Lifeboat Foundation

Wake Forest Institute for Regenerative Medicine (WFIRM) scientists working on CRISPR/Cas9-mediated gene editing technology have developed a method to increase efficiency of editing while minimizing DNA deletion sizes, a key step toward developing gene editing therapies to treat genetic diseases.

CRISPR (clustered regularly interspaced short palindromic repeats) technology is used to alter DNA sequences and modify gene function. CRISPR/Cas9 is an enzyme that is used like a pair of scissors to cut two strands of DNA at a specific location to add, remove or repair bits of DNA. By modifying gene function, scientists hope to treat genetic diseases by halting a diseased cell’s ability to continue replicating the defective DNA. CRISPR/Cas9 is the most versatile genetic manipulation available and has a wide range of potential applications. While CRISPR/Cas9 mainly generates short insertions or deletions at the target site, it may also make large DNA deletions around the specific target site. These large deletions cause safety concerns and may decrease functional editing efficiency.

The WFIRM team is looking for ways to reduce the chances of this happening. The research described in their recent paper, published recently in Nucleic Acids Research, sought to address the generation of unpredictable on-target long DNA deletions and find a way to guard against them, said lead author Baisong Lu, Ph.D., of WFIRM.

Amid much speculation and research about how our genetics affect the way we age, a University of California, Berkeley, study now shows that individual differences in our DNA matter less as we get older and become prone to diseases of aging, such as diabetes and cancer.

In a study of the relative effects of genetics, aging and the environment on how some 20,000 human genes are expressed, the researchers found that aging and environment are far more important than genetic variation in affecting the expression profiles of many of our genes as we get older. The level at which genes are expressed — that is, ratcheted up or down in activity — determines everything from our hormone levels and metabolism to the mobilization of enzymes that repair the body.

“How do your genetics — what you got from your sperm donor and your egg donor and your evolutionary history — influence who you are, your phenotype, such as your height, your weight, whether or not you have heart disease?” said Peter Sudmant, UC Berkeley assistant professor of integrative biology and a member of the campus’s Center for Computational Biology. “There’s been a huge amount of work done in human genetics to understand how genes are turned on and off by human genetic variation. Our project came about by asking, ‘How is that influenced by an individual’s age?’ And the first result we found was that your genetics actually matter less the older you get.”

28 to 34% lifespan increase in mice. I wonder if there would be side effects as a recent study showed Rapamycin and Metformin canceled each other’s side effects.

In a new study published in Aging Cell, researchers have tested several individual drugs and a combination of rapamycin plus acarbose as potential life extension agents in genetically heterogeneous mice [1].

Identification of successful anti-aging interventions is arguably one of the most challenging research problems to date. In addition to the complexity of aging, researchers have to deal with the biological heterogeneity of animals even within the same species and research reproducibility issues due to different experimental designs and approaches.

Continue reading “Combination of Rapamycin and Acarbose Extends Lifespan” »

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Continue reading “Improve Lung Function, Reduce Blood Pressure, Slow Brain Aging?” »

In a study involving marmosets, a primate genetically similar to humans, researchers have come closer to understanding brain evolution.

Summary: Administering a chemical compound called synthetic retinoids to the retina helped restore brain networks associated with vision and prompted the growth of two times more neurons, effectively restoring vision in adult mouse models of the genetic visual disorder LCA.

Source: UC Irvine.

A discovery about how some visually impaired adults could start to see offers a new vision of the brain’s possibilities.

Summary: Brain organoids are helping researchers map the molecular, genetic, and structural changes that occur during brain development.

Source: ETH Zurich.

The human brain is probably the most complex organ in the entire living world and has long been an object of fascination for researchers. However, studying the brain, and especially the genes and molecular switches that regulate and direct its development, is no easy task.

NIH researchers reveal new insights on how genetic architecture determines gene expression, tissue-specific function, and disease phenotype in blinding diseases.

National Eye Institute (NEI) scientists have mapped the organization of human retinal cell chromatin. These are the fibers that package 3 billion nucleotide-long DNA

Continue reading “New Insights Into Eye Diseases: 3D Map Reveals DNA Organization Within Human Retina Cells” »

Two groundbreaking studies recently published in the journals Nature and Genome Medicine found genetic signatures that explain ethnic disparities in the severity of prostate cancer, notably in Sub-Saharan Africa.

By genetically analyzing prostate cancer tumors from Australian, Brazilian, and South African donors, the team developed a new prostate cancer taxonomy (classification scheme) and cancer drivers that not only distinguish patients based on their genetic ancestry but also predict which cancers are likely to become life-threatening, a task that is currently difficult.

“Our understanding of prostate cancer has been severely limited by a research focus on Western populations,” said senior author Professor Vanessa Hayes, genomicist and Petre Chair of Prostate Cancer Research at the University of Sydney’s Charles Perkins Centre and Faculty of Medicine and Health in Australia. “Being of African descent, or from Africa, more than doubles a man’s risk for lethal prostate cancer. While genomics holds a critical key to unraveling contributing genetic and non-genetic factors, data for Africa has till now, been lacking.”