最新研究顯示阿茲海默症與腦細胞的 DNA 變化有關
New study links Alzheimer's disease to DNA changes in brain cells
Updated at: September 14, 2026 at 03:00 AM
數十年來，科學家將阿茲海默症視為大腦中蛋白質纏結與斑塊堆積所致。
For decades, scientists viewed Alzheimer's disease primarily as a result of protein tangles and plaques clogging the brain.
然而，突破性的新研究顯示真相更為深層：存在於我們DNA的結構之中。
However, groundbreaking new research suggests the truth lies deeper: within the very structure of our DNA.
近期的研究揭示，阿茲海默症與基因組不穩定性（即腦細胞內的DNA受損且混亂的狀態）有根本性的連結。
A recent study reveals that Alzheimer's is fundamentally linked to genomic instability—a state where the DNA inside brain cells becomes damaged and disorganized.
受影響的大腦中的基因組並非一成不變的藍圖，而是經歷著持續且有害的變化。
Instead of remaining a static blueprint, the genome in affected brains undergoes constant, harmful changes.
這些變化包括由氧化壓力引起的體細胞突變、擾亂基因表現的結構重組，以及改變腦細胞功能的表觀遺傳轉變。
These include somatic mutations caused by oxidative stress, structural rearrangements that disrupt gene expression, and epigenetic shifts that alter how brain cells function.
甚至大腦的免疫細胞——微膠細胞，也顯現出受損跡象，引發了一場進一步降低神經元健康的發炎循環。
Even the brain's immune cells, the microglia, show signs of damage, creating a cycle of inflammation that further degrades neuronal health.
重要的是，這種損害因大腦修復機制的失效而加劇。
Importantly, this damage is compounded by the brain’s failing repair mechanisms.
這一典範轉移顯示，阿茲海默症不僅是蛋白質錯誤折疊的問題，更是基因組完整性的系統性失效。
This paradigm shift suggests that Alzheimer’s is not just a protein-misfolding issue but a systemic failure of genomic integrity.
透過超越傳統觀點，研究人員現在正尋找新的治療標靶，例如支持少突膠質細胞的健康並穩定基因組，為解決這種複雜疾病的根源提供了治療上的新希望。
By moving beyond traditional views, researchers are now looking toward new therapeutic targets, such as supporting oligodendrocyte health and stabilizing the genome, offering fresh hope for treatments that could address the root causes of this complex disease.
