Even if you don't immediately recognize the words "prion" or "Kuru", the history has seeped into popular culture, like a horrifying fairy tale that just happens to be true. Once, there was a tribe in New Guinea that ate the dead. It wasn't the kind of fakey cannibalism you see in the movies, with hunters rushing out to spear people for sustenance. Instead, it was about respecting your elders. When a member of your family died, you ate them—you took a part of them into yourself. And that included the brain.

But over time, these people found themselves plagued with a terrible illness. Children and perfectly healthy adults, usually women, would suddenly begin to lose control of their limbs. They would jerk and shudder. Within weeks, they wouldn't be able to stand up at all. And then they died. Everybody who had those symptoms died.

Eventually, Western scientists would learn the awful truth. When the people from New Guinea ate their ancestors they were also eating a disease. It attacked their brains—riddling the tissue with holes. The New Guineans, the Fore people, called the disease kuru. In their language it meant "trembling" or "fear".

Today, we know a little bit more about the disease, kuru. We know it's not caused by a virus or a bacterium or a fungus. We know it's related to other brain-damaging diseases, including Creutzfeldt-Jakob disease, which turns healthy adults senile and kills them within a year of the onset of symptoms; scrapie, which affects sheep; and the dreaded bovine spongiform encephalopathy — mad cow disease.

Tying all these diseases together is a scary little something called a prion. On August 16th, I attended a lecture by Jay Ingram, a Canadian journalist who has written a book about prion diseases, called Fatal Flaws. The lecture taught me a lot about prions, but it also taught me about some of the flaws inherent in trying to live-tweet a lecture as I'm listening to it. When the subject is so scary—and so confusing—even well-intentioned live tweets can go awry.

[View the story "Fear and Trembling: Prion diseases on Twitter" on Storify]

Fear and Trembling: Prion diseases on Twitter

A public lecture introduced me to the terrifying world of mad cow disease and kuru. But to really understand what there was to fear, I had to dig deeper.

Storified by Maggie Koerth-Baker · Tue, Sep 11 2012 08:22:17

Drugline

You have probably heard this story before. Even if you don't immediately recognize the words "prion" or "Kuru", the history has seeped into popular culture, like a horrifying fairy tale, or an urban legend that just happens to be true. Once, there was a tribe in New Guinea that ate the dead. It wasn't the kind of fakey cannibalism you see in the movies, with hunters rushing out to spear people for sustenance. Instead, it was about respecting your elders. When a member of your family died, you ate them — you took a part of them into yourself. And that included the brain.

But over time, these people found themselves plagued with a terrible illness. Children and perfectly healthy adults, usually women, would suddenly begin to lose control of their limbs. They would jerk and shudder. Within weeks, they wouldn't be able to stand up at all. And then they died.

Everybody who had those symptoms died.

Eventually, Western scientists would learn the awful truth. When the people from New Guinea ate their ancestors they were also eating a disease. It attacked their brains –riddling the tissue with holes. The New Guineans, the Fore people, called the disease Kuru. In their language it meant "trembling" or "fear".

Prions show up as little brown specks on desktop microscope images of infected brain tissue. #banffscienceMaggie Koerth-Baker

Frontalcortex

That story is true. Mostly. It happened in the 1950s and 1960s. Today, we know a little bit more about the disease, kuru. We know it's not caused by a virus or a bacterium or a fungus. We know it's related to other brain-damaging diseases, including Creutzfeldt-Jakob disease, which turns healthy adults senile and kills them within a year of the onset of symptoms; scrapie, which affects sheep; and the dreaded bovine spongiform encephalopathy — mad cow disease.

I'm at a @jayingram talk about his new book on prion diseases. #banffscienceMaggie Koerth-Baker

Tying all these diseases together is a scary little something called a prion. On August 16th, I attended a lecture by Jay Ingram, a Canadian journalist who has written a book about prion diseases, called Fatal Flaws. The lecture taught me a lot about prions, but it also taught me about some of the flaws inherent in trying to live-tweet a lecture as I'm listening to it.

