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A new long-term study of adults over 51 confirms that people who are overweight or obese at the time of a dementia diagnosis live longer than those in a normal weight range. Researchers found that individuals with class 1 obesity had a 27 percent lower risk of death after diagnosis, even when controlling for other chronic conditions and smoking. While excess weight is a known risk factor for developing dementia earlier in life, having those energy reserves appears to help the body better withstand the physiological wasting that accompanies the disease.

It is tempting to read this as a prescription to gain weight in middle age, but the authors are careful to note the study was not designed to test that question. Instead, it highlights how pre-diagnosis weight loss can distort baseline data, making normal-weight patients look sicker because they have already dropped pounds. The real takeaway is practical rather than prescriptive: nutrition deserves far more clinical attention as the disease progresses, particularly given how difficult eating becomes for many patients.

more: https://www.futurity.org/obesity-death-dementia-3348282/?utm_source=rss&utm_medium=rss&utm_campaign=obesity-death-dementia-3348282

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Yale researchers found that the epilepsy medication lacosamide, when combined with a hydrogel to deliver low doses directly into the joint, can reverse cartilage damage and relieve pain in osteoarthritis. The drug targets Nav1.7 sodium channels, proteins that become overactive in diseased cartilage cells and drive both tissue breakdown and pain signaling. Blocking this specific protein at an optimal low dose prompted chondrocytes to stop degrading tissue and start producing protective signaling proteins like HSP70 and midkine.

Treating the structural root of osteoarthritis rather than just masking symptoms has long been the elusive goal for joint disease therapies. Because these results are currently limited to preclinical testing, it remains to be seen whether this local delivery method will translate safely and effectively to human joints over the long term.

more: https://www.sciencedaily.com/releases/2026/10/261006234528.htm

my other side: ivo.blogspot.com

Researchers at UCSF have developed a two-particle system that delivers CRISPR-Cas9 gene-editing machinery directly to circulating T cells in mice. The method inserts cancer-fighting CAR instructions into a precise genomic location without removing the cells. In tests on mice with aggressive leukemia, a single injection cleared detectable cancer within two weeks.

Current CAR-T therapies require expensive, weeks-long offsite manufacturing and harsh preparatory chemotherapy. Doing this work in vivo could eventually lower costs and widen access, but moving from mice to humans introduces major safety hurdles. Without a chance for post-manufacturing quality control, researchers must be entirely certain the gene-editing machinery targets only the intended cells.

more: https://www.sciencedaily.com/releases/2026/10/261005071532.htm

my other side: ivo.blogspot.com

Sebuah studi terhadap rekam medis anak di puskesmas menemukan bahwa sekitar sepertiga pasien yang didiagnosis pneumonia sebenarnya tidak memenuhi kriteria WHO. Di antara yang diagnosisnya tepat, hanya sebagian kecil yang menerima dosis amoksisilin sesuai anjuran standar, sementara sisanya mendapat dosis terlalu rendah atau tidak diberi sama sekali.

Masalah ini tampaknya tidak bersumber dari kelalaian individu semata, melainkan tumpang tindih antara pedoman internasional dan aturan lokal di fasilitas kesehatan tingkat pertama. Kita perlu membaca temuan ini secara hati-hati karena penelitian tersebut belum memetakan panduan mana yang secara aktual dipakai oleh tenaga kesehatan di lapangan.

more: https://theconversation.com/salah-diagnosis-tak-tepat-dosis-pekerjaan-rumah-di-balik-pneumonia-anak-292446

my other side: ivo.blogspot.com

Stanford researchers found that inhibiting a protein called 15-PGDH can restore cartilage in older mice and in human tissue samples taken during joint surgeries. The protein, which accumulates with age, drives tissue degradation rather than healing. Rather than relying on stem cells, the treatment works by reverting existing cartilage cells to a more youthful state.

This is a notable shift from current osteoarthritis treatments, which focus entirely on managing pain rather than reversing tissue damage. However, the work has only been demonstrated in animals and lab-grown human samples, meaning a safe and effective drug for humans is still a long way off. We will need to see if this mechanism translates safely inside a living human joint before getting ahead of ourselves.

more: https://www.sciencedaily.com/releases/2026/10/261005011249.htm

my other side: ivo.blogspot.com