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Neurodegeneration driven by pathogenic aggregating proteins reorganizes the actin cytoskeleton, causing cellular stiffening and abolishing force generation required for endocytic events.

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.

Traumatic injury leads to functional defects in nucleocytoplasmic transport and TDP-43 pathology in multiple model systems.

Local brain functional activity reductions in bvFTD follow the distribution of serotonergic, GABAergic, and norepinephrinergic neurotransmitter systems, indicating a selective vulnerability and providing novel insights into the underlying disease mechanisms.

Cdk5-mediated stabilization of Acinus in postmitotic neurons promotes autophagy and the removal of protein aggregates linked to neurodegeneration in Drosophila melanogaster.

Signaling at the primary cilium is important to sustain the morphology, connectivity, and survival of a key neural population within the brain.

Serum response factor (SRF) deficient reactive astrocytes are neuroprotective in the mammalian brain.

TGFβ signaling to retinal microglia is central to the regulation of neuroinflammatory responses relevant to age-related macular degeneration (AMD), a leading cause of blindness in the developed world.

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.

Genetic, biochemical, and physiologic analyses reveal differential responses of polyQ SCAs to exercise, and identify Sestrin as a mechanistic target that can be leveraged towards therapeutics for patients unable to exercise, or to supplement the benefits of those who can.