM (#591705) Journal

    I am currently watching my grandmother go through the stages of Alzheimer's disease as my wife and I caretake for her. After watching this I want to make sure that I am able to kill myself if I ever develop the kind of mental deterioration that comes with this (and other) diseases. As part of this a friend of mine and I have been discussing checks that you can make against your brain to confirm your mental ability and then commit these to habit. The goal is to be able to run your own system diagnostics through a series of thought processes to determine you are at a point where you need to take action without returning false positives.

    Being people of intellect I imagine that this is something other soylentels have thought about to. Any ideas?

    Something that I do daily is run through the multiplication tables in my head. Pretty easy, but could be a useful method in this case.

    --
    Ceterum censeo Sinae esse delendam
    • (Score: 2, Interesting) by Anonymous Coward on Friday November 03 2017, @04:06PM

      by Anonymous Coward on Friday November 03 2017, @04:06PM (#591711)

      An OS watchdog timer only works if the kernel itself hasn't become corrupted; I don't think it's possible for system to analyze itself effectively without a rogue component that has been designed to be as independent as possible from the rest of the system.

      I mean, there's a reason it's difficult for a lot of people to keep themselves from drinking too much alcohol; it's hard to be reasonable about something that explicitly diminishes reason.

      Instead of figuring out how to self-check, spend your time figuring out how to kill yourself in a non-violent, peaceful way, which includes figuring out how to prepare yourself to follow through with such a decision. Alzheimer's or not, the longer you live, the more likely you'll need to make that choice (or, like most people, choose not to think about it, and then just futilely claw in fear as the Universe sucks you down its merciless hole of eternal oblivion). Hypoxia by nitrogen gas seems like a good choice.

      None of us knows how the story will go. The only thing we do know is that it won't end well. Prepare accordingly.

    • (Score: 2, Informative) by Ethanol-fueled on Friday November 03 2017, @04:21PM (1 child)

      by Ethanol-fueled (2792) on Friday November 03 2017, @04:21PM (#591716) Homepage

      Music Therapy. Insist that, should your mental condition deteriorate, your family and/or caretakers regularly play music and other media from back when you were younger and stronger.

      So for current old Geezers, this would be stuff like Louis Armstrong, Gershwin, perhaps some fifties and even sixties shit. Old TV shows etc. The sense of association can tie who they were to who they are today.

      Note: I didn't come up with this idea, but I think it's a good one -- who likes the crap media churned out nowadays anyway?

      The second I become incontinent or demented, I'm going to go full-chimp and fling my poo at people while making monkey-noises. That's always been my lifelong dream, just gotta wait until I have the right excuse to do it.

      • (Score: 3, Interesting) by HiThere on Friday November 03 2017, @05:14PM

        by HiThere (866) Subscriber Badge on Friday November 03 2017, @05:14PM (#591743) Journal

        You've been channeling my father's ghost. He got Alzheimer's and towards the end one of his joys was to take his urine bag and swing it around his head...at some point it usually broke.

        --
        Javascript is what you use to allow unknown third parties to run software you have no idea about on your computer.
    • (Score: 1, Interesting) by Anonymous Coward on Saturday November 04 2017, @09:18AM (2 children)

      by Anonymous Coward on Saturday November 04 2017, @09:18AM (#592117)

      As part of this a friend of mine and I have been discussing checks that you can make against your brain to confirm your mental ability and then commit these to habit.

      Once you get past your peak your general trajectory is deterioration for most stuff, BUT you can still enjoy life. And as long as you're having a decent quality of life and not being a big burden or problem for others why kill yourself? Just because you're starting to forget stuff or start not being able to do some stuff?

      Most pet dogs don't think that well but lots of people still love them AND want them to still be around. Even the really stupid ones.

      Similarly lots of us don't mind those kind gentle old folks with good hearts even if they're forgetful. Then it's only near the very end that it becomes a big problem, but that's true for the many other ways you can age to death (cancer, heart problems etc).

