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Genetics, Nutrition, Obesity, Research

Early findings show nutrigenomics could make weight loss more efficient

Early findings show nutrigenomics could make weight loss more efficient

Bieler2“Food is your best medicine,” a wise saying and a book by the late Henry Bieler, MD, holistic doctor to the stars, includes testimonials by Gloria Swanson and Greta Garbo and a recipe for an alkalizing broth comprising four green vegetables to which he attributes all kinds of health benefits. My former ballet teacher (1919-2012) used to eat the broth according to his instructions whenever she was sick, almost sick, or feeling “toxic” for any reason, and I make it now and then just in case it works.

Well, science is moving toward grounding some beliefs about the healing power of certain foods for certain people and the effectiveness of diets tailored to a person’s genetic makeup. A New Scientist piece reports that last week at the European Society of Human Genetics meeting in Milan, University of Trieste researcher Nicola Pirastu, PhD, and colleagues presented findings on nutrigenomics showing that diets shaped according to a person’s metabolism may be more effective than non-specialized calorie reduction in helping him or her lose weight.

From the piece:

The team used the results of a genetic test to design specific diets for 100 obese people that also provided them with 600 fewer calories than usual. A control group was placed on a 600-calorie deficit, untailored diet.

After two years, both groups had lost weight, but those in the nutrigenetic group lost 33 per cent more. They also took only a year to lose as much weight as the group on the untailored diet lost in two years.

I’ll keep eating four green vegetables in their cooking water (and adding Bieler-taboo salt and pepper) until a larger, randomized trial tells me otherwise, but it’s worth considering that “healthy” isn’t one-size-fits-all. The piece continues:

[John Mathers, PhD, director of the Human Nutrition Research Centre at Newcastle University, UK] says the effects of even a healthy diet can vary according to someone’s genetics. For instance, the APOE gene is linked to the breakdown of fat, and one variant of it confers a higher risk of getting cardiovascular disease and dementia. “People with that variant respond differently to certain fats in the diet,” he says. Another gene affects how much vitamin B9 people need.

Previously: Stanford geneticist talks tracking biological data points and personalized medicine, Ask Stanford Med: Genetics chair answers your questions on genomics and personalized medicine and How genome testing can help guide preventative medicine
Photo by Emily Hite

Evolution, Genetics, Research, Science, Stanford News, Stem Cells

It’s a blond thing: Stanford researchers suss out molecular basis of hair color

It's a blond thing: Stanford researchers suss out molecular basis of hair color

blond hair, brighter

It’s all over the news today: Blonds aren’t stupid.

Well, that’s what most of the media would have you believe is the take-home message of the latest research by developmental biologist David Kingsley, PhD. And although I’m happy to see such great coverage, I’m hoping that readers realize that Kingley’s study on human hair color, which was published yesterday in Nature Genetics (subscription required), describes something much more subtle, and less superficial. From our release:

The study describes for the first time the molecular basis for one of our most noticeable traits. It also outlines how tiny DNA changes can reverberate through our genome in ways that may affect evolution, migration and even human history.

Kingsley, who is known for his study of a tiny fish called the threespine stickleback, is interested in learning how organism adapt to new environments by developing new traits. He’s found that this type of adaptation is most-often accomplished by changes in DNA regulatory regions that affect when, where and how a gene is expressed, rather than through (possibly disruptive) changes in the genes themselves.

In this case, he and his colleagues turned his attention to the blond hair common to many northern European and Icelanders. A previous study had shown that a single nucleotide change on human chromosome 12 was a major driver in hair color. As explained in the release:

The researchers found that the blond hair commonly seen in Northern Europeans is caused by a single change in the DNA that regulates the expression of a gene that encodes a protein called KITLG, also known as stem cell factor. This change affects how much KITLG is expressed in the hair follicles without changing how it’s expressed in the rest of the body. Introducing the change into normally brown-haired laboratory mice yields an animal with a decidedly lighter coat — not quite Norma Jeane to Marilyn Monroe, but significant nonetheless.

