Recent genome-wide association studies have catapulted the search for genes underlying human intelligence into a new era. Genome-wide polygenic scores promise to transform research on individual differences in intelligence, but not without societal and ethical implications, as the authors discuss in this Review.
Are humans born with “intelligence” genes, or is human intelligence determined by environmental factors, such as economic status or easy access to education?
When a team of researchers set out to answer this question, they discovered that more than 500 genes were associated with intelligence. The results, published in Nature Genetics, indicate that intelligence is much more complex than previously thought.
Intelligence, as defined by Merriam-Webster, is the ability to learn new information and apply it to different situations. Despite this simple definition, many elements of intelligence are difficult to nail down.
Today, we’re offering another talk from Ending Age-Related Diseases 2019, our highly successful two-day conference that featured talks from leading researchers and investors, bringing them together to discuss the future of aging and rejuvenation biotechnology.
In her talk, Morgan Levine of the Yale School of Medicine discussed epigenetic biomarkers in detail, discussing the ways in which co-methylation networks provide insight into senescent cells and other facets of biological age.
A deadly fungus is spreading through banana plantations, and the cloned bananas we eat are defenseless. In labs around the world, scientists are trying to find ways to genetically alter the fruit to make it resistant.
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Scientists are reporting the first use of the gene-editing tool CRISPR to try to cure a patient’s HIV infection by providing blood cells that were altered to resist the AIDS virus.
The gene-editing tool has long been used in research labs and a Chinese scientist was scorned last year when he revealed he used it on embryos that led to the birth of twin girls. Editing embryos is considered too risky, partly because the DNA changes can pass to future generations.
Wednesday’s report in the New England Journal of Medicine, by different Chinese researchers, is the first published account of using CRISPR to treat a disease in an adult, where the DNA changes are confined to that person.
Evidence that quantum searches are an ordinary feature of electron behavior may explain the genetic code, one of the greatest puzzles in biology.
In July of 2017, doctors in Beijing blasted the patient with chemicals and radiation to wipe out his bone marrow, making space for millions of stem cells they then pumped into his body through an IV. These new stem cells, donated by a healthy fellow countryman, would replace the patient’s unhealthy ones, hopefully resolving his cancer. But unlike any other routine bone marrow transplant, this time researchers edited those stem cells with Crispr to cripple a gene called CCR5, without which HIV can’t infiltrate immune cells.
For the first time, a patient got treated for HIV and cancer at the same time, with an infusion of gene-edited stem cells. The results? Mixed.
San Francisco.
Gene-editing technology offers the potential to treat inherited disorders with selective edits and corrections to an afflicted individual’s genetic code. But with such molecular tinkering comes with the risk of unintended changes to the genome.
Biotech startup Trucode Gene Repair is developing technology that it claims can edit genes in a way that reduces the risk of these so-called “off-target effects.” The South San Francisco company is announcing Tuesday that it has raised $34 million to support its research. Trucode disclosed that its investors in the financing include Kleiner Perkins and GV.
Growing evidence supports the antagonistic pleiotropy theory of mammalian aging. Accordingly, changes in gene expression following the pluripotency transition, and subsequent transitions such as the embryonic–fetal transition, while providing tumor suppressive and antiviral survival benefits also result in a loss of regenerative potential leading to age-related fibrosis and degenerative diseases. However, reprogramming somatic cells to pluripotency demonstrates the possibility of restoring telomerase and embryonic regeneration pathways and thus reversing the age-related decline in regenerative capacity. A unified model of aging and loss of regenerative potential is emerging that may ultimately be translated into new therapeutic approaches for establishing induced tissue regeneration and modulation of the embryo-onco phenotype of cancer.
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Aging is often defined as a progressive deterioration of an organism over time, wherein the risk of mortality increases exponentially with age in the postreproductive years. Although everyday environmental risks from predation or infectious disease (e.g., stochastic risks) necessarily lead to increased mortality over time, they are not considered core to the definition of the aging process per se [1,2]. Thus, an important criterion of aging is that it encompasses virtually every somatic tissue type, including the gonads (though not necessarily the germ-line cells themselves, given their role in potentially perpetuating the species) [3]. In order to distinguish the aging process from damage that occurs stochastically over time, Benjamin Gompertz described aging as a process leading to an exponential increase in mortality with time, that is, Rm = R0eat where ‘Rm’ represents the probability of mortality between ages ‘t’ and ‘t + 1’.
