UCLA HealthとUC San Franciscoの研究者らが、脳細胞内の自然な防御機構を特定した。この機構は毒性のタウ蛋白質を除去するのを助け、一部のニューロンが他のニューロンよりアルツハイマー病の損傷に抵抗する理由を潜在的に説明する可能性がある。同研究は『Cell』誌に掲載され、実験室で培養したヒトニューロンに対するCRISPRスクリーニングを用いてこのシステムを明らかにした。知見は神経変性疾患の新たな治療経路を示唆している。
科学者らは、アルツハイマー病および関連性痴呆の中核となる毒性蛋白質であるタウの清掃班として機能するCRL5SOCS4と呼ばれる蛋白質複合体を特定した。タウの蓄積はニューロンを損傷し細胞死を引き起こすが、一部の脳細胞はより大きな耐性を示す。研究チームは遺伝子サイレンシングツールであるCRISPRiを用い、ヒト幹細胞由来のニューロンにおけるタウ蓄積に対するほぼすべてのヒト遺伝子の影響をテストした。
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Researchers report that tanycytes—specialized cells lining the brain’s third ventricle—can help move tau protein from cerebrospinal fluid into the bloodstream, and that signs of tanycyte disruption in Alzheimer’s patient tissue may be associated with impaired tau removal. The findings, published March 5 in Cell Press Blue, are based on animal and cell experiments and analyses of human brain samples.
Researchers have uncovered how amyloid beta and inflammation may both trigger synapse pruning in Alzheimer's disease through a common receptor, potentially offering new treatment avenues. The findings challenge the notion that neurons are passive in this process, showing they actively erase their own connections. Led by Stanford's Carla Shatz, the study suggests targeting this receptor could preserve memory more effectively than current amyloid-focused drugs.
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A team of researchers led by Professor Yan-Jiang Wang has published a review arguing that Alzheimer's disease requires integrated treatments targeting multiple factors, not single causes. New drugs like lecanemab and donanemab offer modest benefits by slowing decline, but fall short of reversal. The paper, in Science China Life Sciences, emphasizes genetics, aging, and systemic health alongside amyloid-beta and tau proteins.
Researchers are exploring CAR T-cell therapy to slow the advancement of amyotrophic lateral sclerosis (ALS) by targeting overactive immune cells in the brain. The approach aims to reduce neuron damage without curing the disease. Early studies suggest potential benefits for other neurodegenerative conditions as well.
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Researchers at UCLA have identified senescent immune cells, dubbed 'zombie' cells, that accumulate in aging livers and contribute to fatty liver disease. By eliminating these cells in mice, the team reversed liver damage and reduced body weight, even on an unhealthy diet. The findings, published in Nature Aging, suggest similar mechanisms may drive human liver conditions.
Researchers at University College London have found that up to 93 percent of Alzheimer's cases may be linked to variants of the APOE gene, far more than previously estimated. The analysis, published in npj Dementia, also indicates that nearly half of all dementia cases could depend on this gene. The discovery underscores APOE as a key target for future treatments.