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Papers referenced in the video:

Motor skills learning is classically associated with brain regions including cerebral and cerebellar cortices and basal ganglia nuclei. Less is known about the role of the hippocampus in the acquisition and storage of motor skills. Here, we show that mice receiving a long-term training in the accelerating rotarod display marked hippocampal transcriptional changes and reduced pyramidal neurons activity in the CA1 region when compared with naive mice. Then, we use mice in which neural ensembles are permanently labeled in an Egr1 activity-dependent fashion. Using these mice, we identify a subpopulation of Egr1-expressing pyramidal neurons in CA1 activated in short-term (STT) and long-term (LTT) trained mice in the rotarod task. When Egr1 is downregulated in the CA1 or these neuronal ensembles are depleted, motor learning is improved whereas their chemogenetic stimulation impairs motor learning performance. Thus, Egr1 organizes specific CA1 neuronal ensembles during the accelerating rotarod task that limit motor learning. These evidences highlight the role of the hippocampus in the control of this type of learning and we provide a possible underlying mechanism.

SIGNIFICANCE STATEMENT It is a major topic in neurosciences the deciphering of the specific circuits underlying memory systems during the encoding of new information. However, the potential role of the hippocampus in the control of motor learning and the underlying mechanisms has been poorly addressed. In the present work we show how the hippocampus responds to motor learning and how the Egr1 molecule is one of the major responsible for such phenomenon controlling the rate of motor coordination performances.

O.o!!!!!


Changing the number of chromosomes an animal has can take millions of generations to happen in nature through the course of evolution – and now, scientists have been able to make these same changes in lab mice in a relative blink of an eye.

The new technique using stem cells and gene editing is a major accomplishment, and one that the team is hoping will reveal more about how the rearrangement of chromosomes can influence the way that animals evolve over time.

It’s in chromosomes – those strings of protein and DNA inside cells – that we find our genes, inherited from our parents and blended together to make us who we are.

Analysis of the genome and proteome shows that eukaryotic evolution gave rise to the regulatory function of chromatin.

Two meters of DNA

DNA, or deoxyribonucleic acid, is a molecule composed of two long strands of nucleotides that coil around each other to form a double helix. It is the hereditary material in humans and almost all other organisms that carries genetic instructions for development, functioning, growth, and reproduction. Nearly every cell in a person’s body has the same DNA. Most DNA is located in the cell nucleus (where it is called nuclear DNA), but a small amount of DNA can also be found in the mitochondria (where it is called mitochondrial DNA or mtDNA).

This finding “proved” the significance of chromosomal rearrangement, a crucial evolutionary indicator of the emergence of a new species.

Researchers from the Chinese Academy of Sciences (CAS) claim to have found a novel technique for programmable chromosome fusion successfully producing mice with genetic changes “that occur on a million-year evolutionary scale” in the laboratory.

The findings could shed light on how chromosome rearrangements—the tidy packages of organized genes provided in equal numbers by each parent, which align and trade or blend traits to produce offspring—influence evolution, reported Phys.org on Thursday.


Evolutionary chromosomal changes may take a million years in nature, but researchers are now reporting a novel technique enabling programmable chromosome fusion that has successfully produced mice with genetic changes that occur on a million-year evolutionary scale in the laboratory. The result may provide critical insights into how rearrangements of chromosomes—the tidy packages of organized genes, provided in equal number from each parent, which align and trade or blend traits to produce offspring—influence evolution.

In results published today in Science, the researchers reveal that chromosome-level engineering can be achieved in mammals, and they successfully derived a laboratory house mouse with novel and sustainable karyotype, providing critical insight into how may influence evolution.

“The laboratory house mouse has maintained a standard 40-chromosome karyotype—or the full picture of an organism’s chromosomes—after more than 100 years of artificial breeding,” said co-first author Li Zhikun, researcher in the Chinese Academy of Sciences (CAS) Institute of Zoology and the State Key Laboratory of Stem Cell and Reproductive Biology. “Over longer time scales, however, karyotype changes caused by chromosome rearrangements are common. Rodents have 3.2 to 3.5 rearrangements per million years, whereas primates have 1.6.”

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In the Existential Hope-podcast (https://www.existentialhope.com), we invite scientists to speak about long-termism. Each month, we drop a podcast episode where we interview a visionary scientist to discuss the science and technology that can accelerate humanity towards desirable outcomes.

Xhope Special with Foresight Fellow Morgan Levine.

Morgan Levine is a ladder-rank Assistant Professor in the Department of Pathology at the Yale School of Medicine and a member of both the Yale Combined Program in Computational Biology and Bioinformatics, and the Yale Center for Research on Aging. Her work relies on an interdisciplinary approach, integrating theories and methods from statistical genetics, computational biology, and mathematical demography to develop biomarkers of aging for humans and animal models using high-dimensional omics data. As PI or co-Investigator on multiple NIH-, Foundation-, and University-funded projects, she has extensive experience using systems-level and machine learning approaches to track epigenetic, transcriptomic, and proteomic changes with aging and incorporate.
this information to develop measures of risk stratification for major chronic diseases, such as cancer and Alzheimer’s disease. Her work also involves development of systems-level outcome measures of aging, aimed at facilitating evaluation for geroprotective interventions.

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Researchers at Washington University School of Medicine in St. Louis have found a new druggable pathway that potentially could be used to help prevent Alzheimer’s dementia.

Amyloid beta accumulation in the brain is the first step in the development of Alzheimer’s dementia. Scientists have poured countless hours and millions of dollars into finding ways to clear amyloid away before cognitive symptoms arise, with largely disappointing results.

In this study, published Aug. 24 in the journal Brain, researchers found a way to increase clearance of waste products from the brains of mice by ramping up a genetic quirk known as readthrough. This same strategy also may be effective for other characterized by the buildup of toxic proteins, such as Parkinson’s disease, the researchers said.

Basically this means halting and controlling cellular death which would reverse the death process :3.


During pyroptosis, gasdermin D (GSDMD) forms plasma membrane pores that initiate cell lysis. Here, the authors develop optogenetically activatable human GSDMD to assess GSDMD pore behavior and show that they are dynamic and can close, which can be a pyroptosis regulatory mechanism.