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Alzheimer's disease: Plaques and tangles

Visit us (http://www.khanacademy.org/science/healthcare-and-medicine) for health and medicine content or (http://www.khanacademy.org/test-prep/mcat) for MCAT related content. These videos do not provide medical advice and are for informational purposes only. The videos are not intended to be a substitute for professional medical advice, diagnosis or treatment. Always seek the advice of a qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen in any Khan Academy video. Created by Tanner Marshall.

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  • mr pink red style avatar for user serena
    "not very well understood" are we just guessing then?
    (8 votes)
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    • leafers seed style avatar for user PCMSIII
      Research has actually come a long way with Alzheimer's disease (AD). We have studied many of the proteins that deposit in the brain tissue and found the genes that code for them. We have looked at slices of AD patients' brains and seen the tissue changes that take place. We have used those changes to guide MRI-based screening for AD. The unfortunate and unknown thing about AD is that its not readily preventible due to the fact that we don't have a good screening test for it and we also have no good way of treating it. Its hard to predict which patients will get it due to complex genetics. Therefore, patients present with symptoms and its already too late. There are certain medicines that have slowed progression of AD in some patients, but they don't work for everyone, and they don't stop AD from progressing completely.

      I would say that AD treatment is more of educated guessing. Because there isn't really anything we can do besides supportive care, we are still in the discovery phase of learning about AD, as discovering its cause, and how to eventually treat it. Just think, there was once a time when antibiotics didn't exist, and we were "just guessing" about how to treat people with infections! Look at how far we have come!
      (11 votes)
  • starky ultimate style avatar for user alina
    How do these plaques and tangles actually spread? From what I understood from this video, "something" happens and either the tau protein stops working and/or the amyloid precursor protein turns into a plaque. What's the underlying mechanism?
    (6 votes)
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    • male robot hal style avatar for user Akshanth
      The tangles and plaques themselves form numerously so they are kinda everywhere. Scientists think genes are the underlying mechanism. Some genes are supposed to tell the glial cells(cells that support the neuron) to clear the debris but fail to do so. Like the gene in microglia(type of glial cell) called TREM2.
      (1 vote)
  • blobby green style avatar for user Candace Dyck
    Can Alzheimer's affect kids, teens, and/or young adults?
    (3 votes)
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    • duskpin ultimate style avatar for user Cathrin Lionheart
      Candace, excellent question!

      It doesn't affect kids, but you can get something called early onset Alzheimer's, which can effect people in their 30s and 40s. It's quite uncommon though, only about 5% of cases are early onset. And often in early onset it is people who are 50+., but under 65. (Which would be normal Alzheimer's)

      If say a man in his 30s got Alzheimer's it's likely he has a family history of it. So far scientists have figured out that if you have a mutation in one of 3 genes; APP, PSEN 1 or PSEN 2, you WILL get Alzheimer's which can be early onset. (Yet it's kinda confusing because some people don't have these mutations and still get this kind of Alzheimer's).

      If you have a family history you can get genetic testing to see if you have those mutated genes. It might be helpful to think about how a positive result would affect you. How it would alter your life insurance as an example, even though you would be better prepared, but then would you live in fear? Would you even want to know if that was the case?
      (7 votes)
  • ohnoes default style avatar for user Jazmyne  Deither
    do most Alzheimers victims die because the cells die out completely
    (1 vote)
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    • aqualine sapling style avatar for user Trinity Hope
      Alzheimers can acually kill you, my grandma has dementia, and a few months ago went into the hospital, the doctors said her sodium was low because of the alzheimers, the plaque blocks the cells that tell the body to produce sodium and other natural stuff that it needs, so practically, alzheimers can kill you....
      (2 votes)
  • blobby green style avatar for user Mathias Pape
    Under what enzyme class does the specific enzymes that chop off the beta-amyloid protein fragment fall under and why?
    (1 vote)
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  • female robot amelia style avatar for user صفية/ Safia
    At why do enzymes snip off beta-amyloid fragments?
    (1 vote)
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  • blobby green style avatar for user lumosmaximus
    Why is it that extracellular amyloid plaques and intracellular neurofibrillary tangles are often only seen in a post mortem eval of a brain? Can a MRI/CT be used to visualize these structures prior to an autopsy? Thanks in advance!
    (1 vote)
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  • starky tree style avatar for user LJ
    Can someone with Alzheimer's have either plaques or tangles, not both? Or is it more common to have both plaques and tangles?
    (1 vote)
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  • aqualine ultimate style avatar for user emily.windham
    Will scientists ever find a cure and how long is it expected to take?
    (1 vote)
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Video transcript

