Aggregator
Scorpions reinforce their most lethal weapons with metal
Arachnids infuse zinc into their claws or stingers—whichever they depend on most while hunting
Daily briefing: AI forces us to rethink maths, says Fields medallist
Key US science panels are being axed — and others are becoming less open
The politics of playful primates
First detailed ‘smell maps’ reveal how noses track odours
AI data hubs in space: when will they take flight?
Why both trees and technology are important in the race to mitigate carbon emissions
Space diplomacy: bridging the operating gaps between myriad missions
‘World models’ are AI’s latest sensation: what are they and what can they do?
Rhymes on reason: scientific units inspire poetry
Hungarian science has undergone rapid changes
Gulf states must move from efficiency to resilience
To hire good scientists, look at their peer-reviewing records
The equity paradox of environmental DNA for biodiversity monitoring
Author Correction: Quantum error correction below the surface code threshold
China’s latest push to commercialize research: match 680,000 innovators with companies
Fauci aide indicted over federal records violations related to COVID-19
David Morens could face prison time for allegedly concealing back-channel efforts to help nonprofit accused of starting pandemic
Famed Brazilian dinosaur fossil finally heads home
Germany and Brazil reach agreement over controversial spinosaurid fossil, heralding new collaboration between the two nations
Mitochondrial-nuclear crosstalk: A central axis in Alzheimer's disease
Alzheimer's disease (AD) is a progressive neurodegenerative disorder traditionally defined by amyloid-β plaques and tau tangles. However, growing evidence indicates that deeper disruptions in cellular homeostasis contribute to disease onset and progression. Among these, impaired communication between mitochondria and the nucleus has emerged as a central yet underrecognized pathological feature. Mitochondrial-nuclear (mito-nuclear) crosstalk regulates energy metabolism, stress responses, and...
The PM20D1-OLE pathway induces microglia rewiring to ameliorate Alzheimer disease
There is increasing evidence of microglia participation in Alzheimer's disease (AD), which incentives their modulation to intercept the disease. Here, we describe a new mechanism by which the recently AD-associated Peptidase M20 Domain Containing 1 (PM20D1) instructs microglia to tackle AD. We show that the PM20D1-derived N-oleoyl-Leucine (OLE) improves AD pathologies in two animal models of AD. OLE induces microglia association with amyloid beta (Aβ) plaques, reduce their size, number and...