      So maybe what might help is training yourself and your character so that even if you're a forgetful person you'd still be a nice forgetful person that normal people are happy to be with. There are some paranoid and angry forgetful people who accuse other people of stealing stuff, get angry and make a huge fuss for small stuff, etc.

      Unfortunately there are cases of nice people being changed by Alzheimer's to becoming nasty people, not everyone though.

      • (Score: 0) by Anonymous Coward on Saturday November 04 2017, @06:36PM (1 child)

        by Anonymous Coward on Saturday November 04 2017, @06:36PM (#592254)

        Just sayin'.

        • (Score: 0) by Anonymous Coward on Monday November 06 2017, @04:40PM

          by Anonymous Coward on Monday November 06 2017, @04:40PM (#593154)
          Which is what you might want to happen too, but there's probably still like about 10+ years before things get that bad.
  • (Score: 1, Informative) by Anonymous Coward on Friday November 03 2017, @04:21PM (4 children)

    by Anonymous Coward on Friday November 03 2017, @04:21PM (#591715)

    Along with a chorus of others, we have previously argued against the assumption that Aβ accumulation is the primary early pathogenic trigger of AD [4]-[8]. An unintended consequence of that assumption, which contributes to the continued failure of anti-amyloid clinical trials, is that affirmative diagnosis of AD-type dementia can only occur when the presence of Aβ accumulation in the brain is confirmed. However, recent imaging studies confirm previous observations of Aβ accumulation in a significant proportion of non-demented individuals [4],[9],[10]. Conversely, a sizable proportion of patients clinically diagnosed with AD do not display Aβ accumulation-even though neurodegeneration is in progress [4],[11]. Remarkably, rather than concluding that Aβ status is not a reliable marker for the early stages of clinical AD, a consensus has been reached in which clinically diagnosed AD patients without Aβ are classified as not suffering from AD.

    https://bmcneurol.biomedcentral.com/articles/10.1186/s12883-014-0169-0 [biomedcentral.com]

    • (Score: 2) by frojack on Friday November 03 2017, @08:25PM (3 children)

      by frojack (1554) on Friday November 03 2017, @08:25PM (#591853) Journal

      Remarkably, rather than concluding that Aβ status is not a reliable marker for the early stages of clinical AD, a consensus has been reached in which clinically diagnosed AD patients without Aβ are classified as not suffering from AD.

      That wouldn't be the first time that has happened in the field of medicine.
      There are more than a few very common diseases where diagnosis is just wrong. [cnn.com]
      Yet these guys write that is if recognizing the misdiagnosis is somehow a bad thing.

      Behavioral based diagnosis is a tricky business at best. Deciding that Neurodegeneration is in progress really says nothing about the source. If AD is defined as the presence of Aβ accumulation, AND Aβ accumulation is missing, then what would be the point of continuing to treat Aβ accumulation?

      --
      No, you are mistaken. I've always had this sig.
      • (Score: 0) by Anonymous Coward on Friday November 03 2017, @10:12PM

        by Anonymous Coward on Friday November 03 2017, @10:12PM (#591905)

        There doesn't seem to be any point of continuing to treat Aβ accumulation... that is the point.

      • (Score: 2) by TheLink on Saturday November 04 2017, @08:55AM

        by TheLink (332) on Saturday November 04 2017, @08:55AM (#592113) Journal

        I doubt it'll work for everybody (lots of other causes for dementia) but it may work for lot of people. After all many people have type 2 diabetes, so while not all dementia might be "type 3 diabetes" a large percentage might be:
        https://www.nia.nih.gov/alzheimers/clinical-trials/study-nasal-insulin-fight-forgetfulness-sniff [nih.gov]
        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3260944/ [nih.gov]
        http://www.alzforum.org/therapeutics/nasal-insulin [alzforum.org]

        I don't recommend you DIY and bypass professional medical treatment, but hey if you're getting desperate the side effects may not be bad enough for you:
        http://www.lostfalco.com/intranasal-insulin/ [lostfalco.com]