Public lectures are fascinating introductions to a subject. Twitter is a great way to share information with people who can't be in the live audience. But they are both, by necessity, short summaries of much deeper stories. When you combine the two, it's easy to end up with a collection of snappy ideas, rather than a deep, context-laden narrative. And that can be the difference between education and sensationalism.

The tweets I wrote during Jay Ingram's lecture got a lot of attention. But as I looked at the questions and criticisms some of my readers had — and as I started to read Ingram's actual book — I realized that the missing context of Twitter might be leading people to conclusions that weren't correct. That's why I'm writing this up as a Storify. I want to take the disconnected ideas and fit them into a bigger whole. I also want to give you some things to think about the next time that I (or anybody else) live tweet a lecture.

Prions represent a revolution in the study of biology – starts in 1950s with kuru. – @jayingram #banffscienceMaggie Koerth-Baker

I tried to make it clear that I was quoting Ingram here. And, in general, most tweets from a lecture are quotes. But this is one of the places where it becomes difficult to understand the context. Am I, as the tweeter, telling you what I think? Am I simply relaying what was said by someone else? I can tell you what a speaker says, or I can tell you whether what that speaker is saying matches up with the bigger picture of evidence and opinion. The problem is that a live tweet of a public lecture can be a mixture of both. And knowing which perspective you're reading matters. Sometimes, it helps to ask before you re-tweet.

That's not to say that Ingram is incorrect in this quote. Prions do represent a revolution in how we think about biology. That's because prions are simply misfolded proteins.

Proteins are everywhere. Your body is built out of them. There are proteins in your cells that make the cells function. There are proteins in your hair, your skin, your muscles. Proteins control your metabolism, allowing you to turn a sandwich into energy. There are proteins in your brain.

Every protein is made up of amino acids, the little molecular building blocks of biochemistry. In his talk, Jay Ingram had a really nice model that will help you visualize this stuff. Imagine a pearl necklace.

Natural Grey Freshwater Pearl Necklace ~ Accented with Rhodolite Garnets ~ Pearl Drop NecklaceNaomi King

Now, imagine that necklace twisted and turned, folded back on itself in a complex pattern.

Natural Grey Freshwater Pearl Necklace ~ Accented with Rhodolite Garnets ~ Pearl Drop NecklaceNaomi King

Protein folding is an incredibly complex process that happens in fraction of a second. And must be done perfectly. #banffscienceMaggie Koerth-Baker

That's what you should be thinking of when you think about proteins. At its most basic, a protein is just a chain of amino acids. But it gets its power — an individual protein gains specific skills and tools — because of how that chain is folded. In some ways, that's a great system. It allows you to do more things with the same set of tools, as if your screwdriver could suddenly become a hammer.

The catch: The same protein can act in very different ways, depending on how it's folded.

Healthy human brains have "prion proteins" on surface of neurons. Nobody is sure what they do yet. #banffscienceMaggie Koerth-Baker

Healthy prion protein has a tendency to misfold. When it does, it can touch off infectious process and spread misfolding. #banffscienceMaggie Koerth-Baker

To demonstrate this, @jayingram throws a sprung mousetrap into a batch of set ones … so they all spring too. #banffscienceMaggie Koerth-Baker

So there's a nice, healthy protein that sits on the surface of the neuron cells in your brain. Nobody knows what, exactly, it does. But prions seem to be this same protein, folded up all wrong. And that's the revelatory part.

All that stuff I told you about proteins is basic biology. Nobody questions that. But as they studied kuru, scientists began to see evidence of something a lot more controversial — the idea that misfolded proteins could cause deadly disease, and that the disease could be spread by the misfolded proteins, themselves. Somehow, they think, misfolded proteins trigger healthy proteins to also misfold. This idea is way out in left field compared to everything we thought we knew about how disease works. It's still not 100% proven. In fact, there are researchers who think misfolded proteins are only a mere symptom of mad cow and other prion diseases — not their cause. There's a lot we don't know. But it does seem like, the more scientists study this, the more evidence appears supporting the theory that prions — misfolded proteins — can make more of themselves and can, together, make people and animals sick.

