Eric Klann

This study shows astrocytes regulate neuronal translation through secreted proteins, with implications for neurodegenerative diseases.

This study investigates how overexpression of the eIF4E gene in mice affects striatal long-term potentiation (LTP), finding increased LTP that is NMDA receptor-dependent but not blocked by D1/D2 receptor antagonists.

This study shows that border-associated macrophages (BAM) are critical in limiting Alzheimer's Disease progression by clearing beta-amyloid, and their loss accelerates disease pathology.

This study shows that tau mutations slow ribosomal elongation, causing collisions that activate the integrated stress response, impairing memory and contributing to neurodegeneration.

The paper shows microglia support neuronal protein synthesis by coordinating metabolic coupling in response to increased demand from motor tasks.

This study maps the spatiotemporal dynamics of de novo protein synthesis in mice brains after auditory threat conditioning using a novel labelling technique.

The paper identifies neuron-type-specific mRNA translation programs during early memory consolidation and shows they are influenced by mRNA sequence features.

The paper develops a meta-analysis method to identify reproducible differentially expressed genes across single-cell transcriptomic case-control studies and finds shared genes across neurodegenerative diseases.

The paper investigates the role of the TSC-Rheb axis in Oxytocin receptor+ cells in stress-induced anxiety, finding sex-specific behavioral and neural changes in TSC mutant mice.

The paper shows that GADD34, an Integrated Stress Response effector, is used by neurons to enhance eIF2-dependent translation in response to BDNF stimulation.

The paper investigates EEF1A2 mutations linked to autism and epilepsy, showing they impair translation and alter actin bundling in neurons.

This paper introduces Opto4E-BP, an optogenetic tool that inhibits translation initiation in specific cell types and times, showing it blocks long-term memory consolidation.

The paper investigates microglial BDNF expression and its impact on neuronal activity and interactions in the motor cortex, finding that microglia do not express BDNF at levels sufficient to modulate neuronal function.

The paper investigates how cell-type-specific disruptions in cortico-striatal circuits in FXS model mice lead to repetitive behaviors and identifies potential therapeutic targets.

This study shows that astrocytes from ASD patients induce repetitive behavior and impair memory when transplanted into healthy mice, suggesting a primary role for astrocytes in ASD.

The paper shows that reducing S6K1 corrects translation defects in FXS mice by normalizing ribosome translocation and translation efficiency across mRNA lengths.

This study shows that reducing eIF2-P in Alzheimer's mouse models improves protein synthesis, synaptic plasticity, and memory.

The paper investigates early molecular changes in the APP/PS1 mouse model of Alzheimer's disease, finding dysregulation of the de novo proteome in synaptic, lysosomal, and mitochondrial pathways before pathology develops.

This study shows that de novo protein synthesis in specific CeL interneurons is required for storing threat memories and response inhibition.

This study shows that reducing PERK-eIF2α signaling in dopaminergic neurons causes cognitive and age-related motor issues in mice.

The paper develops a chemogenetic tool to inhibit protein synthesis in specific neurons and shows it is required for long-term memory consolidation.

This study shows that NMD regulates synaptic plasticity and cognitive function by controlling GluR1 levels through local mRNA degradation and synthesis in dendrites.

The paper shows that learning regulates protein synthesis in adult rat amygdala axons, identified through TRAP-RNASeq, revealing upregulated mitochondrial and translation-related genes and downregulated synaptic genes.