us the genetic component. i mean, i think i've... i understand that 99% of our genes are all alike but the 1% is crucial. >> exactly. so we've known for a long time that genes play an important role in autism but it's really only been in the last several years that we've had the tools and we're able to really make progress and get a good picture of the genetic landscape and really a lot of that is because the advances in genomic technology have allowed us to look at that 1%, the part of the genome that varies between people in a way we've never been able to before. so in doing that we found there are different types of variation that we either didn't know about or didn't pay attention to that are very important for autism. >> rose: and what are they? >> so we've known for a long time if you look at two people and examine their genome there is will be changes or differences in the letter code of d.n.a. one particular position. we've known that for a long time. what we've now found out through high resolution ge

>> as eric is implying, between the psychology and the genetics is the brain. and the hope is that although there may be three or 400 genetic risk factors, they will converge on common pathways. so this is a diagram of a neuron, all these genes are in that little sphere tucked the nucleus and all that genetic information is read and it main tand the shape of the neurocell and function of the neurocell. and one key function we have all been talking about is the connection that nerve cell makes with the next cell in line called the synapse which literally means to clasp. and some synapses are stimulating the next cell in line and o some inhibit it. and the general theory which i ascribe to is that there is an imbalance between this exciteation and inhibition, almost, the world is too much with us, and the autistic child can't process information because of imbalances in those synapses, in key areas of the brain. perhaps those areas in the temp oral lobe, the superior temp oral gyhus that were pointed out in your diagrams. but there are many, many, many proteins t

ultimately it's a genetic syndrome. it's a extra chromosome but you can sample as you know, you can sample tissue. and again those are examples where as i said the pen transae very high. as a society, if the disease is a suffering is great enough we've decided that's okay to do. we've made that decision. the question now as we read the genome in more deep ways as we read individual genomes in more deep ways are we entering arenas where the moral uncertainties are so great we don't know what to do, we need to have a conversation about. >> rose: is there an urgency to have a conversation. >> there's an absolute urgency to have a conversation. just to give you a couple examples. in about four or five weeks before i finished writing the book, in china there was an attempt to make a genetic, define genetic change in making an embryo. now these were non-viable embryos, they were chosen. so there were some natural limits to the experiments. you couldn't have carried out this experiment but it was nonetheless an experiment that

genetic technology has advanced rapidly since then. the human genome project took ten years and cost $3 billion. today the cost of sequencing a genome is less than $10,000 and can be completed in just a matter of days. these technological advances led to the recent mapping of the neanderthal genome using d.n.a. taken from bones that are 40,000 years old. yet researchers have found that mapping the genome is far easier than understanding everything they want to know. despite some notable achievements, gee no, ma'am i cans has not yet produced a revolution in medicine or biotechnology but scientists say they're on the way. the increasing availability of genetic information, many believe, it's just a matter of time before we understand the biological basis of disease. we begin with nicholas wade he's a 30-year veteran science reporter for the "new york times". he's the author of several books including "the faith instinct" and "before the dawn" which is about human evolution over the past 10,000 years. in recent articles, he's explored th

so here's one thread that comes out of the genetics. schizophrenia, typically, people start to show symptoms as danny did in their late teens in college. but when we look at the genes, we find that many of them are acting in, before birth while you're still in the womb to set up the development of the brain. so the risk is some sort of a vulnerability that set up very, very early that makes the brain show problems much, much later. and that same idea comes up from our understanding of environmental risks tooment one of the most well understood environmental risks for schizophrenia was made based on its discovery after world war ii, after the dutch hunger winter, that children who were born after that winter, 18 years later had a much higher spike of rates of schizophrenia. something about being starved in the womb had created a risk for them so we're learning that we have to think about very early development, not just about what happened when you are an adolescent or teenager or freshman in college. and then we're learning some over th

