A combined analysis using people of Japanese, Chinese, and European ancestry identified five new genes associated with the non-familial, sporadic form of amyotrophic lateral sclerosis (ALS).
These findings further an understanding of the genetic basis of sporadic ALS, and may support the development of new therapies.
Some people are at higher risk of developing obesity because they possess genetic variants that affect how the brain processes sensory information and regulates feeding and behavior. The findings from scientists at the University of Copenhagen support a growing body of evidence that obesity is a disease whose roots are in the brain.
Over the past decade, scientists have identified hundreds of different genetic variants that increase a person’s risk of developing obesity. But a lot of work remains to understand how these variants translate into obesity. Now scientists at the University of Copenhagen have identified populations of cells in the body that play a role in the development of the disease—and they are all in the brain.
“Our results provide evidence that biological processes outside the traditional organs investigated in obesity research, such as fat cells, play a key role in human obesity,” says Associate Professor Tune H Pers from the Novo Nordisk Foundation Center for Basic Metabolic Research (CBMR), at the University of Copenhagen, who published his team’s findings in the internationally-recognized journal eLife.
Two active genetics strategies help address concerns about gene-drive releases into the wild.
In the past decade, researchers have engineered an array of new tools that control the balance of genetic inheritance. Based on CRISPR technology, such gene drives are poised to move from the laboratory into the wild where they are being engineered to suppress devastating diseases such as mosquito-borne malaria, dengue, Zika, chikungunya, yellow fever and West Nile. Gene drives carry the power to immunize mosquitoes against malarial parasites, or act as genetic insecticides that reduce mosquito populations.
Although the newest gene drives have been proven to spread efficiently as designed in laboratory settings, concerns have been raised regarding the safety of releasing such systems into wild populations. Questions have emerged about the predictability and controllability of gene drives and whether, once let loose, they can be recalled in the field if they spread beyond their intended application region.
Continue reading “New Genetic Systems Created by Biologists to Neutralize Gene Drives” »
For the first time, Senckenberg scientist Mónica Solórzano-Kraemer, together with lead authors David Peris and Kathrin Janssen of the University of Bonn and additional colleagues from Spain and Norway, successfully extracted genetic material from insects that were embedded in six- and two-year-old resin samples. DNA—in particular, DNA from extinct animals—is an important tool in the identification of species. In the future, the researchers plan to use their new methods on older resin inclusions, as well. The study was published today in the scientific journal PLOS ONE.
The idea of extracting DNA from resin-embedded organisms inevitably invokes memories of the blockbuster “Jurassic Park.”
“However, we have no intention of raising dinosaurs,” says Dr. Mónica Solórzano-Kraemer of the Senckenberg Research Institute and Natural History Museum. “Rather, our current study is a structured attempt to determine how long the DNA of insects enclosed in resinous materials can be preserved.”
Not too much here, but longevity research fans might like.
Time may be our worst enemy, and aging its most powerful weapon. Our hair turns gray, our strength wanes, and a slew of age-related diseases represent what is happening at the cellular and molecular levels. Aging affects all the cells in our body’s different tissues, and understanding its impact would be of great value in fighting this eternal enemy of all ephemeral life forms.
The key is to first observe and measure. In a paper published in Cell Reports, scientists led by Johan Auwerx at EPFL started by asking a simple question: how do the tissues of aging mice differ from those of mice that are mere adults?
Continue reading “Understanding the effect of aging on the genome” »
A newly identified genetic factor allows adult skin to repair itself like the skin of a newborn babe. The discovery by Washington State University researchers has implications for better skin wound treatment as well as preventing some of the aging process in skin.
In a study, published in the journal eLife on Sept. 29, the researchers identified a factor that acts like a molecular switch in the skin of baby mice that controls the formation of hair follicles as they develop during the first week of life. The switch is mostly turned off after skin forms and remains off in adult tissue. When it was activated in specialized cells in adult mice, their skin was able to heal wounds without scarring. The reformed skin even included fur and could make goose bumps, an ability that is lost in adult human scars.
“We were able to take the innate ability of young, neonatal skin to regenerate and transfer that ability to old skin,” said Driskell, an assistant professor in WSU’s School of Molecular Biosciences. “We have shown in principle that this kind of regeneration is possible.”
David Sinclair wants to slow down and ultimately reverse aging. Sinclair sees aging as a disease and he is convinced aging is caused by epigenetic changes, abnormalities that occur when the body’s cells process extra or missing pieces of DNA. This results in the loss of the information that keeps our cells healthy. This information also tells the cells which genes to read. David Sinclair’s book: “Lifespan, why we age and why we don’t have to”, he describes the results of his research, theories and scientific philosophy as well as the potential consequences of the significant progress in genetic technologies.
At present, researchers are only just beginning to understand the biological basis of aging even in relatively simple and short-lived organisms such as yeast. Sinclair however, makes a convincing argument for why the life-extension technologies will eventually offer possibilities of life prolongation using genetic engineering.
#DigitalTheology #TheologyofDigitalPhysics #PhenomenalConsciousness #CosmicSelf #HolographicPrinciple #DigitalPhysics #theology #pantheism #consciousness
Since we live in a world which isn’t random, but organized at every level, a role for consciousness seems unavoidable. The ‘digital theologian’ shows us compelling evidence from quantum mechanics, mathematics and computer sciences, which not only aligns with a philosophical worldview of the Primacy of Consciousness, but which also assigns a role to information as its modus operandi.
It is quantum mechanics which appears to connect the Universe as a whole to consciousness. A whole, which is more than the sum of its parts and irreducible to mere assumptions deriving from the anatomizing dissection into mental confabulations. Drawing from the holographic principle, perceptroniums and noocentrism, Alex provides crucial keys to unlock the mystery of consciousness to show us how our local consciousness can arise from a non-local cosmic consciousness network.
Continue reading “Theology of Digital Physics: The Universe of Conscious Minds” »
Summary: PLCG2-P522R, a genetic variant that protects against Alzheimer’s disease, enhances key functions of immune cells.
Source: University of Eastern Finland
A new study conducted by researchers at the University of Eastern Finland found that the PLCG2-P522R genetic variant, which protects against Alzheimer’s disease, enhances several key functions of immune cells. The results obtained in the study highlight the importance of immune cells as a target of future development of new therapies for Alzheimer’s disease.
11 epigenetic clocks have been published since 2011, but which is best for predicting aging and age-related disease? In this video, I present findings from a recent publication, “Underlying features of epigenetic aging clocks in vitro and in vivo”, that compared data for 11 epigenetic clocks, and derived a new epigenetic clock, the meta-clock.
