Structural, biophysical, and functional analyses reveal that mutations in TREM2 trigger either misfolding or reduced binding to cell-surface glycosaminoglycans, which segregate with neurodegenerative disease link and highlight a functional surface linked to the pathogenesis of Alzheimer's disease.
Activation of the integrated stress response by stalled translation elongation complexes attenuates neurodegeneration, and demonstrates a protective link between a decrease in the rate of translation initiation and defects in translation elongation.
Zfp106 functions as an RNA binding protein, binds directly to GGGGCC RNA repeats, is required in motor neurons to prevent ALS-like neurodegeneration in mice, and can suppress neurotoxicity in an established fly model of ALS.
Non-invasive imaging of hippocampal neurodegeneration and structural reorganization during epileptogenesis allows the prediction of disease severity in mesial temporal lobe epilepsy, which may facilitate the early pharmacological intervention before seizure onset.
Two seemingly distinct cellular stress response pathways that contribute to neurodegeneration after axonal insults are now revealed to be under the control of a single master regulator of the neuronal injury response, the kinase DLK.