神经炎症
祖细胞
促炎细胞因子
骨髓
髓样
炎症
免疫学
医学
认知功能衰退
下调和上调
祖细胞
干细胞
神经干细胞
癌症研究
T细胞
移植
神经科学
认知
生物
小胶质细胞
巨噬细胞
细胞
作者
Alexander S. Harris,James A. Rouse,郭广冉,Inés Fernández-Maestre,Sujay Pal,Brian Oh,Shuxuan Li,Wen Yi See,Arianna Anderson,Joseph Gewolb,Matthew Soethout,Jill Habel,Rad Utama,Christopher R. Vakoc,Corina Amor
出处
期刊:
[Cold Spring Harbor Laboratory]
日期:2026-09-28
标识
DOI:10.64898/2026.09.27.754777
摘要
Aging is associated with progressive neuroinflammation and cognitive decline, yet the cellular sources that sustain this process and whether they can be targeted peripherally remain unclear. Here, we identify inflammatory border-associated macrophages (BAMs) as key drivers of neuroinflammation in aging and show that their therapeutic and prophylactic elimination through intrathecal CAR T cell therapy restores cognitive performance in mouse models of aging and Alzheimer's disease. Furthermore, targeting of aged inflammatory bone marrow myeloid progenitors through either intravenous CAR T cells, which do not infiltrate the brain, or through transplantation of CAR T-treated progenitors is sufficient to reduce neuroinflammation and cognitive impairment. These findings reveal that bone marrow myeloid progenitors harbor a heritable inflammatory transcriptional state that is transmitted to their BAM progeny, driving neuroinflammation and cognitive deterioration, and conserved in human aging. Critically, this proinflammatory state is marked by the upregulation of surface proteins, enabling precise peripheral CAR T cell targeting of these progenitors for long-lasting therapeutic effects in cognitive aging.
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