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Celebrate women in research and the networks that sustain them
Peanut-processing microbes ward off dangerous allergic shock
Cracked, but still there: the glass ceiling persists for senior women in science
Uncharted: understanding women’s health across the body
Climate change is speeding up — the pace nearly doubled in ten years
What a viral TikTok taught me about personal storytelling in science
The missing pieces of menopause science
Modelling the cosmos and imagining a future without meat: Books in brief
Electric-vehicle batteries toughen up to beat the heat
Briefing chat: What Galileo’s scribbled margin notes reveal about his scientific journey
The glycolytic metabolite phosphoenolpyruvate restricts cGAS-driven inflammation to promote healthy aging
Dietary restriction in aging and longevity
Mining the prodrome of neurodegeneration
A glycolytic metabolite puts the brakes on cGAS-driven aging
Genetically modified pig liver keeps man alive until human organ transplant
Career effects of preprints get mixed reviews from biomedical researchers
Junior researchers are more likely to embrace preprints; grant reviewers and hiring committees express doubts
NIH reneges on recognizing union for early-career researchers
The biomedical research agency says trainees in its labs are not “employees”
Targeting amyloid-β pathology by chimeric antigen receptor astrocyte (CAR-A) therapy
Alzheimer's disease (AD) is the leading cause of dementia and is characterized by progressive amyloid accumulation followed by tau-mediated neurodegeneration. Despite advances in anti-amyloid immunotherapies, important limitations remain, highlighting the need for new therapeutic strategies. Here, we introduce anti-amyloid chimeric antigen receptors expressed in astrocytes (CAR-A) and validate their function in vitro. We show that two CAR-A designs reduce amyloid and associated pathology after...
Astrocytes engineered to fight Alzheimer's plaques
Genetically altered astrocytes reduce a cardinal pathological feature of Alzheimer's disease.
MS4A4A and MS4A6A: New targets to enhance microglia protective function in Alzheimer's disease
MS4A4A and MS4A6A are microglia-expressed genes linked to Alzheimer's disease risk. In this issue of Neuron, Rosner et al.¹ show that these proteins cooperatively restrain TREM2 signaling, dampening protective microglial responses and highlighting MS4A inhibition as a potential strategy to rejuvenate the brain's innate immune system in Alzheimer's disease.