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Experts estimate that 5% of the United States population – at least 15 million people – have weak spots in the arteries of their brains known as aneurysms. Each year about 27,000 of these bulging arteries burst, releasing blood into the space around the brain and potentially leading to stroke, brain damage or death.
The siblings of people who have had a ruptured brain aneurysm are four times more likely to suffer the same fate, suggesting that genes play a part in determining risk. So far, however, studies of families with a history of a brain aneurysm and genes thought to be likely candidates have failed to produce any convincing genetic links.
A new study published online yesterday in <a href="https://dx.doi.org/10.1038/ng.240" target="_blank" rel="noopener noreferrer">Nature Genetics</a> reports three genetic variants that, when combined, can increase the odds of brain aneurysm by almost three-fold. The variants increased risk independent of sex, family history, and age.

Kaya Bilguvar and colleagues began by screening hundreds of thousands of SNPs in two European samples, one from Finland and one from the Netherlands. They then looked for evidence that the most strongly associated SNPs also increased the likelihood of aneurysm in a Japanese sample. All told, more than 2,100 people with a brain aneurysm and 8,000 controls were studied. The authors say that they used a diverse population for their studies so that the results could be extended to a broader segment of the world’s population.
The researchers found associations between SNPs on chromosomes 2, 8, and 9, and brain aneurysm risk. A person with five or six &#8220;risky&#8221; copies (there are six possible — everyone has two copies of each of the three SNPs) has almost three times greater odds of having a brain aneurysm compared to someone who has zero or only one risky copy.
SNPs in the same region of chromosome 9 as rs1333040 have previously been associated with arterial diseases, including brain aneurysms.
In many cases, the first sign of a brain aneurysm is the catastrophic bleeding in the brain that happens when it ruptures. The authors of the current report caution that further work will be needed in this area and that there are most likely more DNA variants to be found. But they say their findings, in combination with assessment of other risk factors, could help identify people with brain aneurysms before it’s too late.
“Effect” is the increase in odds compared to someone with two copies of the non-risk version of each SNP as calculated in Bilguvar et al for the combined Finnish, Dutch and Japanese sample.

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23andMe Blog Team

Genetic Links to Brain Aneurysm

<img loading="lazy" decoding="async" class="alignright size-full wp-image-1890" title="smiling_dalmatian" src="https://blog-api.23andme.com/wp-content/uploads/2008/11/smiling_dalmatian.jpg" alt="" width="350" height="262" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/11/smiling_dalmatian.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2008/11/smiling_dalmatian-300x225.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
When they eat purines, a class of chemicals that are found in many types of food and most abundant in organ meats and some types of fish and shellfish,, most mammals break them down into a substance called allantoin, which is then excreted.
The only exceptions are humans, great apes and Dalmatian dogs, all of which instead convert purines into uric acid.
That little difference in metabolism can have significant consequences. In humans (and presumably great apes), uric acid can build up in the blood and cause gout, a painful inflammatory arthritis that results from deposition of uric acid crystals in joints. Dalmatians don’t get gout from their uric acid. For them, uric acid crystallizes in their bladders, leading to stones that often have to be removed with surgery.
In humans (and presumably great apes), uric acid can build up in the blood and cause gout, a painful inflammatory arthritis that results from deposition of uric acid crystals in joints. Dalmatians don’t get gout from their uric acid. For them, uric acid crystallizes in their bladders, leading to stones that often have to be removed with surgery.
All pure-bred Dalmatians have the genetic mutation that causes uric acid to build up in their blood, a direct result of years of selective breeding to enhance their characteristic spotty coat.
A new report, published online today in <a href="http://dx.plos.org/10.1371/journal.pgen.1000246" target="_blank" rel="noopener">PLoS Genetics</a>, has finally zeroed in on the mutated gene responsible: SLC2A9.

