Lifeboat Foundation

Aera Therapeutics, a startup launched by the CRISPR pioneer Feng Zhang last year to solve one of the biggest bottlenecks in genetic medicine, has laid off a quarter of its staff, the company confirmed to STAT.

The layoffs come as the biotech market remains mired in a now nearly three-year-long downturn that has left startups struggling to attract both private and public funds. Aera attributed the layoffs to those headwinds and indicated it had axed a portion of the company dedicated to developing new gene-editing enzymes.

“In 2023, Aera launched to pursue an ambitious mission to develop transformative genetic medicines by harnessing enabling delivery technologies and precision payloads,” spokesman Dan Budwick said in a statement. “Although Aera remains in a strong cash position today, given the current biotech funding environment, we have chosen to take steps to focus our strategy and investments on the development of our novel delivery platforms, thereby further extending our cash runway.”

Radon, a naturally occurring radioactive gas produced when metals like uranium or radium break down in rocks and soil, is a known cause of lung cancer. Now new research has found exposure to high levels of this indoor air pollutant is associated with an increased risk of another condition in middle age to older female participants with ischemic stroke. The study is published in the January 3, 2024, online issue of Neurology, the medical journal of the American Academy of Neurology. Ischemic stroke is caused by a blockage of blood flow to the brain and is the most common type of stroke.

The condition, called clonal hematopoiesis of indeterminate potential (CHIP), develops when some hematopoietic stem cells, the building blocks for all blood cells, undergo genetic mutations as a person ages. Cells with such mutations replicate more quickly than cells without them. Previous research has shown people with CHIP may have a higher risk of blood cancers like leukemia and cardiovascular disease including stroke.

Continue reading “Is Radon linked to health condition other than lung cancer?” »

Over the past decades, scientists have made substantial progress unveiling the underlying mechanisms behind many psychiatric disorders. Every year, new genetic mutations or protein dysregulations are identified as potential culprits for the symptoms and sometimes even the root causes of complex neurological diseases, including autism spectrum disorder (ASD), schizophrenia, and Alzheimer’s.

Despite these efforts, the precise roles of several proteins involved in brain function remain obscure. Such is the case for indoleamine 2,3-dioxygenase 2 (IDO2), an enzyme expressed in the brain and metabolized by the tryptophan–kynurenine pathway (TKP).

Changes in the metabolites of this pathway have already been linked to many psychiatric disorders, and genetically modified mice have been invaluable tools in such studies. However, the detailed functions of IDO2 in the brain are not known.

In a recent study published in Molecular Psychiatry, researchers explored the effects of a small humanin-like peptide 2 (SHLP2) variant on mitochondrial function.

Mitochondria are implicated in Parkinson’s disease (PD) pathogenesis. Mitochondrial-derived peptides (MDPs) are microproteins encoded from small open reading frames (sORFs) in the mitochondrial DNA (mtDNA). SHLP2 is an MDP with an essential role in multiple cellular processes, and it improves mitochondrial metabolism by increasing biogenesis and respiration and reducing oxidation.

Recent studies link mitochondrial single nucleotide polymorphisms (mtSNPs) within coding regions of MDPs to age-related deficits. For instance, m.2706 A G, an mtSNP in humanin, predicts reduced circulating levels of humanin and worse cognitive decline. Moreover, another mtSNP, m.2158 T C, is associated with reduced PD risk, albeit the underlying mechanisms are unknown.

Animals exhibit a diverse behavioral repertoire when exploring new environments and can learn which actions or action sequences produce positive outcomes. Dopamine release upon encountering reward is critical for reinforcing reward-producing actions^{1 – 3}. However, it has been challenging to understand how credit is assigned to the exact action that produced dopamine release during continuous behavior. We investigated this problem with a novel self-stimulation paradigm in which specific spontaneous movements triggered optogenetic stimulation of dopaminergic neurons. Dopamine self-stimulation rapidly and dynamically changes the structure of the entire behavioral repertoire. Initial stimulations reinforced not only the stimulation-producing target action, but also actions similar to target and actions that occurred a few seconds before stimulation. Repeated pairings led to gradual refinement of the behavioral repertoire to home in on the target. Reinforcement of action sequences revealed further temporal dependencies of refinement. Action pairs spontaneously separated by long time intervals promoted a stepwise credit assignment, with early refinement of actions most proximal to stimulation and subsequent refinement of more distal actions. Thus, a retrospective reinforcement mechanism promotes not only reinforcement, but gradual refinement of the entire behavioral repertoire to assign credit to specific actions and action sequences that lead to dopamine release.

