Lifeboat Foundation

A, C57BL/6J mice were genetically engineered using CRISPR–Cas9 genomic editing to encode 288L and 330R in mDPP4 on one chromosome (heterozygous, 288/330^+/−) or on both chromosomes (homozygous, 288/330^+/+). b, Northern blot of mDPP4 mRNA expression. c, Immunohistochemistry (IHC) of mDPP4 protein in the lungs, brain and kidneys of individual C57BL/6J wild-type (WT), 288/330^+/− and 288/330^+/+ mice. d, Viral titres for MERS-CoV at 3 days post-infection from C57BL/6J WT, 288/330^+/− and 288/330^+/+ (all n = 4) mice infected with 5 × 10⁵ plaque-forming units (p.f.u.) of the indicated viruses. Bar graphs show means + s.d.

If you look up ‘scientific overachiever’ in the dictionary, you’re likely to find a two-word definition: George Church.

The American geneticist, molecular engineer, and chemist splits his time between roles as Professor of Genetics at Harvard Medical School and Professor of Health Sciences and Technology at Harvard and MIT. He’s also a member of the National Academy of Sciences, acts as an advisor to a plethora of cutting edge companies, and heads up synthetic biology at the Wyss Institute for Biologically Inspired Engineering, of which he’s a founding member.

Oh, and George is author to hundreds of published papers, 60 patents and a popular science book (also, theoretically, George Church may live in an alternate reality where there are more than 24 hours in a day).

“Tim Crow must be proud to see his theory being tested at a complex level.” That’s how I tweeted the news on a recent Brain article by van den Heuvel et al (2019). Tim Crow’s theory on schizophrenia as a possible by-product of human brain evolution was quite inspiring and led to many fruitful discussions in our evolutionary psychiatry group when I was a junior trainee (which I wrote about a while ago: EPSIG Newsletter, June 2018). And here it was, the theory was tested by using novel methodology. Now I am pleased to say that the article did not disappoint, so I can enjoy the initial thrill and share my take with the Mental Elf World.

Tim Crow’s original question was intriguing: “Is schizophrenia the price that Homo sapiens pay for language?” (Crow, 1997). He argued that schizophrenia may be considered an extreme variation of brain systems which are relatively new in evolutionary timescale. Brain structures that are mostly implicated in schizophrenia were also unique to humans as mediators of language and higher cognitive functions. Those relatively new (in evolutionary timescale) brain systems may be more vulnerable to insults (e.g. stress, trauma, neurodevelopmental conditions) and manifest as dysfunctional brain circuits in schizophrenia.

The prevalence of schizophrenia is fairly constant across human populations (Jablensky et al. 1992), and the prevalence does not change despite low fecundity rates of people with schizophrenia. This can only be possible in the case of overall genetic predisposition across the population.

Interesting research paper on a new nanobot technology. I’m watching for ways in which suitable substrates for mind uploading can be constructed, and DNA self-guided assembly has potential.

Here are some excerpts and a weblink to the paper:

“…Chemical approaches have opened synthetic routes to build dynamic materials from scratch using chemical reactions, ultimately allowing flexibility in design…”

Continue reading “Dynamic DNA material with emergent locomotion behavior powered by artificial metabolism” »

Scientists at Rutgers University-Newark have discovered that when a key protein needed to generate new brain cells during prenatal and early childhood development is missing, part of the brain goes haywire—causing an imbalance in its circuitry that can lead to long-term cognitive and movement behaviors characteristic of autism spectrum disorder.

“During brain development, there is a coordinated series of events that have to occur at the right time and the right place in order to establish the appropriate number of cells with the right connections,” said Juan Pablo Zanin, Rutgers-Newark research associate and lead author on a paper published in the Journal of Neuroscience.” Each of these steps is carefully regulated and if any of these steps are not regulated correctly, this can impact behavior.”

Zanin has been working with Wilma Friedman, professor of cellular neurobiology in the Department of Biological Sciences, studying the p75NTR protein—needed to regulate cell division—to determine its exact function in brain development, gain a better understanding of how this genetic mutation could cause brain cells to die off and discover whether there is a genetic link to autism or neurological diseases like Alzheimer’s.

Findings from a recent research project, conducted by a Marshall University scientist and assistant professor in the Marshall University College of Science, with researchers in Texas, was recently published in the December issue of the prestigious online journal, Nature Communications.

Dr. Eugene Shakirov is studying the connection between ribosomes and telomeres in plants. Telomeres are the physical ends of chromosomes and they shorten with age in most cells. Accelerated shortening of telomeres is linked to age-related diseases and overly long telomeres are often linked to cancer.

Telomere length varies between individuals at birth and is known to predetermine cellular lifespan, but the genes establishing telomere length variations are largely unknown. The research being done by Shakirov, along with collaborators at the University of Texas at Austin, Texas A&M University, HudsonAlpha Institute for Biology and the Kazan Federal University in Russia focused on the study of the genetic and epigenetic causes of natural telomere length variation in Arabidopsis thaliana, a small flowering plant.

Scientists at the MDI Biological Laboratory, in collaboration with scientists from the Buck Institute for Research on Aging in Novato, Calif., and Nanjing University in China, have identified synergistic cellular pathways for longevity that amplify lifespan fivefold in C. elegans, a nematode worm used as a model in aging research.

The increase in lifespan would be the equivalent of a human living for 400 or 500 years, according to one of the scientists.

The research draws on the discovery of two major pathways governing aging in C. elegans, which is a popular model in aging research because it shares many of its genes with humans and because its short lifespan of only three to four weeks allows scientists to quickly assess the effects of genetic and environmental interventions to extend healthy lifespan.

Scientists at the MDI Biological Laboratory, in collaboration with scientists from the Buck Institute for Research on Aging in Novato, Calif., and Nanjing University in China, have identified synergistic cellular pathways for longevity that amplify lifespan fivefold in C. elegans, a nematode worm used as a model in aging research.

The increase in lifespan would be the equivalent of a human living for 400 or 500 years, according to one of the scientists.

The research draws on the discovery of two major pathways governing aging in C. elegans, which is a popular model in aging research because it shares many of its genes with humans and because its short lifespan of only three to four weeks allows scientists to quickly assess the effects of genetic and environmental interventions to extend healthy lifespan.