Coincidentally, but not really surprisingly, variants in SLC2A9 have also <a href="https://www.ncbi.nlm.nih.gov/pubmed/18327257?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum" target="_blank" rel="noopener">recently</a> <a href="https://www.ncbi.nlm.nih.gov/pubmed/18327256?ordinalpos=2&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum" target="_blank" rel="noopener">been</a> <a href="https://www.ncbi.nlm.nih.gov/pubmed/18487473?ordinalpos=3&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum" target="_blank" rel="noopener">linked</a> to uric acid levels and gout in humans. What is a surprising coincidence (at least to me!) is that a human sample used for one of the genomewide association studies that identified the SLC2A9 variants was from the <a href="https://en.wikipedia.org/wiki/Dalmatia" target="_blank" rel="noopener">Dalmatian Islands</a> in Croatia.
There is hope for eliminating high uric acid levels in Dalmatians. The “Dalmatian-Pointer Backcross Project” advocates breeding pure Dalmatians with the offspring of a single Dalmatian-Pointer mix born in the 1970’s. These mixed dogs carry one normal copy of the SLC2A9 gene, inherited from the pointer. Each time a litter is produced from the mating of a pure Dalmatian with a mix, about 50% of the puppies will inherit the normal gene, while the other 50 percent will remain afflicted with high uric acid. Over time, by mating only dogs with the normal SLC2A9 gene, high uric acid levels should disappear.
The Backcross Project has been underway for some time, but until now it has relied on urine tests to identify puppies unaffected by high uric acid levels. Now that the exact gene mutation is known, breeders will be able to more easily identify unaffected puppies. The <a href="http://www.vgl.ucdavis.edu/" target="_blank" rel="noopener">Veterinary Genetics Laboratory</a> at the UC Davis School of Veterinary Medicine will soon be offering DNA testing for SLC2A9 mutations.

Gene Links Gout in Humans with Bladder Stones in Dalmatian Dogs

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Most children have mastered the complexities of spoken language by age six or seven,. But about 5% of otherwise healthy children struggle with either expressing themselves, understanding what others are saying or both, a disorder known as<a href="http://www.asha.org/about/publications/leader-online/archives/2001/sli.htm" target="_blank" rel="noopener"> specific language impairment (SLI)</a>.
In a report published online yesterday by the <a href="http://content.nejm.org/cgi/content/full/NEJMoa0802828" target="_blank" rel="noopener">New England Journal of Medicine</a>, researchers from the Wellcome Trust Centre for Human Genetics at the University of Oxford present evidence that a gene called CNTNAP2 is involved in specific language impairment.
“It has long been suspected that inherited factors play an important role in childhood language disorders,” Simon Fisher, senior author of the study, said in a statement. “But this is the first time that we have been able to implicate variants of a specific gene in common forms of language impairment.”

Several previous studies have linked broad regions of DNA with SLI, but there has yet to be any consensus on the true genetic underpinnings of the disorder.
The researchers narrowed in on the role of CNTNAP2 in SLI because it interacts with FOXP2, another gene implicated in the development of language skills. Some people with rare speech disorders have mutations in FOXP2, but variations in this gene have not been associated with more typical forms of language impairment.
In a study of children from 184 families with at least one child affected by SLI, the researchers found that each G at decreased the score on a test that measures the ability to hear and repeat nonsense words like “brufid” and “contramponist” by 5.53 points on average. Previous studies have indicated that this test is a good indicator of SLI.
Each G also decreased a child&#8217;s score on the standardized Expressive Language Score, which measures the ability to communicate through spoken language, by an average 3.21 points. Scores can range from 46 to 141 for the nonsense word test, and 50 to 150 for the expressive language test. Most children in the general population get a score between 85 and 115 on both.
Variants in the same region of CNTNAP2 as have also been linked to delayed speech in children with autism. Some experts suggest that the different components of autism-spectrum disorders, such as communication problems, impaired social interaction, and repetitive behaviors, could be due to different genetic influences. Fisher and colleagues suggest that alterations in CNTNAP2 could be a shared mechanism for pure SLI and language problems associated with autism.
The research team plans to investigate whether variants of CNTNAP2 are linked to natural variations in linguistic abilities in the general population. They also plan to investigate other genes that interact with FOXP2.
“Genes like CNTNAP2 and FOXP2 are giving us an exciting new molecular perspective on speech and language development, one of the most fascinating but mysterious aspects of being human,” said Fisher. “This work promises to shed light on how networks of genes help to build a language-ready brain.”
In an accompanying <a href="http://content.nejm.org/cgi/content/full/NEJMe0807813" target="_blank" rel="noopener">editorial</a> in NEJM, Karin Stromswold, who was not associated with the research, said that the findings of the British study and others like it could someday help tease apart the genetic and environmental factors that affect language and language disorders. Stromswold questioned, however, why others studies of SLI have never implicated the DNA region where CNTNAP2 is found, even when the same group of children was studied.

