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Johns Hopkins Medicine neuroscientists say they have found a new function for the SYNGAP1 gene, a DNA sequence that controls memory and learning in mammals, including mice and humans.

The finding, published in Science, may affect the development of therapies designed for children with SYNGAP1 mutations, who have a range of neurodevelopmental disorders marked by intellectual disability, autistic-like behaviors, and epilepsy.

In general, SYNGAP1, as well as other genes, control learning and memory by making proteins that regulate the strength of synapses—the connections between brain cells.

Researchers at the Centre for Genomic Regulation (CRG) have found that the Snhg11 gene is critical for the function and formation of neurons in the hippocampus. Experiments with mice and human tissues revealed that the gene is less active in brains with Down syndrome, potentially contributing to the memory deficits observed in people living with the condition. The findings are published in the journal Molecular Psychiatry.

Traditionally, much of the focus in genomics has been on protein-coding genes, which in humans constitute around just 2% of the entire genome. The rest is “dark matter,” including vast stretches of non-coding DNA sequences that do not produce proteins but are increasingly recognized for their roles in regulating gene activity, influencing genetic stability, and contributing to complex traits and diseases.

Snhg11 is one gene found in the dark matter. It is a long non-coding RNA, a special type of RNA molecule that is transcribed from DNA but does not encode for a protein. Non-coding RNAs are important regulators of normal biological processes, and their abnormal expression has been previously linked to the development of human diseases, such as cancer. The study is the first evidence that a non-coding RNA plays a critical role in the pathogenesis of Down syndrome.

Factors that affect include genes, education, nutrition, and others. Learn more about how genetics impacts

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Strategies differ, but there are some gene edits that all researchers agree must underpin any universal stem-cell-derived therapy. There is also widespread consensus that the optimal product should incorporate as few edits as possible, both to minimize the potential for unintended genetic consequences and to streamline manufacturing and regulatory approval.

Beyond that, the scientific community is divided. The complexities of the immune system have fuelled spirited debates over the exact genetic manipulations necessary to create a cell therapy that is both capable of bypassing immune defences and delivering meaningful health benefits.

“The immune system is pervasive and persistent,” says Charles Murry, a cardiovascular pathologist at the University of Washington in Seattle and chief executive of StemCardia in Seattle, one of a growing number of biotechnology companies developing gene-editing strategies to overcome immune barriers in regenerative cell treatments.

Professor Ronjon Nag presents about his project on AI and healthcare, aiming at creating a multi-faceted approved therapy for extending lifespan and curing aging.

Dr. Ronjon Nag is an inventor, teacher and entrepreneur. He is an Adjunct Professor in Genetics at the Stanford School of Medicine, becoming a Stanford Distinguished Careers Institute Fellow in 2016. He teaches AI, Genes, Ethics, Longevity Science and Venture Capital. He is a founder and advisor/board member of multiple start-ups and President of the R42 Group, a venture capital firm which invests in, and creates, AI and Longevity companies. As an AI pioneer of smartphones and app stores, his companies have been sold to Apple, BlackBerry, and Motorola. More recently he has worked on the intersection of AI and Biology. He has numerous interests in the intersection of AI and Healthcare including being CEO of Agemica.ai working on creating a therapy for aging.

Continue reading “Can We CURE AGING In 7 YEARS With Combination Therapy??” »

Cytotoxic T-lymphocytes are important effectors in the clearance of virally infected and cancerous cells, and defects in their function give rise to many pathologies.

Cytotoxic T lymphocytes (CTLs) are key effectors of the adaptive immune system that recognize and eliminate virally infected and cancerous cells. In naive CD8⁺ T cells, T-cell receptor (TCR) engagement drives a number of transcriptional, translational and proliferation changes over the course of hours and days leading to differentiation into CTLs. To gain a better insight into this mechanism, we compared the transcriptional profiles of naive CD8⁺ T cells to those of activated CTLs. To find new regulators of CTL function, we performed a selective clustered regularly interspaced short palindromic repeats (CRISPR) screen on upregulated genes and identified nuclear factor IL-3 (NFIL3) as a potential regulator of cytotoxicity. Although NFIL3 has established roles in several immune cells including natural killer, Treg, dendritic and CD4⁺ T cells, its function in CD8⁺ CTLs is less well understood. Using CRISPR/Cas9 editing, we found that removing NFIL3 in CTLs resulted in a marked decrease in cytotoxicity. We found that in CTLs lacking NFIL3 TCR-induced extracellular signal-regulated kinase phosphorylation, immune synapse formation and granule release were all intact while cytotoxicity was functionally impaired in vitro. Strikingly, NFIL3 controls the production of cytolytic proteins as well as effector cytokines. Thus, NFIL3 plays a cell intrinsic role in modulating cytolytic mechanisms in CTLs.

CD8⁺ cytotoxic T lymphocytes (CTLs) are key effectors of the adaptive immune response that precisely recognize and eliminate virally infected and cancerous cells. In naive CD8⁺ T cells, T-cell receptor (TCR) engagement induces a number of transcriptional, translational and proliferation changes over the course of hours and days leading to differentiation into CTLs [1,2]. TCR ligation of differentiated CTLs drives a rapid response and the formation of a transient area of plasma membrane specialized in signalling and polarized secretion, termed the immune synapse [3]. CTLs undergo rapid rearrangements in microtubule and actin cytoskeletons as the centrosome and microtubule network polarize towards the synapse and cortical actin is transiently depleted [4–7].

Early language development is an important predictor of children’s later language, reading and learning skills. Moreover, language learning difficulties are related to neurodevelopmental conditions such as attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD).

Children typically start to utter their first words between 10 and 15 months of age. At around two years of age, they may produce between 100–600 words, and understand many more. Each child embarks on its own developmental path of language learning, resulting in large individual differences. “Some variation in language development can be related to variation in the genetic code stored in our cells,” says senior researcher Beate St Pourcain, lead scientist on the study.

Because identical twins develop from a single fertilized egg, they have the same genome, the entire set of genetic material found in an organism. So, any differences between them, even in traits with a significant genetic component – say one develops heart disease and the other doesn’t – are due to their environments. This is known as epigenetics.

Genes in DNA are ‘expressed’ when they’re read and transcribed into RNA, which is then translated into proteins. It’s proteins that determine many of a cell’s characteristics and functions. Epigenetic changes can boost or silence the transcription of specific genes, ramping up or inhibiting associated protein production, but they don’t change the genome. These changes, which are reversible, can affect a person for their entire life and mediate a lifelong dialogue between genes and the environment.