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Some of nature’s mysteries have kept scientists busy for decades—for example, the processes that drive evolution. The question of whether certain differences between and within species are caused by natural selection or by chance processes divides evolutionary biologists even today. Now, an international team of researchers has teased apart a scientific debate concerning the evolutionary theories of Darwin and the Japanese geneticist Kimura. Their conclusion: the debate is unnecessarily convoluted by the co-existence of different interpretations.
Due to his contributions to geological and biological sciences, British naturalist Charles Darwin (1809–1882) is considered one of the most important natural scientists. His influential work “On the Origin of Species” (1859), with its strictly scientific explanation of the diversity of life, forms the basis of modern evolutionary biology. Darwin concluded that species evolve through natural selection: well-adapted organisms survive, others don’t.
However, by the end of the 1960s, the Japanese geneticist Motoo Kimura (1924–1994) proposed that at the genetic level, most changes in the course of evolution do not offer direct advantages or disadvantages to the individual but are simply neutral. According to his “Neutral Theory of Molecular Evolution,” first published in 1968, most of the genetic variation within and between species arises from random fluctuations of neutral mutations.
Centenarians, once considered rare, have become commonplace. Indeed, they are the fastest-growing demographic group of the world’s population, with numbers roughly doubling every ten years since the 1970s.
How long humans can live, and what determines a long and healthy life, have been of interest for as long as we know. Plato and Aristotle discussed and wrote about the ageing process over 2,300 years ago.
The pursuit of understanding the secrets behind exceptional longevity isn’t easy, however. It involves unravelling the complex interplay of genetic predisposition and lifestyle factors and how they interact throughout a person’s life.
New research that helps explain the molecular processes involved in the painful autoimmune disease ankylosing spondylitis, or AS, may reduce the guessing game that health care providers currently play while attempting to treat the condition.
A team from Oregon Health & Science University and the VA Portland Health Care System has found a specific kind of AS treatment that is effective when used by patients who have a particular genetic mutation. Their study was published today in the journal Annals of the Rheumatic Diseases, and its findings could lead to more targeted, timely and patient-specific treatment recommendations.
“This is the first time research has shown that we might be able to use genetic markers to determine which therapy ankylosing spondylitis patients should receive,” said the study’s senior researcher, Ruth Napier, Ph.D., assistant professor of molecular microbiology and immunology, arthritis and rheumatic disease in the OHSU School of Medicine, and principal investigator with VA Portland. “These promising findings are encouraging. This is the first time I can say that I’m on the cusp of making a difference for patients with ankylosing spondylitis who seek relief.”
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The challenge: There are very few ways to slow down Alzheimer’s disease or treat its symptoms, and there’s no cure — in 2021, nearly 120,000 Americans died from Alzheimer’s complications, making it one of the top 10 leading causes of death.
One genetic variant in particular — called APOE-e4 — is strongly tied to the brain disease. Having one copy makes a person 2–3 times more likely to develop Alzheimer’s, while having two copies (one from each parent) increases the risk by 8–12 times.
Antisocial Personality Disorder (ASPD) is a complex mental health condition characterized by a pervasive pattern of disregard for the rights of others and violation of societal norms. Untreated forms of ASPD affect about three percent of the general population. While the exact causes of ASPD remain unclear, researchers have identified several potential factors that may contribute to its development.
1. Genetic Factors: Studies suggest a genetic component in the development of ASPD, with heritability estimates ranging from 40% to 70%. Genetic variants involved in neurotransmitter regulation, such as serotonin and dopamine, have been implicated in antisocial behavior (Ficks & Waldman, 2014).
2. Environmental Factors: Childhood experiences play a crucial role in the development of ASPD. Early exposure to abuse, neglect, or inconsistent parenting has been linked to an increased risk of developing antisocial behavior (Rhee & Waldman, 2011).
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In the quest to overcome the limitations of the human body and mind, scientists worldwide are diligently working on various technologies. The question arises: What will human beings become after undergoing numerous enhancements? Will we retain our identity while embracing the possibilities offered by artificial intelligence? What extraordinary capabilities will biotechnology bestow upon us? And how will our emotions and desires evolve as our bodies undergo transformation?
23andMe, the popular DNA testing company, has launched an investigation after client information was listed for sale on a cybercrime forum this week.
On Oct. 1, a post was published on the forum with a link to a sample of allegedly “20 million pieces of data” from the genetic testing company, claiming that it was “the most valuable data you’ll ever see.” The first leak included 1 million lines of data, but on Oct. 4, the threat actor began offering bulk data profiles ranging from $1 to $10 per account in batches of 100, 1,000, 10,000, and 100,000 profiles.
The information leaked in the breach includes names, usernames, profile photos, gender, birthdays, geographical location, and genetic ancestry results.
Scientists testing a new method of sequencing single cells have unexpectedly changed our understanding of the rules of genetics.
The genome of a protist has revealed a seemingly unique divergence in the DNA code signaling the end of a gene, suggesting the need for further research to better understand this group of diverse organisms.
Dr. Jamie McGowan, a postdoctoral scientist at the Earlham Institute, analyzed the genome sequence of a microscopic organism—a protist—isolated from a freshwater pond at Oxford University Parks. The research was published in PLoS Genetics.