Genetic Variant Linked to Common Form of Language Impairment

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We all know that what a mother eats, drinks, smokes and does during pregnancy can affect her child’s prenatal development. But can it actually affect the baby’s DNA?
Animal studies have shown that transient environmental exposures of a pregnant female can produce “epigenetic” changes in her offspring &#8212; chemical modifications superimposed on the DNA sequence that affects how and when genes are expressed.
It would, of course, be highly unethical to purposefully subject human mothers to environmental insults for the purpose of studying DNA effects in developing fetuses. But history has provided researchers a unique opportunity to study how one environmental factor, maternal nutrition, can affect an unborn child at the genetic level.
In the winter of 1944-1945, the Germans imposed a food embargo in the western part of the Netherlands, leading to a period of famine known as the <a href="https://en.wikipedia.org/wiki/Dutch_famine_of_1944" target="_blank" rel="noopener noreferrer">Dutch Hunger Winter</a>. Food was so scarce that the average daily caloric intake was cut to about 667 calories. Despite the desperate times, birth registries and the health care system remained operational, allowing researchers today to trace people who were prenatally exposed to the famine.
Higher rates of schizophrenia, addiction, obesity and heart disease have <a href="https://www.ncbi.nlm.nih.gov/pubmed/16778567?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum" target="_blank" rel="noopener noreferrer">previously been associated</a> with people conceived during the Hunger Winter. But new results, published online last week in the <a href="https://dx.doi.org/10.1073/pnas.0806560105" target="_blank" rel="noopener noreferrer">Proceedings of the National Academy of Sciences</a>, offer some of the first evidence that there were also epigenetic effects in these people.
Heijmans and colleagues found that people who were conceived during the Hunger Winter, and thus exposed to famine very early in their development, to this day have fewer epigenetic markers called methyl groups attached to a gene called IGF2 than their unexposed siblings. People who had been in the late stages of gestation during the famine did not show these differences.
The protein encoded by the IGF2 gene is a key factor in human growth and development. A reduction in the number of methyl groups attached to the gene affects whether the maternal copy of the gene is expressed and has been associated with an increased risk of colorectal cancer.
Although people exposed to famine during the earliest days of their development show evidence of epigenetic changes all these years later, their average recorded birth weight was no different than what was seen in children born before the famine. But the people who were late in gestation during the famine and didn’t show epigenetic effects were lighter at birth. This suggests that low birth weight, a commonly used proxy measure for compromised prenatal development, might not be sufficient for understanding the true extent of how a mother’s environment has impacted her child.
The authors of the study suggest that future research should focus on the epigenetic effects of environmental exposures that are more common in modern societies, such as over-nutrition and assisted reproductive technologies.
“Understanding how epigenetic control depends on early exposure may shed light on the link between development and health over the lifespan and ultimately suggest new ways to prevent human disease,” the authors conclude.
Photo: Sander van der Molne

Mom’s Experience Can Affect Your Genes

It was a great honor to learn yesterday that the 23andMe Personal Genome Serviceâ„¢ has been named TIME Magazine&#8217;s 2008 Invention of the Year. Today the Blog would like to acknowledge several 23andMe partners who contributed to the innovation behind our service.
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We&#8217;d like to extend our thanks to Illumina, Inc., DNA Genotek, Inc., and LabCorp, and especially to everybody at those companies who shared their ideas, expertise and hard work.
<ul>
<li>DNA Genotek produces the collection system our customers use to collect their saliva samples and ship them to our contracted laboratory. The caps, container and funnel are functional and easy to use.</li>
<li>Illumina is behind the technology we use to generate our customers&#8217; genetic data. The Illumina Human Hap550+ is a customizable DNA array that allows us to determine an individual&#8217;s genetic signature at nearly 600,000 locations on all 23 pairs of chromosomes, plus the mitochondrial DNA. Because Illumina&#8217;s technology lets our scientists select thousands of specific locations in the genome that they want to probe, we think it is the best genotyping platform for personalized genetics.</li>
<li>Labcorp is the company that brings the Spit Kit and the Human Hap550+ together. Their laboratory technicians extract DNA from our customers&#8217; saliva, then run it through Illumina arrays to produce the basic genetic data we use as the starting point for our Personal Genome Service. As a CLIA-certified laboratory with extensive experience in all types of medical diagnostic testing, Labcorp assures our customers genetic data of the utmost accuracy and quality.</li>
</ul>
A big thanks to all who help make our Personal Genome Service possible – including our partners, scientific advisors, investors, team members and customers. We hope everyone is as excited as we are to see not just our service recognized, but also our shared vision of personal genomics for all.

