Biotech/medical – Lifeboat News: The Blog

Mar 10
2026

Abstract: BreastCancer is associated with loss of the sirtuin deacetylase SIRT2, which leads to genomic instability and carcinogenesis, but the precise mechanism has been unclear

David S. Yu & team now show SIRT2 deacetylates MRE11 facilitating DNA binding to promote DNA end resection and ATM-dependent DNA damage signaling:

The figure shows MRE11 K393 deacetylation by SIRT2 promotes DNA end resection after ionizing radiation exposure, in the osteosarcoma cell line U20S.

¹Department of Radiation Oncology and Winship Cancer Institute, Emory University School of Medicine, Atlanta, Georgia, USA.

²Department of Biology, Clark Atlanta University, Atlanta, Georgia, USA.

³Department of Biochemistry, Emory University School of Medicine, Atlanta, Georgia, USA.

Mar 10
2026

Astrocytes engineered to fight Alzheimer’s plaques

Genetically altered astrocytes reduce a cardinal pathological feature of Alzheimer’s disease

Mar 10
2026

How AI is integrated into clinical workflow lowers medical liability perception

Artificial intelligence (AI) is changing the field and practice of medicine, including legal liability and the perception of who is at fault when a patient experiences harm. “AI holds promise to improve the quality and safety of health care and to reduce errors and patient harm, but the risk of legal liability is a potential barrier for investment and development of this technology as well as the quality of care,” said Michael Bruno, professor of radiology and of medicine at Penn State College of Medicine.

Now, Bruno, working alongside a team of researchers from Brown University and Seton Hall University School of Law, found that the understanding of physician liability is influenced by the way in which AI is integrated into a clinician’s workflow. The study was published in the journal Nature Health.

The researchers presented mock jurors with a hypothetical malpractice case where a patient suffered irreversible brain damage because a radiologist didn’t detect a brain bleed from a computerized tomography (CT) scan, even though AI correctly identified the scan as abnormal.

Mar 10
2026

This Therapy Doubled Lifespan in Mice

At the 2026 Biotech Showcase during JPM Week, Immortabio revealed new data from an established aging mouse model.

The results were striking.

Senovax alone improved outcomes.
Stem cells alone performed even better.

But when combined, the therapy doubled lifespan.

Mar 10
2026

Revolutionary single shot helps with healing after a heart attack

Researchers at Texas A&M University have developed a single-injection treatment to aid heart recovery after a heart attack. Following a myocardial infarction, the heart naturally releases atrial natriuretic peptide (ANP), a hormone that reduces cardiac stress and limits long-term damage — but in insufficient quantities. To address this, the team leveraged self-amplifying RNA (saRNA) technology: a one-time intramuscular injection (administered with a standard syringe into the arm) temporarily instructs muscle cells to produce elevated levels of ANP, which then enters the bloodstream and reaches the heart over several weeks. In animal models, the treatment reduced scarring, preserved healthy heart muscle, improved pumping function, and lowered the risk of post-infarction complications. Compared to the team’s earlier approaches — such as surgically implanted cardiac patches — this method is far simpler and more practical, with the potential to meaningfully improve both clinical workflow and patient outcomes.

The new approach uses an injection that prompts the body to release a natural heart protective hormone for weeks.

Mar 10
2026

Mapping human brain cell type origin and diseases through single-cell transcriptomics

Wang P, Zhao D, Lachman HM, Zheng D. Enriched expression of genes associated with autism spectrum disorders in human inhibitory neurons. Transl Psychiatry. 2018;8:13. https://doi.org/10.1038/S41398-017-0058-6

Article PubMed PubMed Central Google Scholar

Mar 10
2026

CD36-Fatty Acid-Mediated Metastasis via the Bidirectional Interactions of Cancer Cells and Macrophages

Tumour heterogeneity refers to the complexity of cell subpopulations coexisting within the tumour microenvironment (TME), such as proliferating tumour cells, tumour stromal cells and infiltrating immune cells.

Mar 10
2026

Avoiding Dementia and Alzheimers: Twelve Key Interventions

This article reviews 12 interventions that the evidence suggests may help protect our brains as we age.

Mar 10
2026

Brain immune cells may help build Alzheimer’s plaques

A new study led by researchers from VIB and KU Leuven shows that immune cells called microglia can actively promote the formation of plaques in Alzheimer’s disease, challenging the long-standing view that these cells serve only as defenders against plaque buildup. The findings were recently published in the Proceedings of the National Academy of Sciences.

“Most studies suggest that microglia are there to clean up the brain and remove the amyloid plaques. What we discovered is that actually they’re part of the problem. They generate plaques,” says Prof. Joost Schymkowitz, co-senior author of the study at the VIB-KU Leuven Center for Neuroscience. “It was thought that plaques aggregate by themselves. And it seems that the microglia, by trying to deal with the problem, amplify it.”

Alzheimer’s disease affects nearly 55 million people worldwide and is characterized by the accumulation of toxic protein aggregates in the brain known as amyloid plaques. These plaques are associated with neuronal death and progressive dementia. The brain’s microglia have been hailed as protectors against plaque accumulation in the disease, being the focus of several therapies. Nonetheless, the study shows how microglia are active producers of amyloid plaques in the earlier stages of the disease, reconsidering the therapeutic paradigm for Alzheimer’s.

Mar 10
2026

TREM2 in neurodegeneration and diseases

Triggering receptor expressed on myeloid cells 2 (TREM2) is a cell surface transmembrane receptor from the TREM receptor family, predominantly expressed on the microglia in the central nervous system (CNS). TREM2-initiated signaling plays a crucial role in regulating neuroinflammation and neurodegeneration, particularly in the context of neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD), through the activation of downstream signaling pathways and transcriptional regulation of relevant genes. In this review, we aim to provide a concise review of the role and mechanistic implications of TREM2 in neurodegeneration and neuroinflammation, with a specific focus on AD and PD. We will discuss the most recent preclinical studies to highlight current advancements in the field. This review is intended to support both basic researchers and clinicians by enhancing their understanding of microglial function in the pathophysiology of AD and PD, as well as its role in neuroinflammation and neurodegeneration. Ultimately, we hope this contribution will pave the way for new discoveries and the development of potential therapeutic interventions.

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