      • (Score: 1) by rylyeh on Saturday November 04 2017, @05:39PM

        by rylyeh (6726) <kadathNO@SPAMgmail.com> on Saturday November 04 2017, @05:39PM (#592222)

        Amyloid-β is definatley not even the biggest problem: Gene variant linked to Alzheimer’s disease is a triple threat [sciencenews.org]

        For more than 20 years, researchers have known that people who carry the E4 version of the APOE gene are at increased risk of developing Alzheimer’s. A version of the gene called APOE3 has no effect on Alzheimer’s risk, whereas the APOE2 version protects against the disease. Molecular details for how APOE protein, which helps clear cholesterol from the body, affects brain cells are not understood.

        But Holtzman and other researchers previously demonstrated that plaques of amyloid-beta protein build up faster in the brains of APOE4 carriers (SN: 7/30/11, p. 9). Having A-beta plaques isn’t enough to cause the disease, Holtzman says. Tangles of another protein called tau are also required. Once tau tangles accumulate, brain cells begin to die and people develop dementia. In a series of new experiments, Holtzman and colleagues now show, for the first time, that there’s also a link between APOE4 and tau tangles.
        Death sentence

        Mouse brain nerve cells (green) making a disease-causing version of the tau protein were grown in lab dishes with supporting brain cells called glia. The glial cells produced different versions of the human APOE protein, or had no APOE. Glia making the APOE4 version of the protein often killed the nerve cells (bottom right).

        Y. Shi et al/Nature 2017

        In one experiment, mice that had no A-beta in their brains developed more tau tangles if they carried the human version of APOE4 than if they had the human APOE3 gene, Holtzman and colleagues found. That finding indicates APOE4 affects tau independently of A-beta.

        Brains of people who died from various diseases caused by tangled tau had more dead and damaged cells if the people carried APOE4. The researchers also tracked 592 people who had low levels of A-beta in their cerebral spinal fluid — a clue that plaques have formed in the brain — and who showed symptoms of Alzheimer’s. Over a five- to 10-year period, the disease progressed 14 percent faster in people with one copy of APOE4 and 23 percent faster in people with two copies than in people who didn’t have that version of the gene, the researchers found. Those worsening symptoms are presumed to be caused by more rapid buildup of tau tangles in the APOE4 carriers.

        APOE4 also seems to make Alzheimer’s worse by causing inflammation, the researchers found. Two kinds of mouse glial brain cells, microglia and astrocytes, making different versions of the APOE protein were grown with brain nerve cells, or neurons, that make disease-causing forms of tau. Mouse neurons grown with glia making no APOE grew well, even though they were making abnormal tau. But neurons grown with glia making APOE4 often died. APOE4 provoked inflammation responses in the normally friendly astrocytes and microglia, leading those cells to kill neurons, the researchers found. Such inflammation can make brain degeneration worse.

        Based on the above research - I think these 'new treatments' will prove to be ineffective.

        --
        "a vast crenulate shell wherein rode the grey and awful form of primal Nodens, Lord of the Great Abyss."
  • (Score: 0) by Anonymous Coward on Friday November 03 2017, @06:29PM (1 child)

    by Anonymous Coward on Friday November 03 2017, @06:29PM (#591791)

    "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."

    how about screw you? why don't you skanks just educate people on their lifelong habits(bad nutrition, etc) and pollutants that are causing the shit and we won't need your expensive, likely poisonous drugs. oh, actually fixing the problem isn't absurdly profitable? i wonder if selling doctors and drug chemists' forcibly harvested organs is profitable...

    • (Score: 2) by frojack on Friday November 03 2017, @08:33PM

      by frojack (1554) on Friday November 03 2017, @08:33PM (#591860) Journal

      lifelong habits(bad nutrition, etc) and pollutants that are causing the shit

      Oh Riiiiight.
      Lets take your pet quasi-religious beliefs and substitute THOSE for actual science. That would be great [gstatic.com]

      --
      No, you are mistaken. I've always had this sig.
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