TIME to Thank Our Friends

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About 3,500 years ago, the Phoenicians expanded from their homeland in present-day Syria and Lebanon, using their superior maritime technology to establish trading posts across southern Europe and North Africa.
<h2>The Rise and Fall of the Phoenicians</h2>
They traded silver from Iberia, copper from Cyprus, and textiles from Morocco. They built cities in Sicily, Malta, and Tunisia that rivaled those in Greece and Rome. However, by the 1st century BC, nearly all evidence of their power and authority over Mediterranean trade routes had vanished.
The Phoenicians&#8217; fate as a maritime power is well documented. The Persians conquered the Phoenician homeland in 539 BC. Two centuries later, Alexander the Great&#8217;s army swept in from the west. Finally, the Roman Empire conquered—and destroyed—the Phoenician city of Carthage in 146 BC following the Third Punic War.
<h2>The Disappearance of the Phoenicians</h2>
But what happened to the Phoenicians themselves? Were they wiped out, too? Or are their descendants still alive today?
In a study published this week, researchers identify Phoenician-specific DNA markers in present-day Mediterranean populations, demonstrating that genetic traces of the ancient civilization still exist in some modern-day peoples. These people could be descendants of the Phoenicians themselves.

It has always been difficult to use genetics to trace specific historical migrations, such as the Jewish Diaspora, the Norman invasion of Britain, or even the Viking expansions into Western Europe.
<h2>Using DNA to Tell a Story</h2>
Attempting to trace migrations across the Mediterranean is even more arduous, as there have been multiple migrations at different times throughout history. How do scientists sort out each unique migration event over the long and complex population history of the region? A team of geneticists from National Geographic and IBM’s Genographic Project believes they have found a way to do just that. They discuss their research in the latest American Journal of Human Genetics issue.
Traditionally, when scientists want to understand the genetic history of an area, they collect DNA samples from the entire region of interest. But in this case, the authors of the AJHG paper collected samples from specific towns and cities that are believed to have been built on or near ancient Phoenician archaeological sites, including Carthage, Cyprus, and Sicily. They reasoned that if descendants of the Phoenicians do indeed exist, they would more likely be found near these sites.
<h2>Tracing Paternal Lines</h2>
Armed with this newly collected data, the authors focused on the Y-chromosome to trace the Phoenicians’ genetic history. According to Chris Tyler-Smith, one of the study’s authors, “We chose the Y-chromosome because its male-specificity means that it would have been carried by the predominantly male Phoenician traders.” They then used a newly devised analytical method of distinguishing any Phoenician migration from other geographically similar migrations. Their results are surprisingly informative.
The authors found a weak — but significant — genetic signature among their samples that could not be explained by chance. Many of the samples belonged to a particular branch of haplogroup J2, which the authors believe points back to distinct migrations by Phoenician traders from the Middle East into Europe and North Africa more than 3,000 years ago.
The applications of the authors’ new approach to studies of population history are incredibly far-reaching. Perhaps similar analyses could be used to trace the genetic footprints of Alexander the Great and his army into Persia during the 4th century BC or migrations along the Silk Road from China during the Middle Ages. The authors even propose that their technique could be used within populations to discover historical migrations that we never even knew existed.
Photograph courtesy of Wikimedia Commons.

