Speaker 0:  for decades, alzheimer brain damage was considered an irreversible one way street, but researchers at oregon state just caught this reversal process live on tape by perfectly targeting rogue metals in the brain. they haven't just halted the disease signature protein clumps. they've actively untangled them. so this is a live reversal of alzheimer's clumping. scientists used a light tracking technique called fluorescence anisotropy. john? i don't know. okay. to watch amyloid beta protein clumps form and untangle in real time. by deploying highly selective copper grappling molecules, they successfully reverse the chemical process that dries the disease. this completely shifts the scientific consensus from merely slowing down dementia to legitimate possibility of reversing brain damage. what do you think about this, john?

Speaker 1:  this is cool. so it's anisotropic, by the way. i was pronouncing it the same way you did, but when you struggled with it, i'm like, shit. maybe i'm wrong again because i was wrong with, with the other one. so,

Speaker 0:  keep in mind, everyone. i do have dyslexia. when i see it, i think i knew how to pronounce it before, but the words start dancing when it's a complicated word and it yeah. anyway, anyway, it is what it is.

Speaker 1:  so i think this is cool. so this is the study itself. it highlights a crucial biochemical driver, which is the metal ion imbalance, particularly copper. so, amyloid beta proteins, they're normally present in the brain. but excess metals like copper bind to them. and so this interaction accelerates misfolding and aggregation into toxic plaques. and these plaques, they disrupt neuron to neuron communication, they trigger inflammation, and they lead to neurodegeneration. so the disease isn't just about protein buildup, it's about chemical interactions between proteins and metals. and so the key intervention in this research involves chelators, which are molecules that bind tightly to metal ions. and there were two important findings here. so what they found was some chelators bind metals broadly, which is less effective, and others selectively target copper, which is more effective. and so the selective chelator, it removed copper from the protein metal complex. it disrupted the aggregation process. and in some cases, it reversed existing clumping, which is huge because it suggests that alzheimer's chemistry is not strictly one way, and and it could be reversible. this is a cool breakthrough. think? do you think this is a viable, study here, craig?

Speaker 0:  well, i hope it's a bible study because what we're reading looks amazing. you know? yeah. think of this update like a massive tangled lot of cables under your desk that are super glued together by rogue drops of copper. older treatments acted like a giant clumsy magnet that yanked all the metals out, destroying your good cables along with the bad. this new selective chelitor is like a microscopic set of smart tweezers that specifically dissolves only the copper glue, allowing the cables to naturally untangle themselves without damaging the whole system. unfortunately, this is in early stage in vitro laboratory, and the science is moving to, next to cellular models. so were years of way of seeing this in yeah. treatments?

Speaker 1:  yeah. yeah. so there's still human clinical trials yet. and alzheimer's it's a it's multifactorial. so it's not just metal driven. so, this is sort of a mechanistic breakthrough, not a cure yet, if that makes sense.

Speaker 0:  absolutely. the breakthrough relies on fluorescence anastropic, technique that measures changes in the polarization of light emitted by the fluorescently tagged molecules. when amyloid beta proteins aggregate, their mass increases causing their rotational diffusion to slow. so this technique detects the sluggish rotation allowing the researchers to plot the exact kinetic rate of the clumping and the unraveling in real time. so, the gelatin therapy actually originated in the nineteen forties to treat heavy metal pros poisoning like, lead and arsenic for industry workers and navy personnel exposed to lead paint, adapting it for, neurodegenerative diseases is a massive modern pivot, so i'm excited to see that. yeah. the failure rate for alzheimer drugs and clinical trials between 2002 and 2012 was a staggering ninety nine point six percent. a major reason for this failure was exactly what this study solves, targeting that plaques after the damage was done without understanding the kinetic formation. so yep. i'm really excited for this. any, more thoughts on this, john?

Speaker 1:  no. this is exciting. exciting to see where this goes next, because, yeah, historically, drug trials have failed. so now we can target early stage chemical triggers potentially. so this is cool.

Speaker 0:  oregon state didn't just find a new chemical compound. they built a real time window into dementia's core mechanics proving that what once was thought permanent might actually be reversible. if this tech makes it pass the blood brain barrier in the next decade, do you think we are finally looking at the end of alzheimer's epidemic, or is this just another lab miracle that won't survive clinical trials? let us know what you think in the chat.