Wow. @jayingram showing 1950s era video of kuru victims. Only affected motor neurons. Still alert. But couldn't move. #banffscienceMaggie Koerth-Baker

When I say that there's a lot we don't know, I mean A LOT. For instance, we have microscopes that can see healthy proteins, but we can't get a good look at a prion. That's because, when proteins misfold, they seem to immediately start clumping together, like one of those magnetic desk toys. We can't see any of the individual units that make up that mess. Which means that when we talk about prions we are talking about something we have not yet directly observed.

Here's another example of how little we know when it comes to prions: As I mentioned in the tweet above, the effects of kuru are centered around the control of limbs. Victims jerk and writhe. Slowly, they lose the ability to walk. But they're lucid and cognitively normal right up until the end. Victims of mad cow disease, on the other hand, have severe problems with memory. They experience hallucinations.

Video of cow with mad cow, terrified of hallucinated threats is heartbreaking. #banffscienceMaggie Koerth-Baker

Jay Ingram wasn't able to get in touch with the researchers who own this video, so I can't share it with you here. But here's what I saw: A cow running aimlessly around its paddock, stopping short in fear of non-existent terrors and hopping over obstacles that weren't actually there. I've never seen an animal behave this way, and it looks nothing like the video of kuru. But the theory is that both these diseases involve the same protein from the surface of neurons.

Why would the same misfolded protein cause such very different symptoms? That's a question we don't have an answer for. When I interviewed him after the lecture, Jay Ingram told me that the best guess that the difference has to do with the structure we can't see.

"They're all misfolded, but in different ways. That's the assumption," he said. "Supposedly that also accounts for the so-called species barrier when it happens. People eat sheep meat infected with scrapie all the time and never get ill. Structural differences probably account for that, and also probably account for where in the brain the damage happens. It's not a great explanation though, because you can't get details yet on the structure, on how they misfold."

Early #FF to @maggiekb1, because she's scaring the crap out of me with her live tweets right now.Alex Knapp

Fair enough. I'm scaring myself, too. Now, on to the cannibalism.

Australian miners and laborers guessed kuru was related to cannibalism before scientists did.#banffscienceMaggie Koerth-Baker

Of course, those miners weren't prescient or anything. They just got lucky in this prediction. Their prejudices against the Fore happened to overlap with the actual mode of transmission. Or, anyway, with what scientists are pretty sure was the actual mode of transmission.

Because here's another thing you need to remember about public lectures: They're edited for time and they're edited to tell a compelling story. There are always details that get left out. And you can see this in the difference between Jay Ingram's lecture and his book. In the lecture, he went with the general consensus: Kuru spread among the Fore because they were eating the brains of kuru victims and ingesting prions. But in the book, he explains why this story can't be said to be the unquestionable truth.

Lots of Western doctors and anthropologists wrote about the Fore eating their dead. But none of those people actually saw them do it. In fact, there's very little direct evidence for cannibalism among the Fore. Scientists believe it happened, though, for two reasons. First, the Fore say it happened. And there's not really an obvious benefit to lying about eating your dead grandmother. Second, it just makes sense. Most prion diseases are not very easy to transmit. Directly eating infected tissue is one of the few ways to do it. Plus, the Fore say they began eating their dead in the early 20th century and that kuru only started killing people after that. And we know that cases of kuru tapered off to almost nothing as soon as the Fore say they stopped eating their dead in the 1950s. But we don't know for sure. It's a story that's never been independently verified.

Square Cowadrian fu

British govt suppressed connection between mad cow and scrapie when first noticed. Hid data for four years. #banffscienceMaggie Koerth-Baker

.@maggiekb1 UK minister at time notoriously fed his young daughter a burger on TV to show editing beef was 'safe'. Not his proudest momentAnsonMackay

That's true. British scientists noticed that there were similarities between the brains of victims of mad cow disease, the brains of sheep infected with scrapie, and the brains of kuru victims. But the government worried that publishing that information could decimate the beef industry. Because the scientists worked for the government, the government was able to prevent them from publishing their work. You can read all about this in several volumes of The BSE Inquiry Report, published in 2000.