Ripples in the Mediterranean: Tracing the Genetic Origins of the Phoenicians

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Editor&#8217;s Note: This week TIME Magazine is naming the 23andMe Personal Genome Service, its Invention of the Year, an honor that the publication has previously bestowed on innovations such as the iPhone and YouTube. This post by Director of Products Alex Wong (back row, second from right) offers a glimpse at how 23andMe came to be, and what makes it such a powerful tool for exploring your DNA.
We&#8217;re thrilled that our product has been named TIME Magazine&#8217;s 2008 Invention of the Year. But what exactly did we invent? To answer that question, let&#8217;s to go back to the early days of 23andMe … .
I first met our co-founders Anne and Linda, together with Serge and Brian, our first two employees, in the summer of 2006 at a bakery in downtown Palo Alto, Calif.. As they were explaining the basic concept behind the company, Linda reached into her bag and pulled out a CD with &#8220;Aveys&#8221; written on it in magic marker.
&#8220;What&#8217;s that?&#8221;, I asked.
Her reply: &#8220;It&#8217;s my family&#8217;s genomes!&#8221;
That&#8217;s a first, I thought to myself – pulling genomes from a handbag. I was hooked. I knew I wanted to join 23andMe and help make this possible for everyone and their family.

But we had a long way to go. DNA chip technology was still fairly new, something that only researchers had access to. Linda, having worked at a DNA chip company, was able to get her own family genotyped. But unless you had an in at a research lab or one of these companies, getting your own genome just was not possible. Even if you did manage to get the genomes of you and yours on a CD, all you&#8217;d find when you looked at it would be a bunch of giant, indecipherable text files filled with &#8220;rs&#8221; numbers and A&#8217;s and B&#8217;s. These are the raw data files of SNP information that the DNA chip analysis produces.
How to make sense of all that data? The good news was that years of research, starting with the <a href="https://www.genome.gov/10001772" target="_blank" rel="noopener">Human Genome Project</a> and the International HapMap Project, had produced a wealth of publicly available information about human genetics. The bad news was, it was all locked inside databases designed by researchers, for researchers. Want to know what one of your SNPs means? A logical place to start, you would think, would be <a href="https://www.ncbi.nlm.nih.gov/projects/SNP/" target="_blank" rel="noopener">dbSNP</a>, a massive database of SNPs run by the National Institutes of Health.
Good luck. Assuming you can wade through its dense user interface, make sure you get your alignment, genome build, major and minor alleles, orientation, and stranding right, or you&#8217;re liable to get your interpretation backwards and think you&#8217;re supposed to have wet earwax when you really have dry! Don&#8217;t know what stranding, genome builds, or any of those other things are? Trust me, you&#8217;d rather not.
Not only did these government and academic databases sport slow and unfriendly user interfaces, but some of them also had data quality and consistency problems and few of them were linked together.
So it was going to require more than just building a website to make all the fruits of ongoing genetic research accessible, useful, and compelling to regular people like you and me. We had to create a whole architecture and process for cleaning up, aggregating and integrating all of this human genetic information, combining it with an individual&#8217;s own genotype data, running comparisons and algorithms on it, blending it with great educational content, and serving it back to our customers through a friendly user interface – all in under 500 milliseconds, which is how long you have before people start to complain that your website is slow.
On top of that, we wanted personal genetics to be social, so our customers could see their genetic data in context and learn about what makes us all different and similar at the same time. That meant building in the ability for customers to share their data with family or friends without sacrificing privacy or security.
It&#8217;s taken the combined talents of all the different kinds of people we have at our company, from bioinformaticians, to engineers, to writers, to UI designers, but we&#8217;re all so excited about having made it possible in 2008 for anyone with $399 to explore their own genome.
Of course, if you&#8217;d like to rock it 2006-style, you can still get your own gigantic text file full of SNPs using our Download Your Raw Data feature. You can even burn it onto a CD and stick it in your handbag!

