Neil R. Cashman

Reliable repurposing of the antibody interactome inside the cell

The paper develops methods to improve the solubility and stability of intrabodies by optimizing linker design, domain orientation, and charge properties, enabling effective intracellular targeting of cytoplasmic proteins.

Relationship between therapeutic activity and preferential targeting of toxic soluble aggregates by amyloid-beta-directed antibodies

The paper examines how the binding selectivity of amyloid-beta antibodies to toxic oligomers correlates with therapeutic efficacy and reduced risk of adverse effects in Alzheimer's disease.

Rational Generation of Monoclonal Antibodies and Intrabodies Selective for Pathogenic TDP-43

This paper generates monoclonal antibodies and intrabodies that selectively target misfolded TDP-43 aggregates in disease, showing they inhibit transmission and promote degradation in cell models.

Amyloidogenic regions in beta-strands II and III modulate the aggregation and toxicity of SOD1 in living cells

The paper identifies amyloidogenic regions in beta-strands II and III of SOD1 that modulate aggregation and toxicity in ALS mutants, showing that proline mutations reduce these effects.

Analysis of protein levels and solubility in distinct brain regions reveals several elements of the protein homeostasis network that are impacted by aging

The paper analyzes protein levels and solubility in brain regions of aged mice, revealing age-related changes in proteostasis and inflammation markers.

TNF receptor associated factor 6 interacts with ALS-linked misfolded superoxide dismutase 1 and promotes aggregation

The paper identifies TRAF6 as an interactor of misfolded SOD1 in ALS, showing it promotes aggregation through ubiquitination.

Spatial patterning of tissue volume loss in schizophrenia reflects brain network architecture

This study links tissue volume loss in schizophrenia to structural and functional connectivity, finding that 25-35% of regional deformation variance is explained by these factors.

In Silico Determined Properties of Designed Superoxide Dismutase-1 Mutants Predict ALS-like Phenotypes In Vitro and In Vivo

The paper designs and tests SOD1 mutants using computational methods, showing that a destabilizing mutant causes ALS-like phenotypes while a stabilizing mutant rescues them in zebrafish.