[ARCHIVED CONTENT] The BSE Inquiry Report: HomeThis site is an archive of the BSE Inquiry. It is no longer being updated and some links from the site may no longer work. This site co…

At the peak, in 1993, 45,000 British cows were dying per year. #madcow #banffscienceMaggie Koerth-Baker

Somewhat reasonable that they didn't suspect risk to humans at first; scrapie has never infected ppl. #madcow #banffscienceMaggie Koerth-Baker

Cow disease peaked in 1993. Human disease peaked 2001. But incubation period was a decade. #banffscienceMaggie Koerth-Baker

One woman who died of mad cow had been a vegetarian for 8 years. #banffscienceMaggie Koerth-Baker

"@maggiekb1: One woman who died of mad cow had been a vegetarian for 8 years. #banffscience"'Splain THAT one!Diana McIntosh

@dianamcintosh that shows you how long the incubation period is.Maggie Koerth-Baker

The incubation period for prion diseases is another thing we don't understand very well. I mentioned that kuru cases dropped off to "almost nothing" after the Fore say they stopped practicing cannibalism. I worded it that way for a reason. No Fore born after 1960 has ever developed kuru. But people who were alive during the time when cannibalism happened do still occasionally die from the disease. In his book, Ingram notes that 11 people died from kuru between 1996 and 2004. Assuming they were infected before 1960, that gives them a good 40-odd years of living, symptom-free with an incubating prion disease.

But why would some people, including children, die within a few years of exposure, while others lived to a ripe old age? I asked Jay Ingram about this. He told me there are two factors that likely account for the wide variety of incubation periods we see in prion diseases.

First, it might have to do with how well-adapted the prions are to their host species. Some prion diseases — like mad cow — seem to be able to jump from one species to another. Mad cow can infect cows, and humans … and cats. In fact, Ingram told me that it was the death of a housecat named Max in 1990 that really got people seriously considering the idea that mad cow wasn't limited to cows.

But it does seem like prions can get better at infecting a specific species over time. You can infect a mouse with mad cow disease from a cow, Ingram told me. And if you take the brain of that mouse and use it to infect more mice, something weird starts to happen.

"If you continue in the lab and infect mice, and then infect more mice, eventually the incubation period seems to start to shrink," he said. Nobody understands why that happens. But it could be a form of adaptation as the prions "figure out" how to better infect a new species. Basically, it could be a form of natural selection. Remember, we can't see the prion, itself. There's a possibility that every prion disease actually represents a variety of specific types of protein misfoldings. In a new a host, a previously small-potatoes type of misfold could turn out to be a better match for the host's proteins. Over several generations of infection, that type could come to dominate the mix, allowing the infection operate more efficiently.

Genetics might also affect how long it takes an individual person to develop symptoms of a prion disease. Remember that healthy prion proteins — the ones we all have on the surface of our neurons — are long chains of amino acids. It seems to be very important to have specific amino acids at a specific place in the chain.

The place is called position 129. There are two amino acids at this spot and what pairing you get is determined by who your parents are. You can have two methionine amino acids, two valine amino acids, or one of each.

"That seems to determine resistance to prion diseases," Ingram said. "We know that people who are heterozygous, with a methionine-valine pair, were most resistant for kuru. For instance, a lady who was incubating it for 50 years was methionine-valine."

Again, we don't know for certain what's going on here, but there seems to be evidence that some people are more susceptible to prion diseases than others. And that has implications for mad cow disease. The peak of human deaths has long since passed. But there's a possibility that that was only the first peak — as the most susceptible people died. Others could still be carrying the disease.

"We don't know whether it will someday pop up again," Ingram said. "And we don't know, if people are carrying it, whether the incubation period will turn out to be long enough that they all die of something else first."

Today, though, mad cow is no longer the most critical prion disease to pay attention to.

