Blaine Russell Roberts

This paper identifies a novel mechanism by which manganese disrupts mitochondrial transcriptome processing, leading to dsRNA accumulation and neuroinflammation through MDA5 activation.

The paper compares the effects of copper deficiency in CTR1- and COX17-deficient cells using multiomics approaches, revealing distinct signaling mechanisms and proteome responses.

This study identifies how host glycosylation of bacterial antigens in nucleic acid vaccines reduces immune recognition by shielding epitopes and altering antibody binding.

This study shows that zinc-deficient SOD1 forms toxic heterodimers with wild-type SOD1, contributing to ALS pathology through enhanced redox activity and motor neuron toxicity.

The paper quantifies post-translational modifications of Aβ in brain tissue to distinguish amyloidosis stages in Alzheimer's Disease and related conditions.

The paper investigates how neuronal cells adapt to copper deficiency by increasing protein synthesis through mTORC1 activation and reduced PERK signaling in multiple model systems.

The paper investigates copper availability in sporadic ALS and suggests CuII(atsm) may be therapeutically relevant by improving copper bioavailability.

This study shows that microglial ferroptotic stress leads to non-cell autonomous neuronal death in ALS, with a novel inhibitor reducing neurotoxicity.

The paper uses heparin affinity chromatography to enrich plasma proteomes in Alzheimer's disease, identifying matrisome-associated proteins correlated with AD biomarkers.

The paper compares proteomic profiles of cerebrospinal fluid from African Americans and Caucasians with and without Alzheimer's disease to identify shared and divergent biomarkers.

The paper identifies asymmetric thinning of the cerebral cortex across aging and Alzheimer's Disease, showing that the initially thicker hemisphere thins faster, with this pattern replicated across multiple cohorts.

This study shows that Golgi-dependent copper homeostasis, mediated by ATP7 and COG, is essential for maintaining mitochondrial function and synaptic integrity in neurons.

This study shows that reducing SCN2A function with an antisense oligonucleotide improves survival and behavior in a mouse model of early seizure onset DEE.