Creating the Invention of the Year: A Look Behind the Scenes

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Even though European populations have been studied for years, there are still many lingering questions as to the continent’s population history — especially with regards to isolated peoples.   Understanding the history of the Basque of northern Spain has long been a topic of interest among geneticists, as has the origins of the indigenous Saami of northern Finland.
Now, a study published by geneticists at the University of Helsinki supports the conclusion of <a id="k1oa" title="Some recent studies" href="../2008/08/13/a-different-kind-of-gene-mapping-comparing-genetic-and-geographic-structure-in-europe/" target="_blank" rel="noopener">some recent studies</a> that have hinted that the Finnish people themselves are more genetically isolated than other European populations.
Traditional methods of examining genetic ancestry are focused on two areas of our genome: our mitochondrial DNA, which is passed down from mothers to children, revealing information on our maternal ancestry, and the Y-chromosome, which is passed down from fathers to sons, revealing our paternal ancestry.
But these are only two relatively small regions of our entire genome, and geneticists have often said that to truly understand a person’s ancestry we must examine human DNA much more broadly.   One way to do this is to use a genome-wide analysis, examining hundreds of thousands of genetic markers.   The new University of Helsinki <a id="bt3m" title="study" href="http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0003519" target="_blank" rel="noopener">study</a> did just that, analyzing more than 250,000 unique SNPS across the entire human genome.
What the researchers found was quite intriguing.   First they investigated German and British populations as a basis for comparison and found them to be genetically close to one another – hardly a surprise considering their historical closeness.   But when the researchers looked at populations from Finland in comparison to other parts of Europe, they found few enough similarities to conclude that Finnish people are genetically isolated from other parts of Europe.

This study is important for a few reasons.   First, it illustrates that using genome-wide analysis, rather than only using the Y-chromosome or the mitochondrial DNA, can reveal much about population history.   Second, it confirms previous hypotheses that Finland — which is both geographically and linguistically isolated from other parts of Europe — is genetically isolated as well.
The ancestors of the modern Finns, once they arrived in this cold land thousands of years ago, remained relatively separate from even their closest European neighbors.   Although modern travel and telecommunications have likely reduced this isolation, the remnants of it are still evident in the genetics.

Not So Close Neighbors: The Genetically Isolated People of Finland

The Blog has pointed out several times in the last few months that when researchers look for evidence of interbreeding between early humans and Neanderthals, they often fail to find any.
But there are still several geneticists who would like us to heed the words of former defense secretary Donald Rumsfeld, who once pointed out that &#8220;the absence of evidence is not evidence of absence.&#8221;
During a briefing for science writers this morning at Stanford University, geneticist Bruce Lahn argued that interbreeding with Neanderthals may have introduced a mutation that appears to confer an evolutionary advantage about brain development into the human gene pool.
&#8220;We argue that in modern humans, there may actually be some Neanderthal genes,&#8221; Lahn said at the Council for the Advancement of Science Writing&#8217;s New Horizons in Science briefings.

Lahn based his argument on a gene known as microcephalin. Because certain gene mutations can cause brain underdevelopment, microcephalin is assumed to be involved in that organ&#8217;s development.
Lahn described research he and several colleagues first described two years ago in the <a href="https://www.pnas.org/content/103/48/18178.full?sid=a8247834-aa24-4260-b390-4213ac428291" target="_blank" rel="noopener noreferrer">Proceedings of the National Academy of Sciences</a>. The researchers sequenced microcephalin in 89 people from populations around the world. They found that the sequences fell into two very different groups – so different, in fact, that they apparently traced back to a common ancestor older than the human species itself.
Moreover, each of the two groups appeared to have a very distinct history. One appeared to have arisen about a million years ago and diversified at a steady pace since then. The other group appeared to have arisen just 37,000 years ago and spread rapidly throughout 70% of the human population. That kind of pattern suggests what evolutionary biologists call a &#8220;selective sweep,&#8221; the introduction of an advantageous genetic variant that quickly wipes out older versions of the gene.
Usually, when geneticists see a selective sweep in action, the new variant appears to arise out of the pre-existing one. But in this case, Lahn argues, the new genetic variation traces back to a common ancestor that precedes both populations. He believes Neanderthals could have been that population and that they could have transferred the &#8220;new&#8221; variation into the human gene pool through interbreeding about 40,000 years ago.
It&#8217;s just a hypothesis at this point – and one that many geneticists consider challenging to <a href="https://www.nature.com/hdy/journal/v98/n4/full/6800953a.html" target="_blank" rel="noopener noreferrer">confirm</a>. But suppose ongoing efforts to sequence the Neanderthal genome find a version of the microcephalin gene identical to the one currently sweeping through the human population. In that case, Lahn will have strong evidence for his claim.

Latest Posts — Page 204