Elk SculptureInAweofGod'sCreation

What is the most important prion disease today? @jayingram say chronic wasting disease in deer and moose. #banffscienceMaggie Koerth-Baker

CWD is different than mad cow. Terrifyingly so. Not just brain is infectious. Saliva, flesh, bones, the soil a deer dies on. #banffscienceMaggie Koerth-Baker

Normally, it's not easy to get a prion disease. We're talking about something that infects the brain, and passing it on usually requires direct contact. Kuru was probably spread when people ate the infected brains of other people. Mad cow passed from cow to cow via "protein meal" — a cattle feed made from scrap meat like brain and nervous system tissue. Humans most likely picked up mad cow from nervous system tissue in ground hamburger meat. Creutzfeldt-Jakob disease, which appears spontaneously in humans, is probably linked to unlucky genetics. But it has been spread from person-to-person in the past by surgical transplants of brain dura matter.

Chronic wasting disease (CWD) is different. It's spreading among wild deer, but they aren't getting invasive brain surgery. They aren't eating each other's brains. And they're dying anyway. It's not exactly clear how this is happening, but researchers have found prions in deer saliva. It's present in urine and feces. And deer have become infected simply by having contact with the bones of a deer that died from CWD, or the ground the bones were lying on. Meanwhile, scrapie, the sheep disease, has been known to hide out in the soil, too. Sheep have been infected by grazing on land that played host to a scrapie outbreak two years before.

Which, of course, brings up an interesting question: Is CWD transmissible to humans?

Annnnnd, there goes my love of summer sausage. #banffscienceMaggie Koerth-Baker

Firefighters in rural New York accidentally served CWD infected deer to 80 ppl. Five yrs gone by. So far, so good. #banffscienceMaggie Koerth-Baker

.@maggiekb1 eek! 80 people with potentially infectious saliva?Adam Kent

Another problem with live-tweeting public lectures: Not everything from the lecture makes it to the tweets. I type quickly. But I don't type that quickly. Sometimes, what gets left out ends up being important. This is one of those times.

On March 13, 2005, more than 200 people attended the Sportsman's Feast, hosted by a fire company in Oneida County, New York. By that point, CWD had already been detected in local deer populations so any deer harvested from a domestic deer farm — like the ones eaten at the Sportsman's Feast — had to be tested. Unfortunately, there were no laws preventing the meat from being fed to anyone before the test results came back. People only found out that one of the deer had CWD after the feast was already over.

Since then, 81 of the people who went to the feast have agreed to participate in long-term monitoring. In 2008, researchers published a study documenting various risk factors: Who ate the deer meat and what parts did they eat; who was involved in cooking; did they wear gloves; that kind of thing. The study also documents any risk factors that happened outside the 2005 feast. For instance, whether or not any of the participants are regular hunters. If, someday, any of these people do start dying of prion diseases, researchers will be able to look back at this data and learn a lot more about whether the prion disease in question is likely to be CWD and, if so, which activities are risky and which aren't.

Environmental Health | Full text | Risk behaviors in a rural …… one and can be found online at: http://www.ehjournal.net/content/7/1/31 … (http: //creativecommons.org/licenses/by/2.0), which per…

The really important information is at the end of that paper. Turns out, there's good reason to think that CWD is not transmissible to humans at all.

The Sportsman's Feast research is an ongoing, observational study. Researchers are watching these people to see what happens to them. But there are other ways you can study something like this. In 2001 and 2006, other scientists published papers that looked backwards in time, to see if they could spot any evidence that CWD is already affecting humans.

Creutzfeldt-Jakob disease in unusually young patients who consumedArch Neurol. 2001 Oct;58(10):1673-8. Creutzfeldt-Jakob disease in unusually young patients who consumed venison. Belay ED, Gambetti P, …

The first of these two studies looked at three people who died of Creutzfeldt-Jakob disease while extraordinarily young — all before the age of 31. Dying that young of Creutzfeldt-Jakob can be a sign that the victims acquired their prion disease from another source. (That was the case with mad cow disease.) But it doesn't necessarily mean that. It could just be that these people were extraordinarily unlucky. Their healthy prion proteins just shifted into prions spontaneously.

