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Biotech Medicine

Hibernation Protein May Halt Alzheimer's 79

BarbaraHudson writes The BBC is reporting that tests show a protein called RBM3, involved in hibernation, may hold the key to regenerating synapses. In the early stages of Alzheimer's, and other neurodegenerative disorders, synapses are lost. This inevitably progresses to whole brain cells dying. But during hibernation, 20-30% of the connections in the brain — synapses — are culled as the body preserves resources over winter, and are reformed in the spring, with no loss of memory. Memories can be restored after hibernation as only the receiving end of the synapse shuts down. In a further set of tests, the team showed the brain cell deaths from prion disease and Alzheimer's could be prevented by artificially boosting RBM3 levels. Prof Mallucci was asked if memories could be restored in people if their synapses could be restored: "Absolutely, because a lot of memory decline is correlated with synapse loss, which is the early stage of dementia, so you might get back some of the synapse you've lost."

Further reading: here, here, and here"
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Hibernation Protein May Halt Alzheimer's

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  • by Anonymous Coward

    Could this be the last hurdle for successful cryostasis?

    My wife works with people that have Alzheimer's and dementia. What a terrible way to go.

    • Re:Exciting! (Score:4, Interesting)

      by BarbaraHudson ( 3785311 ) <barbara.jane.hud ... minus physicist> on Sunday January 18, 2015 @03:34PM (#48846187) Journal

      My wife works with people that have Alzheimer's and dementia. What a terrible way to go.

      It's one of the reasons we legalized assisted suicide here (and probably elsewhere in the world). Nobody wants to end up that way. Maybe this will be a second option.

      • i hope not. i can't imagine anybody choosing suicide over this. (IF this ever moves beyond the usual "lab rats regain memory" stage)

        • Re:Exciting! (Score:4, Interesting)

          by BarbaraHudson ( 3785311 ) <barbara.jane.hud ... minus physicist> on Monday January 19, 2015 @09:33AM (#48849453) Journal

          i hope not. i can't imagine anybody choosing suicide over this. (IF this ever moves beyond the usual "lab rats regain memory" stage)

          I've already told everyone that if that happens, take me "out behind the barn and shoot me, and donate my body to science." What makes me me is my mind, not my arms, legs, heart, liver, or kidneys. When that's gone, the rest is just meat anyway, so might as well not consume further resources, and put people through the hassle of feeling guilty because they didn't visit "me" (even though nobody's home any more) often enough.I do NOT want to put that burden on my kids.

          I keep my dogs until they can no longer live a quality life, then I take them to the vet and stay with them while they're killed. Doing otherwise (keeping a dog when it's terminally ill and suffering) would probably (and rightfully) get me investigated for cruelty. I think people have at least as much of a right to a life with some quality of life, and when that's no longer possible, help them end it. Apparently so do enough others to convince lawmakers to pass right to die legislation.

          So hopefully this research will pay off and it won't come to that, but if it does, I'm going to pull the plug while I still can.

  • by Anonymous Coward

    Given that humans do not, in fact, hibernate, there is little reason to think the mechanism present in the test species is identical and fully intact in humans. Furthermore, for all we know, the loss of hibernation ability is a necessary enabler of human-scale intellegence, and recovery of hibernation could cause retardation or something.

    • Because Alzheimer's doesn't cause "retardation".

    • Because Alzheimer's doesn't cause "retardation".

      Obviously I couldn't put everything in the summary (I provided 4 links) A few points: First, the same protection was observed with higher levels or RBM3 in mice that didn't undergo induced hibernation as with those who underwent induced hibernation:

      In the grand finale set of experiments, the researchers bypassed cooling and injected lentiviruses expressing RBM3 directly into the hippocampi of mice early in prion disease. They achieved a threefold overexpression of RBM3 that afforded the mice the same synaptic, behavioral, and survival benefits that early cooling had, and rescued flagging protein synthesis observed in neurons nine weeks post-infection. Boosting RBM3 expression also allowed synapses in both neurodegenerative disease models to recover completely after cooling. Conversely, knocking down expression of RBM3 accelerated disease progression in the prion model, and hastened synapse loss in both models. Synapses and memory even took a hit in normal mice deprived of RBM3 expression, as they lost synapses and did not recognize novel objects as well as control mice. This suggested that the cold-shock protein may play an important physiological role in normal synapse upkeep.

      Mallucci hypothesized that RBM3 promotes synaptic plasticity and staves off neurodegeneration by raising levels of protein synthesis in dendrites. “Synapses are so dependent on their key synaptic proteins for assembly and function,” said Mallucci. Because synapses often reside distant from the cell body, local translation at the dendrite is important to ensure a ready supply of such proteins and thus facilitate synaptic recovery, she added.

      So we know that RBM3 protects regardless of whether it was produced by hibernation or artificial elevation of just the protein RBM3.

      Second we already know cooling of the brain in humans is also protective:

      A state of hypothermia is known to protect the brain. People have been survived for hours after a cardiac arrest without brain damage after falling into icy water. Similiarly, cooling the brains of babies that have suffered a loss of oxygen at birth is also used to protect against brain damage.

      "We’ve known for some time that cooling can slow down or even prevent damage to brain cells, but reducing body temperature is rarely feasible in practice: it’s unpleasant and involves risks such as pneumonia and blood clots," said Professor Giovanna Mallucci, who led the research team, at the Medical Research Councils Toxicology Unit at the University of Leicester. "But, by identifying how cooling activates a process that prevents the loss of brain cells, we can now work towards finding a means to develop drugs that might mimic the protective effects of cold on the brain."

      So there is reason to think that the same mechanism might work in other mammals, and not just those who hibernate. We'll only know when human trials commence, but considering what's at stake, there will be literally millions volunteering to be test subjects.

  • Use it or lose it (Score:1, Interesting)

    by Anonymous Coward

    I expect we'll be hearing more about video game fitness and therapy for senior citizens. Not necessarily FPS type games, but perhaps light strategy games, possibly with a kinesthetic component.

  • by Anonymous Coward

    I don't want those memories back. Just want my brain to work right. I spent many dollars buying booze to forget; why would I wast that money!

  • by account_deleted ( 4530225 ) on Sunday January 18, 2015 @02:05PM (#48845765)
    Comment removed based on user account deletion
  • I think we all know how that works out.

  • craving honey and salmon.

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