Excerpt from an episode of Longevity by Design, hosted by Dr. Gil Blander and Ashley Reaver, MS, RD, CSSD, who were joined by Dr. George Church, Professor of Genetics at Harvard Medical School.
To watch the entire conversation clic here: https://youtu.be/6XnXeVS1m2U
The accident at reactor four of the Chernobyl Nuclear Power Plant in 1986 generated the largest release of radioactive material into the environment in human history. The impact of the acute exposure to high doses of radiation was severe for the environment and the human population. But more than three decades after the accident, Chernobyl has become one of the largest nature reserves in Europe. A diverse range of endangered species finds refuge there today, including bears, wolves, and lynxes.
Radiation can damage the genetic material of living organisms and generate undesirable mutations. However, one of the most interesting research topics in Chernobyl is trying to detect if some species are actually adapting to live with radiation. As with other pollutants, radiation could be a very strong selective factor, favoring organisms with mechanisms that increase their survival in areas contaminated with radioactive substances.
The world has one more sloth species in it than previously thought. Maned sloths live in a small belt of forest in Brazil and an analysis now suggests those in the south are a different species from those found farther north.
Three-toed sloths were conventionally thought to be divided into four species. One — the maned sloth (Bradypus torquatus) — sports a thatch of coarse, brown hair, making the head resemble a husked coconut.
Maned sloths were thought to be one species but a genetic and physical analysis suggests there are actually two.
Continue reading “Newly recognised species of sloth has a head like a coconut” »
A team of researchers affiliated with several institutions in Switzerland and the U.S. reports evidence that the genetics of longevity are influenced by both gender and age. In their paper published in the journal Science, the group describes their study of aging in mice and humans. João Pedro de Magalhães, with the University of Birmingham, has published a Perspective piece in the same journal issue outlining the technical challenges to understanding how aging works and the work done by the team on this new effort.
Scientists have been studying the aging process for many years but still do not have a good explanation for why organisms age and why some live longer than others. In this new effort, the researchers wondered if something in the genome plays a role in how long a species lives on average.
Noting that another team had created a very large dataset of information regarding aging in nearly 3,000 mice, the researchers found that it also contained genetic information. After obtaining access to the database, they analyzed that genetic information—more specifically, they conducted quantitative trait locus mapping. They found multiple loci that they could associate with longevity, some that were specific to one or the other gender. They also found that mice who weighed more during their early years or who had small litter sizes tended to die younger. They suggest the same genes that were associated with aging may have also played a role in the other two traits. The researchers also found that the aging-related genes they isolated appeared to remain dormant until the latter stages of a given individual’s life.
Without altering the genetic code in the DNA, epigenetic modifications can change how genes are expressed, affecting an organism’s health and development. The once radical idea that such changes in gene expression can be inherited now has a growing body of evidence behind it, but the mechanisms involved remain poorly understood.
A new study by researchers at UC Santa Cruz shows how a common type of epigenetic modification can be transmitted via sperm not only from parents to offspring, but to the next generation (“grandoffspring”) as well. This is called “transgenerational epigenetic inheritance,” and it may explain how a person’s health and development could be influenced by the experiences of his or her parents and grandparents.
The study, published the week of September 26 in the Proceedings of the National Academy of Sciences (PNAS), focused on a particular modification of a histone protein that changes the way DNA is packaged in the chromosomes. This widely studied epigenetic mark (called H3K27me3) is known to turn off or “repress” the affected genes and is found in all multicellular animals—from humans to the nematode worm C. elegans used in this study.
Illumina Inc. says it can read a person’s entire genetic code for as little as $200 with its new sequencing machine, bringing the company within reach of its long-promised goal of the $100 genome.
This year’s Breakthrough Prize in Life Sciences has a strong physical sciences element. The prize was divided between six individuals. Demis Hassabis and John Jumper of the London-based AI company DeepMind were awarded a third of the prize for developing AlphaFold, a machine-learning algorithm that can accurately predict the 3D structure of proteins from just the amino-acid sequence of their polypeptide chain. Emmanuel Mignot of Stanford University School of Medicine and Masashi Yanagisawa of the University of Tsukuba, Japan, were awarded for their work on the sleeping disorder narcolepsy.
