Aug 2026· Cell Metabolism· Vol 38 8, pp.
1527-1528
· 0 citations· 8 references
Medicine
TL;DR
It is shown that a brain-penetrant GLP-1 receptor agonist rewires astrocyte-neuron metabolic coupling through lactate-driven histone lactylation, linking astrocytic glycolysis to neuronal lipid homeostasis and positioning metabolite signaling as a therapeutic axis in neurodegeneration.
Abstract
Metabolic dysfunction is a defining but poorly understood feature of Alzheimer's disease. Du et al. show that a brain-penetrant GLP-1 receptor agonist rewires astrocyte-neuron metabolic coupling through lactate-driven histone lactylation, linking astrocytic glycolysis to neuronal lipid homeostasis and positioning metabolite signaling as a therapeutic axis in neurodegeneration.
In a recent study, Adler and colleagues demonstrated that microglia regulate blood glucose delivery to fuel the astrocyte-neuron lactate shuttle. As neuronal protein translation supported by this mechanism is essential for motor learning, these findings reveal how coordinated interactions among microglia, astrocytes, a...
E. Zimmer, Anne-Karine Bouzier-Sore, Luc Pellerin· Trends in Neurosciences· 0 citations
Tau pathology closely tracks neuronal loss in Alzheimer's disease, but how phosphorylated tau becomes lethal has remained unclear. Chen et al. identify a dual-hit mechanism: glucose hypometabolism removes a protective A20-mediated brake on necroptosis while phosphorylated tau scaffolds RIPK1 activation, driving tau-ass...
The brain is a highly complex organ composed of diverse, specialized cell types whose coordinated functions underpin cognition and behavior. While extensive research has elucidated neuronal signaling mechanisms, the metabolic interactions between distinct brain cells that sustain energy homeostasis are not yet comprehe...
Carmen Lahr, Elle Wilson, Melanie Sengupta et al.· Neurobiology of Disease· 0 citations
Metabolic dysfunction, altered adenosine signaling, and white matter abnormalities are implicated in tauopathies, but their relationship to network disconnection remains unclear. Myelinating oligodendrocytes may represent a metabolically vulnerable hub linking these processes to circuit dysfunction.
Synaptic dysfunction is an early feature of Alzheimer's disease (AD) and proper localization of proteins involved in pre‐ and post‐synaptic composition is dependent on endosomal recycling and trafficking, cellular processes involving the AD risk gene sortilin‐related receptor 1 (SORL1).
C. Williams, Shannon E. Rose, Vera Stamenković et al.· Alzheimer's & Dementia· 0 citations
It is demonstrated that S-nitrosylation of the cyclic GMP-AMP synthase (cGAS) stimulator of interferon genes (STING) pathway sustains pathological neuroinflammation in AD, identifying a promising therapeutic target for this devastating disease.
A. A. Pieper, Emiko Miller, O. Khalimonchuk et al.· Cell Chemical Biology· 0 citations
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