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A large, multimodal molecular characterization of the adult human hippocampus provides evidence for sustained neurogenesis and identifies a stalled neurogenic process in major depressive disorder (MDD). Cell- and circuit-specific genetic, epigenetic, stress, immune, metabolic and synaptic mechanisms are identified that underlie impaired hippocampal plasticity, providing a framework for disease subtyping and therapeutic development.
Toxidromes are characteristic patterns of clinical features caused by specific toxic mechanisms that support clinical management of the poisoned patient. In this Primer, Roberts et al. summarize the epidemiology of poisonings and discuss the mechanisms underlying key toxidromes, and their role in diagnosis and treatment of the poisoned patient.
As pancreatic β-cells age, CBX4 levels fall. Restoring CBX4 stabilizes the transcription factor NEUROD1 via SUMOylation and phase separation, counteracting its degradation to rejuvenate β-cell function and offering a new diabetes treatment avenue.
Tobias Lerchner and Stephane Heymans discuss the study that provided seminal evidence linking genetic variation to susceptibility to acute myocarditis.
A large, multimodal molecular characterization of the adult human hippocampus provides evidence for sustained neurogenesis and identifies a stalled neurogenic process in major depressive disorder (MDD). Cell- and circuit-specific genetic, epigenetic, stress, immune, metabolic and synaptic mechanisms are identified that underlie impaired hippocampal plasticity, providing a framework for disease subtyping and therapeutic development.
Tipack Shanmugam discusses a study showing that microparticles released from atherosclerotic plaque can increase thrombotic risk and proposes that these extracellular vesicles might be therapeutically altered to prevent plaque rupture.
Tsiartas and Bennett discuss the discovery that atheroclerotic plaque vulnerability to rupture arises from the interaction between plaque composition and vessel biomechanics.
