Casper C. Hoogenraad

This paper develops scalable human neuron models of Alzheimer's disease to reveal mechanisms linking Tau fibrillization to synaptic dysfunction and identifies therapeutic targets.

This study identifies six microglial transcriptional profiles linked to specific morphological phenotypes and shows AD risk genes disrupt morpho-transcriptomic coupling and phagocytic capacity.

This study identifies Notch signaling in hypothalamic oligodendrocytes as a regulator of systemic energy balance, showing that inhibiting Notch ligands leads to weight loss and metabolic changes.

Soma-seq measures both RNA and intracellular proteins in single human brain cells, revealing protein states linked to transcriptional programs in Alzheimer's disease.

The paper shows that subinhibitory concentrations of orthosteric SARM1 inhibitors can activate SARM1, leading to NAD consumption, neurodegeneration, and biomarker release in neurons.

This study identifies axonal ER tubules and P180/RRBP1 as regulators of local mRNA translation in axons, showing their role in ribosome interactions and proteome dynamics.

The paper shows that NMDA receptor-mediated long-term synaptic depression causes rapid endocytosis of sodium channels from the distal AIS, revealing a mechanism for activity-dependent AIS reorganization.

The paper quantitatively maps transcriptome and proteome changes during human iPSC-derived neuron polarization, identifying extensive remodeling of gene and protein expression.

This study identifies Tpm3.1 as essential for maintaining AIS structure and function by stabilizing actin filaments in the axon initial segment.

This study shows that loss of BICD2 in muscle drives motor neuron loss in SMALED2 through a non-cell autonomous mechanism involving impaired secretory pathways.

The paper uses proteomics and phosphoproteomics to study mGluR-LTD in neurons, identifying key kinases and pathways involved in synaptic plasticity.

The paper provides a high-resolution proteomic signature of human iPSC-derived neurons using mass spectrometry, revealing key proteins and signaling pathways involved in neuronal development.

This study identifies Sema4D's role in stabilizing presynaptic boutons and forming inhibitory synapses through MET activation and actin remodeling.