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--- aging [2026/08/04 08:59] – [ageing] gary1
+++ aging [2026/08/12 09:56] (current) – [why do we age?] gary1
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     * in aging and certain brain diseases, the balance of tryptophan use is disrupted. This can reduce the production of serotonin and melatonin while increasing harmful byproducts that are toxic to nerve cells. When SIRT6 levels drop, tryptophan is used more for energy production, creating toxic compounds and leaving the brain without enough protective neurotransmitters, however, an enzyme called TDO2 appears able to reduce the harmful byproducts and protect brain tissue (([[https://english.news.cn/20251221/775610872f2a45beb67d9ae45792cb73/c.html|2025: Researchers discover protein protecting brain from aging damage]]))
     * between ages 50 and 75yrs, microglia that originate during embryonic development decline substantially and are replaced by cells with molecular signatures that resemble immune cells from the blood and which exhibit elevated inflammatory signatures, suggesting they may contribute to chronic neuroinflammation in the aging human brain (([[https://www.science.org/doi/10.1126/science.adt8307|2026: Epigenetic and 3D genome reprogramming during the aging of the human hippocampus]]))
+    * a study suggests brain immune cells in senescence  begin secreting a protein called DLK1 which disrupts other brain cells, in particular neurons and the oligodendrocytes that help protect nerve fibers(([[https://www.cell.com/neuron/fulltext/S0896-6273(26)00577-5|2026: Senescent microglia with shortened telomeres secrete soluble DLK1 to induce aging-associated hypomyelination and neuronal dysfunction]]))
   * **infections can trigger cellular senescence**
     * infection-driven senescence (IDS), can help limit pathogen replication but may also prolong inflammation, reduce healing and slow recovery, particularly in older adults and during chronic infections