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Science

Blocking a Key Enzyme May Reverse Memory Loss, MIT Study Finds (mit.edu) 29

A better treatment for Alzheimer's patients may be on the horizon thanks to new research from MIT. Researchers at MIT's Picower Institute for Learning and Memory have discovered that they can reverse memory loss in mice by blocking an enzyme called HDAC2. From the study: For several years, scientists and pharmaceutical companies have been trying to develop drugs that block this enzyme, but most of these drugs also block other members of the HDAC family, which can lead to toxic side effects. The MIT team has now found a way to precisely target HDAC2, by blocking its interaction with a binding partner called Sp3. "This is exciting because for the first time we have found a specific mechanism by which HDAC2 regulates synaptic gene expression," says Li-Huei Tsai, director of MIT's Picower Institute for Learning and Memory and the study's senior author. Blocking that mechanism could offer a new way to treat memory loss in Alzheimer's patients. In this study, the researchers used a large protein fragment to interfere with HDAC-2, but they plan to seek smaller molecules that would be easier to deploy as drugs. Picower Institute postdocs Hidekuni Yamakawa, Jemmie Cheng, and Jay Penney are the lead authors of the study, which appears in the Aug. 8 edition of Cell Reports.
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Blocking a Key Enzyme May Reverse Memory Loss, MIT Study Finds

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  • by LordHighExecutioner ( 4245243 ) on Wednesday August 09, 2017 @04:29PM (#54978755)
    ...uh, oh, I do not remember which one it is.
    • Is that because you have Alzheimer's or because you've been smoking the reefer to prevent it [nih.gov]? I mean I guess this could be good news for you on that count, but it would also mean you'd have to give up getting high. At least unless you develop any of the other conditions that allow for a medical card. I personally recommend general anxiety (about your glaucoma) that's giving you migraines.
  • Good Stuff (Score:5, Informative)

    by Mr D from 63 ( 3395377 ) on Wednesday August 09, 2017 @04:33PM (#54978795)
    Sounds like an important development. These are the kind of stories I'd love to see more of, no agenda, an accurate non-clickbait headline, no opinionated assumptions in the summary. Refreshing.
    • The failure of Western governments to throw stupid amounts of money at the two diseases - Alzheimers and Type II Diabetes - that are costing taxpayers rapidly escalating sums of money, is depressing. We need these to be cured - and spending $100bn to do so would be GOOD VALUE.

      • Re: (Score:3, Insightful)

        by ChrisMaple ( 607946 )

        We already know what causes most cases of type 2 diabetes, excessive body fat usually brought on by eating too much sugar. I suppose a medical cure for the disease might be possible, but it's akin to finding a cure for the affects of repeatedly smashing your finger with a hammer: it's the wrong approach.

        Alzheimer's is a different case, and progress is being made, but it's not the government's proper job.

        • by Bruce66423 ( 1678196 ) on Thursday August 10, 2017 @02:13AM (#54981525)

          In reality taxpayers are on the hook for many of the costs associated with Alzheimer's therefore it makes perfect sense for governments to invest in research to reduce those costs in the long term.

          Whilst type II diabetes may indeed be 'caused' by body fat, the mechanism by which the fat causes diabetes may, or may not, be disruptable. Given that it is costing the British NHS billions every year, clearly the identification of the link and finding a way to disrupt it would be worth spending money on since we aren't going to end obesity in a hurry.

          In both cases the discovery of a 'cure' would be a public good which the private sector has failed to find, the exact recipe for government action. Of course the downside is that this would lead to a further rise in life expectancy, which will also cost taxpayers money. However that seems like a bad reason to decline to do the research.

        • by Anne Thwacks ( 531696 ) on Thursday August 10, 2017 @04:17AM (#54981767)
          We already know the claim that what causes most cases of type 2 diabetes, excessive body fat usually brought on by eating too much sugar is completely wrong.

          However, I can tell you, as someone who does not like sugar and has actively avoided it most of my life, that undiagnosed, and therefore untreated diabetes can make you crave sugar.

          There is plenty of evidence that most type II diabetes is caused by a problem with gut bacteria.

          Also, everybody gradually develops insulin intolerance as they age - it is just a question of how fast, and whether they live long enough for it to be classified as diabetes.

  • by Anonymous Coward

    And the purpose of this useless enzyme is?

    • Re:Useless enzymes. (Score:5, Informative)

      by arth1 ( 260657 ) on Wednesday August 09, 2017 @05:04PM (#54979053) Homepage Journal

      And the purpose of this useless enzyme is?

      It's a gene disabler. Those are very important, because every new cell in the body has a full set of DNA and the potential to grow into any type of cell if genes aren't disabled. In other words, it helps prevent your body from growing hundreds of organs instead of one or two, or bone in your eyelids for that matter.

  • Side Effects? (Score:5, Interesting)

    by lobiusmoop ( 305328 ) on Wednesday August 09, 2017 @04:45PM (#54978897) Homepage

    A certain degree of memory loss is important; removing it completely might lead to hyperthymesia [wikipedia.org], Jill Price [wikipedia.org] being a notable example. For her, time does not heal all wounds.

    • I have to admit, I was somewhat curious (and didn't RTFA): Does it reverse memory loss, in that things you couldn't remember you will now be able to? Or will it prevent memory loss--things you didn't remember before, you still won't remember but you won't forget new things.

      • Does it reverse memory loss, in that things you couldn't remember you will now be able to?

        It reverses the inability to transfer information from short-term memory to long-term memory.
        I don't think anyone knows whether old memories would come back - mice generally don't have a lot of them.

  • by Tablizer ( 95088 ) on Wednesday August 09, 2017 @05:03PM (#54979047) Journal

    Being around a good while I see the following news patterns:

    Promising Alzheimer lab breakthrough may end the disease...

    Promising flying car tech close to delivering flying cars for all...

    Promising fusion power lab breakthrough close to delivering cheap safe green power...

    Coffee proven good/bad/good/bad/ [alternates...]

    Small amounts of wine proven good/bad/good/bad/ [alternates...]

    Mild gaming proven good/bad/good/bad/ [alternates...]

    New coding/platform paradigm increases reuse, magic abstraction that reads your mind, separation of concerns without concern-interface bloat, magic defaults, closer to customer's needs, maintainable RAD, blah blah blah...

    (I've actually built frameworks that have a lot of those, but the huge caveat is that you have to settle on a fixed set of conventions that fit a particular shop and avoid the temptation or peer pressure to stuff it with snazzy UI toys.)

  • I've heard of waiting till SP1 hits, but now it looks like I should wait till SP3.
  • Bringing Gamma Back [radiolab.org]

    The guest, Li-Huei Tsai, director of some august learning and memory institute at MIT, eventually confesses that transfer from mice models to humans in this line or research has about a 1% success rate.

    It's a great episode.

    Memories retrieved in mutant 'Alzheimer's' mice [nature.com] — 16 March 2016

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