Joel N. Meyer

This study shows that sodium arsenite requires additional mitochondrial or redox stress to cause dopaminergic neurotoxicity in C. elegans, but not fluoroacetic acid.

This study investigates the neurotoxic effects of a PAH mixture across three species, finding neurotoxicity occurs through a non-AhR mechanism.

This study shows that inhibiting mitochondrial complex III with pesticides causes dopaminergic neurotoxicity in C. elegans through redox stress, which can be mitigated by antioxidants.

This study shows that newer insecticides like flupyradifurone cause dopaminergic neurodegeneration in C. elegans, marked by dendritic blebbing and oxidative stress, which can be mitigated by antioxidants or genetic interventions.

The paper identifies specialized high-capacity mitochondria in C. elegans anchor cells that generate elevated ATP to fuel basement membrane invasion.

This study identifies Rab12 as a negative regulator of mitophagy and mitochondrial homeostasis, showing its loss increases mitochondrial clearance and sensitivity to stress.

This study shows that UVC irradiation changes TFAM's DNA binding specificity and increases mtDNA compaction, but does not protect against DNA damage.

This study demonstrates that a small epigenome-wide association study (EWAS) with high methylmercury exposure variance can identify differentially methylated CpG sites and pathways related to MeHg toxicity.

This study identifies efk-1/eEF2K as a key factor in C. elegans starvation survival by enhancing DNA repair and reducing oxidative stress through a translation-independent mechanism.

This study identifies MOZT, a mitophagy process at the oocyte-to-zygote transition, which removes damaged mitochondria and preserves mitochondrial health, ensuring species continuity.

The paper studies epigenetic memory at the CYP1A gene in PAH-tolerant killifish, showing reduced gene induction and persistent expression linked to cancer risk.

This study evaluates the effects of developmental neurotoxicants on neuronal architecture and function in C. elegans, identifying morphological and behavioral changes consistent with mammalian DNT literature.

This study characterizes mitochondrial bioenergetics in C. elegans across larval stages, revealing that OCR changes depend on normalization methods and showing an earlier shift to oxidative metabolism than previously reported.

The paper shows that morphological changes in dopaminergic neurons of C. elegans correlate with functional impairments, as worms with dendrite degeneration paralyze more in dopamine solutions.

This study investigates the effects of cadmium and Aflatoxin B1 on mtDNA mutagenesis in C. elegans, finding no effect on mutation frequency or spectrum despite mitophagy defects.

This study identifies lutein as a potential therapeutic for mitochondrial dysfunction-induced neurodevelopmental defects in C. elegans by restoring neuroligin expression.

This study shows that swim exercise in C. elegans improves healthspan and protects against neurodegeneration, even when exercise stops early in adulthood.