Associate Professor of Biological Engineering and Brain and Cognitive Sciences Ed Boyden explains optogenetics and how it is used in neurological research.
Video: Emily Heusted
Associate Professor of Biological Engineering and Brain and Cognitive Sciences Ed Boyden explains optogenetics and how it is used in neurological research.
Video: Emily Heusted
In this episode, I talk to world-renowned biologist David Sinclair about aging and longevity. David rejects the notion that the deterioration of health is a natural part of growing old and asserts that aging is a disease itself that we need to reverse. But how will a reset of our biological clocks affect our interactions, responses to adversity, morality, and how we live our lives? We discuss the ethical implications of limitless lifespans and also touch on the topics of death, evolution, genetics, medicine, and data tracking.
Bio.
Dr. David Sinclair is a professor in the department of genetics and co-director of the Paul F. Glenn Center for Biology of Aging Research at Harvard Medical School and co-founder of the scientific journal Aging. He is best known for his work on understanding why we age and how to slow its effects. In addition to being a co-founder of several biotechnology companies, he’s the author of the book Lifespan: Why We Age – and Why We Don’t Have To. Dr. Sinclair was listed by TIME magazine as one of the “100 most influential people in the world”.
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Circa 2019
Researchers of Sechenov University and University of Pittsburgh described the most promising strategies in applying genetic engineering for studying and treating Parkinson’s disease. This method can help evaluate the role of various cellular processes in pathology progression, develop new drugs and therapies, and estimate their efficacy using animal disease models. The study was published in Free Radical Biology and Medicine.
Parkinson’s disease is a neurodegenerative disorder accompanied by a wide array of motor and cognitive impairments. It develops mostly among elderly people (after the age of 55–60). Parkinson’s symptoms usually begin gradually and get worse over time. As the disease progresses, people may have difficulty controlling their movements, walking and talking and, more importantly, taking care of themselves. Although there is no cure for Parkinson’s disease, medicines, surgical treatment, and other therapies can often relieve some symptoms.
There’s also been a lot of interest in creating more versatile “living inks” made up of bacteria, which can be genetically engineered to do everything from deliver drugs to clean up pollutants. But so far, approaches have relied on mixing microbes with polymers that help provide the ink with some structural integrity.
Now, researchers have developed a new living ink that more closely lives up to the name by replacing the polymers with a protein made by genetically engineered E. coli bacteria. The researchers say this opens the door to seeding large-scale, living structures from nothing more than a simple cell culture.
The key to the breakthrough was to repurpose the proteins that E. coli cells secrete to stick together and form hard-to-shift biofilms. In a paper in Nature Communications, the researchers describe how they genetically engineered bacteria to produce two different versions of this protein known as a “knob” and a “hole,” which then lock together to form a robust cross-linked mesh.
Western intelligence agencies fear Beijing could within decades dominate all of the key emerging technologies, particularly artificial intelligence, synthetic biology and genetics.
China’s economic and military rise over the past 40 years is considered to be one of the most significant geopolitical events of recent times, alongside the 1991 fall of the Soviet Union which ended the Cold War.
MI6, depicted by novelists as the employer of some of the most memorable fictional spies from John le Carré’s George Smiley to Ian Fleming’s James Bond, operates overseas and is tasked with defending Britain and its interests.
Kind of starts out with a no but ends in a yes. Just a few minutes long.
An increasing number of studies suggest the presence of a “metabolic clock” that controls aging. This clock involves the accumulation of metabolic alterations and a decline in metabolic homeostasis and biological fitness. There are nine cellular hallmarks of aging: telomere attrition, genomic instability, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, loss of proteostasis, deregulated nutrient sensing, epigenetic alterations, and altered intercellular communication. Metabolic alterations have been implicated in each of these processes.
A new type of cell has been identified in the heart that is linked to regulating heart rate – and the discovery promises to advance our understanding of cardiovascular defects and diseases, once these cells have been more extensively studied.
The new cell is a type of glial cell – cells that support nerve cells – like astrocytes in the central nervous system (the brain and spinal cord). Named nexus glia, they’re located in the outflow tract of the heart, the place where many congenital heart defects are found.
The new cell type was first found in zebrafish, before being confirmed in mouse and human hearts too. Experiments on zebrafish found that when the cells were removed, heart rate increased; and when genetic editing blocked glial development, the heartbeat became irregular.
For the first time, researchers appear to have effectively treated a genetic disorder by directly injecting a CRISPR therapy into patients’ bloodstreams — overcoming one of the biggest hurdles to curing diseases with the gene editing technology.
The therapy appears to be astonishingly effective, editing nearly every cell in the liver to stop a disease-causing mutation.
The challenge: CRISPR gives us the ability to correct genetic mutations, and given that such mutations are responsible for more than 6,000 human diseases, the tech has the potential to dramatically improve human health.
There are synergies between the two kinds of intelligence. The brain serves the genes by improving the organism’s capability to survive and reproduce. In exchange, evolution favors genetic mutations that improve the brain’s innate and learning capacities for each species (this is why some animals are born with the ability to walk while others learn it weeks or months later).
At the same time, the brain comes with tradeoffs. Genes lose some of their control over the behavior of the organism when they relegate their duties to the brain. Sometimes, the brain can go chasing rewards that do not serve the self-replication of the genes (e.g., addiction, suicide). Also, the behavior learned by the brain does not pass on through genes (this is why you didn’t inherit your parents’ knowledge and had to learn language, math, and sports from scratch).
As Lee writes in Birth of Intelligence, “The fact that brain functions can be modified by experience implies that genes do not fully control the brain. However, this does not mean that the brain is completely free from genes, either. If the behaviors selected by the brain prevent the self-replication of its own genes, such brains would be eliminated during evolution. Thus, the brain interacts with the genes bidirectionally.”
Scientists have discovered a way to stop the COVID-19 virus from replicating in infected human cells, marking major progress towards a definitive treatment for the deadly illness and accentuating the potential of genetic engineering to cure viral diseases.
The study explores the use of CRISPR, a genome editing tool, and builds on research that started at Australia’s Peter MacCallum Cancer Center in 2019, when Dr. Mohamed Fareh and Prof. Joe Trapani showed that CRISPR could be used to eliminate abnormal RNAs that drive children’s cancers.
At the beginning of the pandemic, and in collaboration with Director Prof. Sharon Lewin and Dr. Wei Zhao from the Doherty Institute, the scientists reprogrammed the same CRISPR tool to suppress replication of the RNA virus SARS-CoV-2 — and importantly, its “variants of concern” — in a test tube model. SARS-CoV-2, which is short for Severe Acute Respiratory Syndrome Coronavirus 2, is the virus that causes COVID-19.