The involvement of KITLG, with its critical role in stem cell biology, is certainly interesting. But there’s also a more global lesson about the specificity of gene expression their effect on phenotype:

The study shows that even small, tissue-specific changes in the expression of genes can have noticeable morphological effects. It also emphasizes how difficult it can be to clearly connect specific DNA changes with particular clinical or phenotypic outcomes. In this case, the change is subtle: A single nucleotide called an adenine is replaced by another called a guanine on human chromosome 12. The change occurs over 350,000 nucleotides away from the KITLG gene and only alters the amount of gene expression about 20 percent — a relatively tiny blip on a biological scale more often assessed in terms of gene expression being 100 percent “on” or “off.”

“What we’re seeing is that this regulatory region exercises exquisite control over where, and how much, KITLG expression occurs,” said Kingsley. “In this case, it controls hair color. In another situation — perhaps under the influence of a different regulatory region — it probably controls stem cell division. Dialing up and down the expression of an essential growth factor in this manner could be a common mechanism that underlies many different traits.”

And now, the hook that excited most of the news media:

[Kingsley] added: “It’s clear that this hair color change is occurring through a regulatory mechanism that operates only in the hair. This isn’t something that also affects other traits, like intelligence or personality. The change that causes blond hair is, literally, only skin deep.”

Previously: Something fishy: Threespine stickleback genome published by Stanford researchers, Hey guys, sometimes less really is more , Tickled by stickle(backs) and Blond hair evolved more than once, and why it matters
Photo by Traci Lawson

Big data, Genetics, Stanford News, Technology

Computing our evolution

Computing our evolution

Last week, as the 2014 Big Data in Biomedicine conference came to a close, a related story about the importance of computing across disciplines posted on the Stanford University homepage. The article describes research making use of the new Stanford Research Computing Center, or SRCC (which we blogged about here). We’re now running excerpts from that piece about the role computation, as well as big data, plays in medical advances.

The human genome is essentially a gigantic data set. Deep within each person’s 6 billion data points are minute variations that tell the story of human evolution, and provide clues to how scientists can combat modern-day diseases.

To better understand the causes and consequences of these genetic variations, Jonathan Pritchard, PhD, a professor of genetics and of biology, writes computer programs that can investigate those linkages. “Genetic variation effects how cells work, both in healthy variation and in response to disease, which ultimately regulates organism-level phenotypes,” Pritchard says. “How natural selection acts on phenotypes, that’s what causes evolutionary changes.”

Consider, for example, variation in the gene that codes for lactase, an enzyme that allows mammals to digest milk. Most animals don’t express lactase after they’ve been weaned from their mother’s milk. In populations that have historically revolved around dairy farming, however, Pritchard’s algorithms have shown that there has been strong long-term selection for expressing the genes that allow people to process milk. There has been similarly strong selection on skin pigmentation in non-Africans that allow better synthesis of vitamin D in regions where people are exposed to less sunlight.

The methods used in these types of investigations have the potential to yield powerful medical insights. Studying variations in gene regulation within a population could reveal how and where particular proteins bind to DNA, or which genes are expressed in different cell types – information that could be applied to design novel therapies. These inquiries can generate hundreds of thousands of data sets, which can only be parsed with clever algorithms and machine learning.

Pritchard, who is also a Stanford Bio-X affiliate, is bracing for an even bigger explosion of data; as genome sequencing technologies become less expensive, he expects the number of individual genomes to jump by as much as a hundredfold in the next few years. “There are not a lot of problems that we’re fundamentally unable to handle with computers, but dealing with all of the data and getting results back quickly is a rate limiting step,” Pritchard says. “Having access to SRCC will make our inquiries go easier and more quickly, and we can move on faster to making the next discovery.”

Previously: Learning how to learn to readPersonal molecular profiling detects diseases earlier and New computing center at Stanford supports big data

Applied Biotechnology, Cancer, Genetics, otolaryngology, Research, Stanford News

Stanford researchers identify genes that cause disfiguring jaw tumor

Stanford researchers identify genes that cause disfiguring jaw tumor

jawPatients with the rare jaw tumor ameloblastoma have few treatment choices. Radiation and drugs have failed to stop this slow-growing cancer, leaving jaw removal as the only option. The surgery also takes out facial nerves and blood vessels, and so patients need reconstructive surgery and rehabilitation just to smile and chew again.

In a new study, published in Nature Genetics, Stanford researchers discovered two gene mutations that cause this tumor. Their findings point to FDA-approved drugs that are effective against these mutations in other types of cancer.

