Walker S. Jackson

This study identifies fast-conducting mechano-nociceptors as essential for mechanical nocifensive behaviors and sensitization in mice and humans.

The paper measures PrP half-life in vivo and shows it limits the time to effect of PrP-lowering therapies, with implications for drug development and clinical trial design.

This study shows that vaccination reduces prion shedding in feces and urine of CWD-infected mice, potentially breaking the transmission cycle.

The paper introduces a new mouse line expressing FlpO recombinase specifically in NaV1.8-expressing sensory neurons, enabling selective intersectional targeting of C-fiber mechanoreceptors and nociceptors.

This paper introduces a new NefhCreERT2 knock-in mouse line for selectively targeting myelinated primary afferent neurons, enabling genetic studies of these fibers while excluding unmyelinated C fibers.

The paper identifies Rps24c/S24-PKE as a novel marker for neuroinflammation and neurodegeneration through cell type-specific alternative splicing in mouse brains.

This study investigates the impact of a natural Disc1 deletion in 129S4 mice on social behavior in a semi-natural environment, finding minimal effects.

The paper identifies a fast nociceptive pathway that mediates rapid reflexive behavior but not affective pain.

The paper compares the interactomes of mouse and bank vole prion proteins in brain tissue to determine if differences in protein interactions explain the bank vole's susceptibility to prions.

The paper shows DNA G-quadruplex regulates gene expression in neurons, affecting memory formation and fear extinction.

This study shows that knock-in mice with specific prion protein mutations spontaneously develop prion disease, producing atypical prion strains with similar properties regardless of mutation type.

This study tests anle138b in mouse models of prion disease, finding improved survival in RML strain models but no clear endpoints in genetic mutation models.

The paper identifies cell type-specific transcriptomic changes in cerebellar neurons of a Huntington's disease mouse model, highlighting cyclin D1 upregulation in granule cells.

The paper identifies early translatome changes in specific neural cell types before EEG and neuropathological signs of prion disease in mice.

The paper compares behavioral traits between C57Bl/6 and 129S4 mice, establishes a new Cre mouse line for astrocyte study, and investigates calcium signaling and gene expression in astrocytes.

This study identifies CalDAG-GEFI mutations causing psychomotor symptoms and bleeding in multiple species, revealing conserved signaling deficits in striatal function.

The paper shows that in a mouse model of AD, memory recall is impaired due to the superimposition of new neurons onto the memory trace during retrieval.