John R. Lukens

Mitochondrial NADK2-dependent NADPH controls Tau oligomer uptake in human neurons

The paper shows that mitochondrial NADK2-dependent NADPH synthesis mediates Tau oligomer uptake in neurons via LRP1, creating a cycle that exacerbates TauO toxicity.

Structural and functional damage to neuronal nuclei caused by extracellular tau oligomers

This study investigates how extracellular tau oligomers cause structural and functional damage to neuronal nuclei in tauopathies, showing increased invaginations and altered gene expression.

The meningeal transcriptional response to traumatic brain injury and aging

This study investigates the meningeal transcriptional response to traumatic brain injury and aging using scRNA-seq and bulk RNA-seq in mice, revealing age-related differences in immune and extracellular matrix gene expression.

Meningeal lymphatic dysfunction exacerbates traumatic brain injury pathogenesis

This study shows that traumatic brain injury causes severe and prolonged meningeal lymphatic dysfunction, leading to increased neuroinflammation and cognitive deficits.

miR-206 family is important for mitochondrial and muscle function, but not essential for myogenesis in vitro

The paper shows that the miR-206 family is not essential for myogenesis in vitro but affects mitochondrial function and muscle performance in vivo.

Oligomeric amyloid beta prevents myelination in a clusterin-dependent manner

This study shows that clusterin, produced by oligodendrocyte progenitor cells (OPCs), inhibits their differentiation into oligodendrocytes and prevents myelin repair in Alzheimer's disease by reducing IL-9 production.

tRNA-derived fragments and microRNAs in the maternal-fetal interface of a mouse maternal-immune-activation autism model

The paper examines tRNA-derived fragments (tRFs) and microRNAs in the maternal-fetal interface of a mouse model to assess their expression patterns and response to maternal immune activation.

Necroptosis and apoptosis contribute to cisplatin and aminoglycoside ototoxicity

This study shows that apoptosis and necroptosis contribute to cisplatin and aminoglycoside ototoxicity, with potential for therapeutic intervention.