In fact, that's what researchers think happened. Even though all three had regularly eaten deer meat during their lives (two were hunters and one was the daughter of a hunter) their illnesses looked more like classic, spontaneous Creutzfeldt-Jakob than any acquired prion disease. For instance, we already talked about how people who die quickly from acquired prion diseases tend to share a particular pairing of amino acids at Position 129 in their prion protein. None of these people had that.

Human prion disease and relative risk associated with chronic wastingEmerg Infect Dis. 2006 Oct;12(10):1527-35. Human prion disease and relative risk associated with chronic wasting disease. Mawhinney S, …

The second study evaluated 22 years' worth of death certificates from counties in Colorado where CWD is endemic. Looking at hunting licenses, the researchers knew that people who hunted in those counties also tended to live in those counties. So, if people who lived there were more likely to die from from Creutzfeldt-Jakob disease than people who lived in other counties in the state, that might be a sign that hunters and their families were quietly acquiring CWD from the deer they killed and ate.

But the researchers saw no difference between the people who lived in counties with lots of CWD and those who didn't. What's more, rates of Creutzfeldt-Jakob disease in CWD-infected counties haven't gone up over time. Together, these results suggest that humans can't be infected with CWD. It's not absolute proof. Personally, I'm still feeling a little squeamish about eating venison. But it tells us that there's a pretty good chance all those people in New York (and whoever they've been kissing for the past seven years) are going to be okay.

That's not to say there's no reason to worry about the effects of CWD. We're still talking about a disease that could drive deer and elk in North America to extinction. If that happens, it'll have big impacts on the food chain, human culture, and economic activity — especially in parts of Canada where people rely on these animals for food. But those are different concerns than a killer disease that can be spread by saliva.

ποντίκι / μυς, mouse (Mus musculus) by George Shuklindullhunk

Finally, we need to talk about mice. Lab mice, specifically.

In Jay Ingram's lecture, I learned that scientists have been using mice to study some interesting connections between exotic prion diseases and far more common illnesses, including Alzheimer's disease. This is a good example of why tweeting a public lecture can be really tricky. The ideas I'm talking about here aren't crazy. They aren't conclusions promoted by fringe scientists who don't know what they're doing. But it's also really, really easy to blow these particular ideas out of proportion. In a space like Twitter, the act of discussing interesting early findings can very quickly turn into accidental fear-mongering. Especially when the tweeter (in this case, me) hasn't heard about the research before.

ALS, parkinsons, alzheimers are all also related to misfolded proteins, though not prions. Could still be infectious … #banffscienceMaggie Koerth-Baker

Brain material from human alzheimer patient injected into healthy mice equals mice with same kind of misfolded proteins #banffscienceMaggie Koerth-Baker

There is a lot we don't know. But medical world is starting to look at connections between prion disease and alzheimers. #banffscienceMaggie Koerth-Baker

So, is alzheimers infectious? Researchers say "welll probably not. But might not have done right epidemiology" @jayingram #banffscienceMaggie Koerth-Baker

@Lewis_Lab @maggiekb1 Suggesting AD is infectious is incredibly dangerous and possibly damaging to patient care. Grammy WILL NOT give you ADDarren Boehning

Darren Boehning is right. But, at the same time, my tweets (and Jay Ingram's speech) aren't incorrect.

There really is evidence that Alzheimer's disease (along with a host of other disorders, including, believe it or not, Type 2 diabetes) might be related to protein misfolding, and that these misfolded proteins can create more misfolded proteins and spread through a brain — just like prions do. In these cases, the proteins being misfolded aren't the same ones as in prion diseases. But the misfolded proteins do seem to be able to spread from one part of a person's brain to another. For instance, in people with Parkinson's disease who received grafts of healthy brain tissue, the misfolded proteins involved in Parkinson's appeared in the donor tissue ten years later. Nobody knows how that could happen, unless the misfolded proteins spread on their own by converting healthy proteins, the same way that prions spread.