To find the mutations, the researchers sequenced mRNA – messages copied from genes that tell the cell how to make proteins – from slices of preserved tumor. In 80% of the samples, they found a mutation in either the SMO or the BRAF gene. Interestingly, the SMO mutations occurred predominantly in the upper jaw, while BRAF mutations were found mainly in the lower jaw.

From our press release:

“These genes are essential for delivering signals of growth and development, particularly in developing organs,” said Robert West, MD, PhD, associate professor of pathology at Stanford and a senior author on the study. “But it’s increasingly apparent that they are often mutated in cancers.”

Perhaps most promising, researchers found that there are already FDA-approved drugs for cancers with mutations in the same developmental pathway. A drug called vemurafenib is toxic to ameloblastoma cell cultures that harbor a BRAF mutation, they found. This drug is effective against melanomas that carry the same mutant gene. Researchers also found that a compound called arsenic trioxide, an approved anti-leukemia drug, is affective at blocking the mutant SMO protein.

West and his colleagues, A. Cain McClary, MD, a co-author and chief pathology resident at Stanford Hospital, and A. Dimitrios Colevas, MD, an associate professor of oncology at Stanford, have already submitted an application to the biotech company Genentech, which manufactures the most popular brand of vemurafenib. Their pilot study would test whether the drug could shrink tumors in people with ameloblastomas.

Also from the release:

Throughout this project, McClary has engaged with an ameloblastoma Facebook group to hear members’ stories and to learn about what a patient goes through during the initial surgery and subsequent facial reconstruction. He plans to conduct a webinar with the group, and can’t wait to share his findings with them.

“It’s a great motivator,” he said about his involvement with the group. “Our face is a special place. I couldn’t imagine not smiling.”

Patricia Waldron is a science writing intern in the medical school’s Office of Communication & Public Affairs.

Previously: Gene panel screens for dozens of cancer-associated mutations, say Stanford researchers
Photo by Gray’s Anatomy Plates/Wikimedia Commons

Big data, Genetics, Research, Stanford News, Technology

Personal molecular profiling detects diseases earlier

Personal molecular profiling detects diseases earlier

Today, as the 2014 Big Data in Biomedicine conference continues, a related story about the importance of computing across disciplines posted on the Stanford University homepage. The article describes research making use of the new Stanford Research Computing Center, or SRCC (which we blogged about here). Over the next few days we’ll run excerpts from that piece about the role computation, as well as big data, plays in medical advances.

snyder - smallOur DNA is sometimes referred to as our body’s blueprint, but it’s really more of a sketch. Sure, it determines a lot of things, but so do the viruses and bacteria swarming our bodies, our encounters with environmental chemicals that lodge in our tissues and the chemical stew that ensues when our immune system responds to disease states.

All of this taken together – our DNA, the chemicals, the antibodies coursing through our veins and so much more – determines our physical state at any point in time. And all that information makes for a lot of data if, like genetics professor Michael Snyder, PhD, you collected it 75 times over the course of four years.

Snyder, who is a member of Stanford Bio-X and the Stanford Cancer Center, is a proponent of what he calls ‘personal omics profiling’, or the study of all that makes up our person, and he’s starting with himself. “What we’re collecting is a detailed molecular portrait of a person throughout time,” he says.

So far, he’s turning out to be a pretty interesting test case. In one round of assessment he learned that he was becoming diabetic and was able to control the condition long before it would have been detected through a periodic medical exam.

If personal omics profiling is going to go mainstream, serious computing will be required to tease out which of the myriad tests Snyder’s team currently runs give meaningful information and should be part of routine screening. Snyder’s sampling alone has already generated a half of a petabyte of data – roughly enough raw information to fill about dishwasher-size rack of servers.

Right now, that data and the computer power required to understand it reside on campus, but new servers will be located at SRCC. “I think you are going to see a lot more projects like this,” says Snyder. “Computing is becoming increasingly important in medicine.”

Previously: New computing center at Stanford supports big data, Stanford researchers work to translate genetic discoveries into widespread personalized medicine, Stanford geneticist talks tracking biological data points and personalized medicine, How genome testing can help guide preventative medicine and ‘Omics’ profiling coming soon to a doctor’s office near you?
Related: Big data
Photo of Snyder by Saul Bromberger

Bioengineering, Genetics, Neuroscience, Pregnancy, Research, Stanford News

Step away from the DNA? Circulating *RNA* in blood gives dynamic information about pregnancy, health

Step away from the DNA? Circulating *RNA* in blood gives dynamic information about pregnancy, health

blood on fingertip - 260

I read a lot of scientific papers. And while they’re all interesting, they don’t all make me snap to attention like the latest from Stanford bioengineer Stephen Quake, PhD. I even remarked to my husband that it’s rare to get the immediate sense that a discovery will significantly change clinical care.

