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The pathway they study is conserved from mice to humans so the results may be relevant. That being said I don't know whether this pathway is involved in Alzheimer's disease. What's more interesting is the mechanism of the curing. One often proposed model for dealing with neurodegeneration is to enhance naturally existing pathways in a cell that deal with misfolded proteins. The authors of this paper do the opposite. They found that this natural response was being overinduced in mice with prion disease and inhibiting it actually made them better. Certainly worth trying in other mouse models.

Why is the 5S being tested in a case?

Is it possible that Apple will settle for lower market share as long as they retain a majority of the profits? I mean look at the PC market where Apple sells relatively few units but controls nearly half of the profit. What does it matter if you only control 10% of the market if you control 90% of the profit in the long run.

Of course the issue in this argument is the App store. You could argue that by building a huge user base could allow you to shift your profits from hardware to software in the long run.

Micromet was developing a set of bi-functional antibodies that pretty much accomplished this same thing. That is directing the immune system to tumors. One side of the antibody would bind the tumor, while the other bound the T-cells. They were bought out by Merck a year or two ago and I believe the therapies are in clinical trials. You can read about the antibodies here: http://cancerres.aacrjournals.org/content/69/12/4941.full.pd...

The added benefit here is that the antibodies can be produced en masse and delivered as a drug rather than reprogramming the person's T-cells.

Known makers make up less than half of known hereditary cases of ALS. That is in families with a history of ALS, only about 30-40% cases have been tracked down to mutations in a single gene. SOD1 mutations are the most common form of familial ALS but like I said, if you had a novel mutation, meaning one that hadn't been observed before, you'd really have no idea. Also if you have one of many previously identified mutations that have been observed in only a few or even a single patient, you still couldn't be sure you'd get ALS.

I'm a SOD1 researcher and my heart goes out to you and the many patients suffering with this terrible disease and their families. Though rest assured, we're working hard to uncover why this happens and what we can do about it.

I just wanted to clarify some points. I'm not sure what you mean about "the mutated gene". SOD1 mutations definitely cause ALS. It's just that there isn't a single SOD1 mutation that's responsible. Over 100 different mutations of the same gene can lead to the disease. Other genes are also implicated in ALS, such as TDP-43 and FUS. Sure there are other genetic factors responsible for ALS, many of which are yet unknown. But these are known factors.

I would be very hesitant to sequence my SOD1 gene to be honest. Let's say it came up with a new mutation. Not all mutations will lead to disease. So while this may not cause you to get ALS in the long run, it may lead to you worrying incessantly as you get older. Furthermore, most of these 100+ mutations have only been found in a single family or even a single patient. It's quite possible there are other genetic polymorphisms in these families that make these patients susceptible to their SOD1 mutations. Also there are examples of SOD1 mutations that aren't 100% penetrant. That is if you have the mutation, you aren't 100% guaranteed to get the disease. For instance, in scandinavian populations the aspartate 90 to valine mutation is recessive.

Basically there are a lot of complicating factors. Even if your SOD1 gene comes back as the normal sequence, you couldn't know you were safe. That is unless you knew that your grandfather and aunt actually had SOD1 mutations. Of course these are only my opinions as a scientist. I am not a physician.

I think this method of teaching cannot succeed without some dramatic shift in the education system, which given its sheer size is nearly impossible. Furthermore, it may not even be optimal. The basis of this change is individualized education. Yet how can we teach students individually when there are millions of kids that have to be taught? Where are the teachers to facilitate this form of delivery? Who will pay for the increased cost in education? How will we even classify children? It has been demonstrated that children do better in school when they are placed in higher performing groups. Should we put all of the underperforming kids in a class where they see no one superior to them? Finally, I think there is a certain set of knowledge that everyone should know and K-12 does a decent job of teaching that. We can certainly improve the system without replacing it outright.

I'm inclined to agree with the ENCODE scientists. You could argue that even protein binding sites that have no biological outcome titrate away transcription factors from other "active" regions. The system would have evolved with these sinks in place and therefore they constitute an active, useful part of the genome. Another way to look at it is that if you were trying to generate a computer model of the entire genome, you would have to account for the extra binding sites, even if they had no output in terms of protein or even RNA.

I see minecraft pocket edition on that list as well and it is neither a $0.99 game or a free to play. I think this is evidence that people are willing to pay for a well-made product. For me this article is simply a rehash of Zynga's whale strategy and we know how manipulative and frankly evil that is.

I think the idea that something like Siri will end Google is silly. Siri is just an input-output platform for a search. I think the more likely outcome is that the best search engine will power the best Siri-like app. There's no reason why Google would miss out on being that search engine.

It is also worth noting that Google dominates mobile search even more than it does traditional search.

I can answer some of your questions. The longevity and age of onset of patients with familial ALS is partially dependent on the mutation they harbor. That being said, genetic background is an important contributor. Fortunately or unfortunately, familial ALS isn't common enough to have significant statistics on the matter. To my knowledge there is no solid proof that environmental factors play a role in ALS. I'm fairly certain some will be discovered, but to date specific factors that enhance or prevent ALS are not known. On the issue of veterans, it is thought that the enhanced physical activity may be the cause for the increased risk of ALS, though the increase is merely 2 fold and once again the statistics are poor. If I remember correctly, this increased risk was present for both combat veterans and those that didn't see any combat. Once again outcomes are identical with the civilian population.

I don't believe that his longevity decreases the urgency for research into the matter. However, compared with disorders such as Alzheimer's disease, cancer, and heart disease, which combined will affect some large percentage of the population, the 1:1000 lifetime risk for ALS makes it somewhat insignificant.

I did ALS research in grad school and his case seems to be an outlier. Generally ALS is late onset (55+) and rapidly lethal (<3 years expected survival). That being said, early onset cases are often slower to progress and if I remember correctly his onset was in his late 20s, which is very early. There are really no medications or treatments that are effective for ALS, no matter how much money you have.