F.C. is the Director of Open Ephys Production Site.

Memorial Sloan Kettering Cancer Center (MSK) has spearheaded revolutionary research unveiling groundbreaking strides in cancer treatment and understanding disease mechanisms.

Their discoveries include CAR T cell therapy targeting specific antigens in acute myeloid leukemia (AML), insights into the genetic element LINE-1, revelations on blood stem cell regulation, and a promising immunotherapy technique targeting CD47, showcasing potential breakthroughs in cancer therapy.

In the battle against acute myeloid leukemia (AML), traditional CAR T cell therapies faced hurdles due to varying antigens in AML cells and their similarity to normal blood stem cells, risking broader immune system damage.

I believe nanomachines or new advanced rna antivirals that can target one’s own variants of viruses will be game changers to prevent future global pandemics. Also eventually new genetic engineering could allow for the end to all viruses with some sorta Omni vaccine.

Measurement(s) Pandemic-and epidemic-prone disease outbreaks Technology Type(s) Text mining using R Sample Characteristic — Organism Disease outbreaks Sample Characteristic — Environment spatiotemporal region Sample Characteristic — Location Global.

Every year I compile what I think were some important contributions to longevity research. Here is my list for 2023.\
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Intro — 00:00\
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What causes aging? — 00:32\
Hallmarks Of Aging: An Expanding Universe \
The DREAM Complex Functions As Conserved Master Regulator Of Somatic DNA-Repair Capacities \
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Biomarkers — 02:00\
The Aging Biomarker Consortium Represents A New Era For Aging Research In China\
Longitudinal fundus imaging and its genome-wide association analysis provide evidence for a human retinal aging clock\
A Foundation Model For Generalizable Disease Detection From Retinal Images\
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Cellular reprogramming — 04:30\
Chemically induced reprogramming to reverse cellular aging\
Loss of epigenetic information as a cause of mammalian aging\
In vivo reprogramming leads to premature death linked to hepatic and intestinal failure\
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Lifespan extension — 07:30\
Astaxanthin and meclizine extend lifespan in UM-HET3 male mice; fisetin, SG1002 (hydrogen sulfide donor), dimethyl fumarate, mycophenolic acid, and 4-phenylbutyrate do not significantly affect lifespan in either sex at the doses and schedules used\
Taurine deficiency as a driver of aging\
Dietary supplementation of clinically utilized PI3K p110α inhibitor extends the lifespan of male and female mice\
Optogenetic Rejuvenation Of Mitochondrial Membrane Potential Extends C. Elegans Lifespan\
Reversal Of Biological Age In Multiple Rat Organs By Young Porcine Plasma Fraction\
Multi-Omic Rejuvenation And Life Span Extension On Exposure To Youthful Circulation\
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Biotechnology — 13:50\
Intravascularly infused extracellular matrix as a biomaterial for targeting and treating inflamed tissues\
Intradermally delivered mRNA-encapsulating extracellular vesicles for collagen-replacement therapy\
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Why we age — 15:15\
Ageing as a software design flaw\
The Longevity Bottleneck Hypothesis: Could Dinosaurs Have Shaped Ageing In Present‐Day Mammals?\
Reconsidering Life History Theory Amid Infectious Diseases\
Blood Group A Enhances SARS-CoV-2 Infection\
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What’s next? — 16:50\
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There are many items missing from this list — these are only the papers I found time to read. Please post below any I missed! \
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ICYMI\
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2022 longevity papers\
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2021 longevity papers\
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Please note that The Sheekey Science Show is distinct from Eleanor Sheekey’s teaching and research roles at the University of Cambridge. The information provided in this show is not medical advice, nor should it be taken or applied as a replacement for medical advice. The Sheekey Science Show and guests assume no liability for the application of the information discussed.\
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Icons in intro; \.

Join us on Patreon! https://www.patreon.com/MichaelLustgartenPhDDiscount Links: Telomere, Epigenetic Testing: https://trudiagnostic.com/?irclickid=U-s3Ii2r7x…