If anyone’s going to shake up the status quo, however, it would be Quake. You may remember that Quake has made waves before with his pioneering discoveries involving the analysis of tiny bits of DNA circulating in our blood. His 2008 discovery that it’s possible to non-invasively detect fetal chromosomal abnormalities with a maternal blood sample has revolutionized prenatal care in this country. It’s estimated that, in 2013, hundreds of thousands of pregnant women used a version of this test to learn more about the health of their fetuses. And, in 2012, Quake showed its possible to sequence an entire fetal genome from a maternal blood sample.

Now he and his lab have gone one step further by turning their attention to another genetic material in the blood, RNA. Although information conveyed in the form of DNA sequences is mostly static (the nucleotide sequence of genes, for example), RNA levels and messages change markedly among tissues over time and at various developmental points. The difference in available information is somewhat like comparing a still photo with a high-resolution video when it comes to sussing out what the body is actually doing at any point in time.

The study was published today in the Proceedings of the National Academy of Sciences. As I explain in my release:

In the new study, the researchers used a technique previously developed in Quake’s lab to identify which circulating RNA molecules in a pregnant woman were likely to have come from her fetus, and which were from her own organs. They found they were able to trace the development of specific tissues, including the fetal brain and liver, as well as the placenta, during the three trimesters of pregnancy simply by analyzing blood samples from the pregnant women over time.

Quake and his colleagues believe the technique could also be broadly useful as a diagnostic tool by detecting distress signals from diseased organs, perhaps even before any clinical symptoms are apparent. In particular, they found they could detect elevated levels of neuronal-specific RNA messages in people with Alzheimer’s disease as compared with the healthy participants.

Quake and the lead authors, graduate students Winston Koh and Wenying Pan, liken their technique to a “molecular stethoscope.” They believe it could be broadly useful in the clinic. More from my release:

“We’ve moved beyond just detecting gene sequences to really analyzing and understanding patterns of gene activity,” said Quake. “Knowing the DNA sequence of a gene in the blood has been shown to be useful in a few specific cases, like cancer, pregnancy and organ transplantation. Analyzing the RNA enables a much broader perspective of what’s going on in the body at any particular time.”

Previously: Whole-genome fetal sequencing recognized as one of the year’s “10 Breakthrough Technologies” and Better know a bioengineer: Stephen Quake
Photo by Alden Chadwick

Cancer, Genetics, Public Health, Research, Stanford News, Technology

Odd couples: Resemblances at molecular level connect diseases to unexpected, predictive traits

Odd couples: Resemblances at molecular level connect diseases to unexpected, predictive traits

odd coupleStanford big-data king Atul Butte, MD, PhD, has made a career out of mining publicly available databases to unearth novel and frequently surprising relationships between, for example, diseases and drugs, nature and nurture, and pain and sexual status.

In his latest Big Dig, Butte (along with his colleagues) has combed through mountains of electronically available data to identify molecular idiosyncrasies linking specific diseases to easily observed traits that on first glance wouldn’t be thought to have any such connection. The results, written up in a study published in Science Translational Medicine, may allow relatively non-invasive predictions of impending disorders.

For example, who would think that magnesium levels in the blood might be an early-warning marker for gastric cancer? Or that platelet counts in a blood sample would predict a coming diagnosis of alcohol dependency? Or that a high PSA reading, typically associated with potential prostate cancer, would turn out to be predictive of lung cancer? Or that a high red-blood-cell count might presage the development of actute lymphoblastic leukemia?

Answer: No one. That’s the beauty of Big Data. You find out stuff you were never specifically looking for in the first place. It just pops out at you in the form of a high, if initially inexplicable, statistical correlation.

But by cross-referencing voluminous genetic data implicating particular gene variants in particular diseases with equally voluminous data associating the same gene variants with other, easily measured traits typically considered harmless, Butte and his associates were able to pick out a number of such connections, which they then explored further by accessing anonymized electronic medical records from Stanford Hospital and Clinics, Columbia University, and Mount Sinai School of Medicine. “We indeed found that some of these interesting genetic-based predictions actually held up,” Butte told me.