if this is a genetic disorder, how can this happen?t may well be that there are certain environmental influences but i believe, i think many believe that there is an increase in the genetic risk. and autism is not inherited in the usual sense, if you think of it. autistic children don't often grow up to have families, large families. so why is it increasing? why isn't autism decreasing? and the thought is that there's a phenomenon called denovo, new mutations that happen every generation. when sperm and egg cells are developed, there are mistakes. not mistakes, there are changes that happen where you are a combination of your mother and father. for every protein in your body, you inherit one gene from your mother and one from your father to make up a pair. but that copying function is not precise. you're different from your mother and from your father. and from your siblings. and you're different because you don't copy all the dna exactly. there can be spelling mistakes or there can be middle pieces of dna, submicroscopic chunks of dna

everyone knows when we do that, when we have the genetic land scain, when we understand what the genetic risk factors are, then we have to find out where in the brain these genes are working, when in the brain they're operative. is it prenatal during the first, second or third trimester of birth or is it in certain critical periods later in development? there's evidence that some autism follows a pattern of regression, children that develop normally for a period of time. although this is a strong debate in the literature but it may be there are different critical periods. autism is not going to be a simple one gene one disease phenomenon. in fact the best estimates i know of suggest there may be more than 100 genes that enhance the risk of autism. and they may act at different times in different ways. that's what challenge is. >> charlie: the most important thing is identifying these genes or are there other things that we're making dramatic progress in autism because it is something i've heard more and more about over the last four or five years. is that because there are more cases or

and hope is if people can really understand the genetics and specifically target what is wrong with the cancer instead of hitting it with chemotherapy or radiation, going after what is driving that particular cancer to grow, then maybe they can actually stop it, or even kill it. and change the whole nature of the disease. that is the dream. >> that still doesn't seem like it is really me that has the disease, in a lot of ways it seems -- it seems too coincidental, too ironic that it would actually happen to me, wilalmost see myself as detachen one way from being a patient versus being a leukemia doctor. >> it has been an interesting interaction between the two of us. i am his physician but i am also his boss. i am his colleague. i was involved in his recruitment as a fellow and then as a faculty member. i work closely with his mentors, who are really invested in him and completely committed to his success. so it is almost -- it is almost an objection more reason in, oxymoron in medicine but it is almost like a family affair .. the. >> we conclude with "the new york times" hong kong bure

and hope is if people can really understand the genetics and specifically target what is wrong with the cancer instead of hitting it with chemotherapy or radiation, going after what is driving that particular cancer to grow, then maybe they can actually stop it, or even kill it. and change the whole nature of the disease. that is the dream. >> that still doesn't seem like it is really me that has the disease, in a lot of ways it seems -- it seems too coincidental, too ironic that it would actually happen to me, wilalmost see myself as detachen one way from being a patient versus being a leukemia doctor. >> it has been an interesting interaction between the two of us. i am his physician but i am also his boss. i am his colleague. i was iv captioning sponsored by rose communications from our studios in new york city, this is charlie rose. >> rose: we want to talk this evening about cancer. there is new research signaling a major shift in the treatment and diagnosis of the disease breakthroughs in dna science are at the heart of this change, the emerging ability of scientists to analyze ge

warinner: the genetics were incredibly stable through time.his was fascinating to us because we saw big changes. for example, between the mebrak and the samdzong period, we suddenly see defleshing. that's a new thing, that's a religious change, and yet we don't see any change in the underlying genetics of the population. narrator: but researchers have spotted one genetic change specific to high-altitude peoples of the himalaya. it's an ancient mutation, or gene variation, a change in the order of the chemical bases-- the as, ts, cs and gs that make up the gene. the variant prevents people from getting sick at high altitude where the available oxygen is low. warinner: there are a few places in the genome, a few traits in which we have experienced very recent evolution. so one of these would be the adaptation to high altitude. there's only a handful of these genes that are very, very recently undergoing selection, and this is one of them. narrator: most of the himalayan people that live here now have this variant. the team wants to know if the a