- [Voiceover] If we take a look at the brain tissue that's been affected by Alzheimer's Disease under a microscope, there's almost always two common factors that we'll see, and these are called plaques and tangles. Let's just look at these plaques for a minute. Well, actually, they're called beta-amyloid plaques. Amyloid is the name we use for fragments of proteins, so it's like not the whole protein, just little bits of it. And these are produced normally in the body. Beta-amyloids are protein fragments that have been snipped off of the larger protein by specific enzymes. So, you have your neuron with this protein called amyloid precursor protein sort of sticking out through the cell's membrane. And so, how beta-amyloid forms is when these enzymes swing by and chop off our beta-amyloid protein fragment. These little beta-amyloid snippets are somewhat sticky, and they'll start to clump together. And as they clump, they mix with other molecules and even other neurons, forming what's eventually called beta-amyloid plaques. Now, it's thought that these clumps of plaques, especially the smaller ones, may interfere with the cell-to-cell communication between the neurons, essentially blocking the signal at the synapse. It's also thought that they might activate the immune response as well, which triggers inflammation and also tells your immune cells to root out and destroy the disabled cells. Now, it's super, super important to note that this process is still not very well understood. It's especially unclear whether beta-amyloid plaques themselves contribute to causing Alzheimer's Disease or if they're essentially just a result of the progression of Alzheimer's Disease. So, those are the plaques. Now, let's talk about these tangles. Another more fancy name you might hear is neurofibrillary tangles. And these, unlike the beta-amyloid plaques, actually show up inside the neurons. So, usually, healthy neurons are internally supported by and partly made up of these structures called microtubules. These microtubules are like tracks that guide nutrients and other molecules from the cell's body down to the cell's axon, which is usually connected to another neuron. And this is basically how the neighboring neurons communicate. So, you could think of these microtubules like rails that carry a mining cart with a bunch of sweet ores and minerals, which are like the nutrients and the messages, to the other miners, which are like the other neurons. Now, a special protein simply called "tau" binds and stabilizes our rails. Kind of like how railroad spikes keep our rails in place, these tau proteins keep our microtubules in place. In Alzheimer's Disease, these railroad spikes, the tau proteins, are chemically changed and basically aren't the right type of spikes. And instead of holding the tracks together, they pair with other tau proteins. And when they do that, they get all tangled up with each other. And since the tracks don't have anything holding them together anymore, what do they do? Well, they start to fall apart, and so our microtubules fall apart, and these tau proteins become tangled. And since our track is all messed up, this disrupts our whole transport system. And when this happens, we call them neurofibrillary tangles. Since the tangles are sort of like these thread-like fibers or fibrils, we say "fibrillary." And since they're in the brain, we say that they're "neurofibrillary." And it's thought that the disruption of our rail system causes some communication issues between our neurons. And since they can't communicate or transport our materials, they eventually are decomissioned and undergo nerve cell death. Now, these plaques and tangles can be found in brains of many elder people, but they're found to a much, much greater extent in the brains of those with Alzheimer's Disease. And for Alzheimer's, they tend to start forming and spread from the cortex in a pretty predictable way, as Alzheimer's progresses. The earliest areas affected are usually those associated with learning and memory, here in the temporal lobe. And as it spreads and more neurons are affected, it usually goes up to the frontal lobe, where thinking and planning become affected. And then, more of the temporal lobe, as speaking and communicating become affected as well. And then, it kind of moves up into your parietal lobe, where your sense of where your body is in relation to objects around you becomes affected. In severe and late-stage Alzheimer's Disease, these plaques and tangles have spread throughout most of the cortex. And as this happens, the cortex gets seriously, seriously damaged. And due to this widespread cell death, the brain actually shrinks dramatically. But since Alzheimer's progresses at different rates for every patient, the rate of spreading of these plaques and tangles varies a lot from patient to patient.