Because checking blood levels of one or another substance is far simpler and less invasive than doing a biopsy, and because altered levels of the substance may appear well before observable disease symptoms, this approach may lead to early, more inclusive and less expensive diagnostic procedures.

Butte is one of the speakers at Stanford’s upcoming Big Data in Biomedicine conference. Registration for the May 21-24 event is open on the conference website.

Previously: Nature/nurture study of type 2 diabetes risk unearths carrots as potential risk reducers, Mining medical discoveries from a mountain of ones and zeroes, Newly identified type-2 diabetes gene’s odds of being a false finding equal one in 1 followed by 19 zeroes, Women report feeling more pain than men, huge EMR analysis shows and Cheap Data! Stanford scientists’ “opposites attract” algorithm plunders public databases, scores surprising drug-disease hook-ups
Photo by cursedthing

Genetics, NIH, Research, Science, Stanford News

Tissue-specific gene expression focus of Stanford research, grant

Tissue-specific gene expression focus of Stanford research, grant

It’s abundantly clear by now that the sequence of our genes can be very important to our health. Mutations in some key areas can lead to the development of diseases such as cancer. However, gene sequence isn’t everything. It’s necessary to know when and at what levels that mutated gene is expressed in the body’s cells and tissues.

This analysis is complicated by the fact that most of us have two copies of every gene – one from our father and one from our mother (the sex chromosomes X and Y would be an exception; people with conditions like Down syndrome that are caused by abnormal chromosomal copy numbers, another). The two copies, called alleles, are not always expressed in the same way (a phenomenon called allele-specific expression). In particular, structural changes or other modifications to the alleles, or the RNA that is made from them, can significantly affect levels of expression. This matters when one copy has a mutation that could cause a disease like cancer. That mutation could be very important if that allele is preferentially expressed, or less important if its partner is favored.

Understanding relative levels of allele expression is therefore critical to determining the effect of particular mutations in our genome. But it’s been very difficult to accomplish – in part because allele-specific expression can vary among our body’s tissues.

Recently, Stanford researchers Stephen Montgomery, PhD, an assistant professor of pathology and genetics, and Jin Billy Li, PhD, an assistant professor of genetics, devised a way to use microfluidic and deep-sequencing technology to measure the relative levels of expression of each allele in various tissues. (The research was published – subscription required – in January in Nature Methods.) Now they’ve taken the research one step further to look at the varying expression of potentially damaging alleles across ten tissues from a single individual. As Montgomery explained in an e-mail to me:

We were able to learn that as many as one-third of personal genome variants (that is, potentially damaging mutations that would be detected by genome sequencing within an individual) can be modified by allele-specific expression in ways that could influence individual outcomes. Therefore, just knowing a variant exists is only one step towards predicting clinical outcome in an individual. It is also necessary to know the context of that variant. Is the damaging allele in a gene that is abundantly expressed within and across an individual’s tissues?

Montgomery and Li published their most recent findings in today’s issue of PLOS Genetics. They were recently awarded a grant from the National Human Genome Research Institute to study allele-specific expression in thousands of tissues from 100 donors  during the next three years. The grant is part of the institute’s Genotype-Tissue Expression effort, or GTEx.

Previously: We are what we….aren’t? Cataloging deletions and insertions in the human genome

Aging, Genetics, NIH, Research

Sequencing a supercentenarian’s genome to unlock the secrets of longevity

DNA_043014In an effort to determine the genetic underpinnings of longevity, scientists at Stanford and elsewhere are mapping the human genomes of supercentenarians, individuals that have lived beyond 110 years old.

A recent entry on the NIH Director’s blog offers an in-depth overview of one such project involving a 115-year-old Dutch woman named Hendrikje “Hennie” van Andel-Schipper, who died in 2005 and donated her body to medical research. Scientists examined the genome of her blood and brain tissue and analyzed the number of somatic mutations, the type of DNA mutations that are acquired over the course of a lifetime rather than inherited. The results raised some interesting questions:

You might imagine that someone who reaches the extreme age of 115 may have a low number of somatic mutations because his or her cells have exceptional protection against DNA damage. [Scientists] rather expected this to be the case for Hennie, particularly because she’d never had leukemia, lymphoma, or any other type of blood cancer. To the researchers’ surprise, the DNA sequencing results showed that Hennie’s blood cells had accumulated about 450 mutations since she was born. That is consistent with a mutation rate of about four mutations per year of life, which is in line with previous work suggesting that laboratory-grown cells derived from younger, healthy people acquire about five mutations annually.

