Marcelo A. Wood

This study investigates FLASH-RT's neuroprotective effects by showing sustained AMPAR activation in CA3 neurons through early transcriptional upregulation of glutamate receptor genes.

This study shows that inhibiting LSD1, a histone demethylase, restores learning and memory in aged mice by reversing age-related defects in H3K4me3 dynamics and synaptic plasticity.

This study investigates the role of the GluA1 cytoplasmic tail in AMPA receptor trafficking and synaptic transmission in dentate gyrus GABAergic interneurons, revealing its impact on behavior and neuronal activity.

This study shows that dendrite injury causes mitochondrial contraction and increased dendrite branching, regulated by KCNJ2 and Drp1.

This study evaluates the reproducibility and temporal evolution of FLASH and CONV irradiation effects on mice, showing FLASH sparing at late but not early time points.

The paper uses CRISPR-Cas9 to edit the App gene in mice, reducing Alzheimer's disease symptoms and showing long-term benefits.

The paper shows that inhibiting the CPEB3 ribozyme increases CPEB3 protein and enhances memory by promoting mRNA polyadenylation and translation.

This study shows that inhibiting C5aR1 reduces excessive synaptic pruning and synaptic loss in AD mouse models, improving LTP in an age and region-dependent manner.

This study shows that inhibiting Acss2 reduces fear memory formation and anxiety in mice and rats by decreasing histone acetylation and gene expression in the hippocampus.

This paper characterizes the 3xTg-AD mouse model of Alzheimer's Disease across its lifespan and compares it with the 5xFAD model to assess pathology and model drift.

The paper performs a comprehensive phenotypic analysis of the 5xFAD mouse model across its lifespan, identifying novel age-related pathological features.

The paper shows that the CPEB3 ribozyme regulates hippocampal-dependent memory by modulating mRNA maturation and translation of plasticity-related genes.

The paper identifies PP4-dependent HDAC3 dephosphorylation as a mechanism distinguishing axonal regeneration from regenerative failure in nerve injuries.

This study shows that HDAC3 restricts long-term memory and synaptic plasticity in aging hippocampus by repressing Per1, a circadian gene, without affecting circadian rhythms.

This study shows that HDAC3 negatively regulates habit formation in the dorsal striatum, with distinct roles in the dorsolateral and dorsomedial striatum.