And there have been several animal studies that suggest it might be possible to transmit Alzheimer's from one individual to another by injecting infected brain material into a second animal. These aren't perfect studies. For instance, this research has mostly been done in mice, which aren't the ideal models of human disease. And only one study — conducted by Claudio Soto at the University of Texas — has been done in mice that weren't already genetically engineered to be more susceptible to Alzheimer's.

We need more information. But we have enough information to know that this isn't something we can just brush off. In May 2012, the New England Journal of Medicine published an article that will give you a good overview of this research.

The Spread of Neurodegenerative Disease — NEJMMay 31, 2012 … Clinicians who care for patients with neurodegenerative disease often believe that their patients' diseases are sp…

Alzheimer's and mad cow might operate in similar ways, but they are two very different things. And, as far as anybody can tell, Alzheimer's disease is not being spread from person to person.

Jay Ingram said the researchers he spoke with didn't think Alzheimer's was contagious, but they also thought the right kinds of epidemiological studies hadn't been done to really know for sure. That matters, because "as far as anybody can tell" only covers what we can see. If we haven't done the right kinds of studies, we could easily be missing evidence.

When Ingram that, one of the researchers he had in mind was Neil Cashman, a neurologist and neuroscientist at the University of British Columbia. I spoke with Cashman for this story and asked him what the "right kind" of study would look like.

For one thing, he said, it would take a long time to do. His ideal scenario would be to look at blood donors and recipients. Researchers could find older donors, who later turned out to have Alzheimer's, and then follow what happened to the people who received that donated blood. You'd have to follow the recipients for 20 years or so, he said, but in the end you'd have the information you need to get an idea of whether receiving blood from an Alzheimer's victim increased your risk of getting it. Without a study like that, we really don't know whether Alzheimer's can spread from person to person or not.

But what does that mean for caregivers now? We're swimming in a sea of scary studies, none of which are yet telling us enough to know much about real-world risks. It's completely possible that all these little clues could end up not being clues to anything, at all. Sometimes things happen in the lab that don't happen in reality. Sometimes we see patterns where patterns don't actually exist.

Cashman says it puts researchers, doctors, and (yes) journalists in a difficult position. "We're trained not to alarm people with unproven possibilities," he said. "One side of me says it's not a good idea to publish or even discuss the possibility that Alzheimer's is transmissible. But another part of me says there's a legitimate public health concern here. Where's the balance between not panicking people, but giving them enough information to know that this is something that really needs to be investigated? Right now, there's not enough evidence to worry about it. But there's not enough evidence to not worry about it, either."

On the plus side, he said, if Alzheimer's is actually infectious, it's probably nowhere near as infectious as prion diseases like mad cow. You can see that just by looking at the epidemiological data we do have, Cashman said. "You didn't need a lab to tell you that Chronic Wasting Disease and kuru were incredibly contagious. That was clear from the patterns of infection," he said. "With Alzheimer's, if it is contagious it must be much less contagious. Otherwise, we'd see much larger outbreaks of Alzheimer's happening, and it would be clear from day one."

Basically: Alzheimer's is not like Chronic Wasting Disease. Unfortunately, from reading my twitter posts, it was easy to get the impression that it might be. The information about the two topics just came too close to each other. Implications happened: Whether I meant them to or not.

Even the best-intentioned live tweets can be misleading.

I'm not exactly sure what I'm going to do with this realization, myself. I enjoy live-tweeting at conferences and lectures. From my perspective, it seems like the people who read my Twitter stream enjoy it, too. But, clearly, there are downsides I had not previously considered. I'll be thinking about it. But, when you read Twitter, you should think about it, too.

Read Jay Ingram's book:

Fatal Flaws: Amazon.ca: Jay Ingram: BooksMost people have never heard of prions. Indeed, most are only barely aware of the diseases caused by them, except, perhaps, for mad cow…

Another good story to check out:

Infectious proteins on the brain: Alzheimer's and prions | SmartPlanetFeb 21, 2012 … Scientists seeking to understand the fundamental pathology of Alzheimer's disease have long debated the merits of …