The remainder of the prize went to Clifford Brangwynne of Princeton University and Anthony Hyman of the Max Planck Institute of Molecular Cell Biology and Genetics in Germany for discovering that the molecular machinery within a cell—proteins and RNA—organizes by phase separating into liquid droplets. This phase separation process has since been shown to be involved in several basic cellular functions, including gene expression, protein synthesis and storage, and stress responses.
The award for Brangwynne and Hyman shows “the transformative role that the physics of soft matter and the physics of polymers can play in cell biology,” says Rohit Pappu, a biophysicist and bioengineer at Washington University in St. Louis. “[The discovery] could only have happened the way it did: a creative young physicist working with an imaginative cell biologist in an ecosystem where boundaries were always being pushed at the intersection of multiple disciplines.”
In adult mice with loss of CHD8 gene function, FDA-approved drug partially restores disrupted brain cell production
CINCINNATI, Sept. 23, 2022 /PRNewswire/ — Research led by a scientist at Cincinnati Children’s who primarily studies brain tumors may open doors for improved treatment of autism.
Autism spectrum disorder (ASD) affects about one in 40 children between ages 3 and 17, according to the National Survey of Children’s Health. Those affected often experience difficulty socializing, impaired language development, repetitive behaviors, and other symptoms. Of those tested for various genes linked to the condition, nearly everyone with disruptive mutations of the gene CHD8 has autism.
Neurodegenerative diseases—like amyotrophic lateral sclerosis (ALS, or Lou Gehrig’s disease), Alzheimer’s, and Parkinson’s—are complicated, chronic ailments that can present with a variety of symptoms, worsen at different rates, and have many underlying genetic and environmental causes, some of which are unknown. ALS, in particular, affects voluntary muscle movement and is always fatal, but while most people survive for only a few years after diagnosis, others live with the disease for decades. Manifestations of ALS can also vary significantly; often slower disease development correlates with onset in the limbs and affecting fine motor skills, while the more serious, bulbar ALS impacts swallowing, speaking, breathing, and mobility. Therefore, understanding the progression of diseases like ALS is critical to enrollment in clinical trials, analysis of potential interventions, and discovery of root causes.
However, assessing disease evolution is far from straightforward. Current clinical studies typically assume that health declines on a downward linear trajectory on a symptom rating scale, and use these linear models to evaluate whether drugs are slowing disease progression. However, data indicate that ALS often follows nonlinear trajectories, with periods where symptoms are stable alternating with periods when they are rapidly changing. Since data can be sparse, and health assessments often rely on subjective rating metrics measured at uneven time intervals, comparisons across patient populations are difficult. These heterogenous data and progression, in turn, complicate analyses of invention effectiveness and potentially mask disease origin.
Additionally, epigenetic changes were suggested to be a possible link [30, 31] between adverse childhood experiences and mortality as well as higher morbidity burden in late life [32]. It was proposed that this link could be mediated by health-adverse coping mechanisms (activated as a result of high levels of anxiety and depression) that are associated with adverse childhood experiences [33]. Some of these coping strategies, such as smoking, alcohol abuse and and a high BMI resulting from unhealthy eating habits, were shown to be associated with DNAmAA in some studies [34,35,36]. However, these results were not unequivocally replicated [37,38,39] (reviewed in ref. [40]).
Previous studies that examined the relationship between DNAmAA and stress operationalized stress as low socioeconomic status (SES) [41, 42], (childhood) trauma [26, 43,44,45], racial discrimination [46], or exposure to violence [47]. Many previous studies on the topic focused on changes in DNAm age during childhood as this period is known to be particularly prone to stress-related epigenetic changes [29].
In contrast, in this work we focus on older age which was shown to be the second most vulnerable phase in a person’s life in terms of epigenetics [29]. As epigenetic modifications remain even after the psychological stimulus has ceased there is the possibility of cumulating effects on the epigenome exerted by repeated psychological stressors [29]. Specifically, we analyzed the association between the amount of experienced stress (measured by Cohen’s Perceived Stress Scale [PSS] [48]) and several DNAm age estimators (i.e. the 7-CpG clock [49], Horvath’s clock [50], Hannum’s clock [51], PhenoAge [34], GrimAge [52]) in 1,100 older adults. While the PSS represents a well-established marker of perceived stress [48], to our knowledge it has not been investigated in the context of epigenetic aging before. While we were able to replicate well-established associations with perceived stress, none of the five epigenetic clocks analyzed in the current study were associated with the perception of stress.