Recognizing that circulating blood cells are derived from a large pool of stem cells in the bone marrow, and that each stem cell may have acquired a different set of mutations during life, researchers thought it would be challenging to detect any mutations in a collection of millions of blood cells. After all, in healthy adults, bone marrow contains about 11,000 hematopoietic stem cells, of which about 1,300 are actively dividing and replenishing our blood cells. If just one of those stem cells had undergone a mutation of an A to a T, the sensitivity of current DNA sequencing technology would be very unlikely to discover it.

However, further study of Hennie’s blood genome revealed that most of her circulating white blood cells were derived from just two hematopoietic stem cells. Not only did that make the process of detecting Hennie’s somatic mutations much easier, it raised fascinating questions about how the aging process affects bone marrow. While the work still must be reproduced in other older people, the researchers speculate that as we age, the pool of hematopoietic stem cells may shrink, until all of our white blood cells are clones of just a few parent cells.

Previously: She’s so 19th century: Women pushing their hundred-and-teens and California’s oldest person helping geneticists uncover key to aging
Photo by Duncan Hull

Aging, Genetics, Neuroscience, Podcasts, Research, Stanford News

The state of Alzheimer’s research: A conversation with Stanford neurologist Michael Greicius

The state of Alzheimer's research: A conversation with Stanford neurologist Michael Greicius

My colleague Bruce Goldman recently wrote an expansive blog entry and article based on research by Mike Greicius, MD, about how the ApoE4 variant doubles the risk of Alzheimer’s for women. I followed up Goldman’s pieces in a podcast with Greicius, who’s the medical director of the Stanford Center for Memory Disorders.

I began the conversation by asking about the state of research for Alzheimer’s: essentially, what do we know? As an aging baby boomer, I’m interested in the differences between normal, age-related cognitive decline versus cognitive declines that signal an emerging disease. Greicius said people tend to begin losing cognitive skills around middle age:

Every cognitive domain we can measure starts to decline around 40. Semantic knowledge – knowledge about the world – tends to stay pretty stable and even goes up a bit. Everything else… working memory, short term memory all tends to go down on this linear decline. The difference with something like Alzheimer’s is that the decline isn’t linear. It’s like you fall off a cliff.

Greicius’ most recent research looks at the certain increased Alzheimer’s risk ApoE4 confers on women. As described by Goldman:

Accessing two huge publicly available national databases, Greicius and his colleagues were able to amass medical records for some 8,000 people and show that initially healthy ApoE4-positive women were twice as likely to contract Alzheimer’s as their ApoE4-negative counterparts, while ApoE4-positive men’s risk for the syndrome was barely higher than that for ApoE-negative men.

In addition to the increased risk of Alzheimer’s for women with the ApoE4 variant, I asked Greicius how he advises patients coming into the clinic who ask about staving off memory loss. At this point, he concedes, effective traditional medication isn’t really at hand. “Far and away our strongest recommendations bear on things like lifestyle and particularly exercise,” he said. “We know, in this case from good animal models, that physical exercise, particularly aerobic exercise, helps brain cells do better and can stave-off various insults.” So remember, a heart smart diet along with aerobic exercise.

One last question for Greicius: What about those cognitive-memory games marketed to the elderly and touted as salves for memory loss – do they have any benefit? He’s riled now: “I get asked that all the time, and smoke starts coming out of my ears.” He says the games are nothing more than snake oil.  His advice when he gets asked the question: “Give that money to the Alzheimer’s Association or save it and get down on the floor with your grandkids and build Legos. That’s also a great cognitive exercise and more emotionally rewarding.”

Previously: Having a copy of ApoE4 gene variant doubles Alzheimer’s risk for women but not for men, Common genetic Alzheimer’s risk factor disrupts healthy older women’s brain function, but not men’s and Hormone therapy halts accelerated biological aging seen in women with Alzheimer’s genetic risk factor

Stanford Medicine Resources: