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MRI age clocks reveal how each organ ages differently and predict who develops disease or lives longer

Researchers developed seven MRI-based biological age clocks across major organs using UK Biobank imaging, linking each to proteins, metabolites, genetics, disease risks, mortality, and cognitive decline. These organ-specific age gaps reveal how uneven aging shapes vulnerability to conditions such as diabetes, hypertension, and dementia, opening new paths for precision prevention and clinical trial stratification

MIT’s new precision gene editing tool could transform medicine

MIT scientists have found a way to make gene editing far safer and more accurate — a breakthrough that could reshape how we treat hundreds of genetic diseases. By fine-tuning the tiny molecular “tools” that rewrite DNA, they’ve created a new system that makes 60 times fewer mistakes than before.

Disease-associated radial glia-like cells with epigenetically dysregulated interferon response in MS

Li et al. report that Edwardsiella piscicida employs HigA, an anti-toxin protein, to facilitate the diversion of tryptophan metabolism to the kynurenine pathway, rather than the serotonin pathway, by directly activating IDO1 in a T6SS-dependent manner as a cross-kingdom effector. The serotonin-level fluctuation modulates host intestinal histological damage and bacterial infection.

How To Track And Optimize Biomarkers: Blood Test #6 in 2025

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Discount Links/Affiliates:
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Epigenetic, Telomere Testing: https://trudiagnostic.com/?irclickid=U-s3Ii2r7xyIU-LSYLyQdQ6…M0&irgwc=1
Use Code: CONQUERAGING

NAD+ Quantification: https://www.jinfiniti.com/intracellular-nad-test/

Tyk2 Targeting in Immune-Mediated Inflammatory Diseases

The Janus kinase (Jak)/signal transducer and activating protein (STAT) pathways mediate the intracellular signaling of cytokines in a wide spectrum of cellular processes. They participate in physiologic and inflammatory cascades and have become a major focus of research, yielding novel therapies for immune-mediated inflammatory diseases (IMID). Genetic linkage has related dysfunction of Tyrosine kinase 2 (Tyk2)—the first member of the Jak family that was described—to protection from psoriasis. Furthermore, Tyk2 dysfunction has been related to IMID prevention, without increasing the risk of serious infections; thus, Tyk2 inhibition has been established as a promising therapeutic target, with multiple Tyk2 inhibitors under development.

🌿 International Conference “Anti-Aging: Science and Practice of Healthy Longevity” —

October 21–22, 2025 (Online) 🌿

Dear colleagues and friends.

We are pleased to invite you to the International Scientific Conference “Anti-Aging: Science and Practice of Healthy Longevity”, organized by the Gerontology Section of the Moscow Society of Naturalists (MOIP) at Lomonosov Moscow State University, with the support of the Gerontology Society of the Ural Branch of the Russian Academy of Sciences (URAN).

📅 Dates: October 21–22, 2025 🕛 Time: 12:00–16:00 (Moscow time) 💻 Format: Online participation (free of charge) 🗣️ Working language: Russian.

🔹 October 21 — “Hypoxic Training (Therapy): Modern Aspects of Healthy Longevity Medicine” 🔹 October 22 — “Fundamental and Clinical Gerontology as the Basis of Healthy Longevity Medicine”

The conference will feature leading scientists from Russia, Germany, Belarus, Kyrgyzstan and other countries. Topics include: • Hypoxic therapy and adaptive mechanisms; • Geroprotection and the biology of aging; • Epigenetic reprogramming and cellular rejuvenation; • Applied aspects of active and healthy longevity.

🔗 Connection links: • Day 1 (October 21): https://my.mts-link.ru/j/38630705/5798697072

Surprising gene mutation in brain’s immune cells linked to increased Alzheimer’s risk

In a study published in Neuron, a research team at the Department of Neurology at Massachusetts General Hospital, aimed to understand how immune cells of the brain, called microglia, contribute to Alzheimer’s disease (AD) pathology. It’s known that subtle changes, or mutations, in genes expressed in microglia are associated with an increased risk for developing late-onset AD.

The study focused on one such mutation in the microglial gene TREM2, an essential switch that activates microglia to clean up toxic amyloid plaques (abnormal protein deposits) that build up between in the brain. This mutation, called T96K, is a “gain-of-function” mutation in TREM2, meaning it increases TREM2 activation and allows the gene to remain super active.

The researchers explored how this mutation impacts microglial function to increase risk for AD. The team generated a mutant mouse model carrying the mutation, which was bred with a mouse model of AD to have brain changes consistent with AD. They found that in female AD mice exclusively, the mutation strongly reduced the capability of microglia to respond to toxic amyloid plaques, making these cells less protective against brain aging.

Genome-Wide Variation Profile of the Genus Tobamovirus

The genus Tobamovirus belongs to the family Virgaviridae, and the genome consists of monopartite, positive, single-strand RNA. Most species contain four open reading frames encoding four essential proteins. Transmission occurs primarily through mechanical contact between plants, and in some cases, via seed dispersal. Tobamovirus fructirugosum (tomato brown rugose fruit virus, ToBRFV), the most recently described species in the genus, was first reported in 2015. It overcame genetic resistance that had been effective in tomato for sixty years, causing devastating losses in tomato production worldwide, and highlights the importance of understanding Tobamovirus genomic variation and evolution. In this study, we measured and characterized nucleotide variation for the entire genome and for all species in the genus Tobamovirus.

Cancer cells reactivate embryo-like gene editors to fuel growth, research reveals

Cancer cells are known to reawaken embryonic genes to grow. A new study reveals the disease also hijacks the proteins, or “editors,” that control how those genes are read.

The findings, published in the journal Nucleic Acids Research, help explain why tumors grow so fast and adapt so well, and may point the way to new treatments.

Embryonic cells have to grow fast and must be able to transform into many different tissue types. The cells rely on genetic programs that are eventually switched off as tissues mature. Cancer reawakens these programs, giving the disease embryonic-like potential to fuel growth.

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