Subhojit Roy

The paper shows that single-molecule bouncing at a presynaptic interface enables protein enrichment without slowing diffusion.

This study shows that Hrs, an ESCRT-0 protein, modulates AMPA receptor currents and Ca2+-dependent signaling by sensing and responding to neuronal activity at synapses.

The paper shows spectrin condensates facilitate the formation of the periodic axonal structure by acting as local assembly hubs that later develop into a stable lattice.

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

This study shows that phosphorylation of α-synuclein at Serine-129 is a physiologic trigger for protein interactions and synaptic function, challenging its previous association with pathology.

The paper identifies the synapsin E-domain as essential for α-synuclein function, showing it binds to α-synuclein and is necessary for its synaptic effects.

DeepMosaic detects mosaic single nucleotide variants without control samples using deep convolutional neural networks, achieving high accuracy and uncovering many variants missed by existing methods.

This study develops non-viral nanocapsules for in vivo CRISPR-Cas9 delivery to edit neuronal DNA in mice, achieving efficient and safe genome editing in specific neuron types.

The paper evaluates brain somatic mosaicism in the adult human to identify rules governing cellular distribution during embryogenesis.

The paper investigates the mechanisms and organization of clathrin transport and presynaptic targeting in neurons, revealing stable transport-packets and their role in synaptic clathrin organization.

This paper shows that excess α-synuclein impairs synaptic vesicle recycling by sequestering Hsc70, and that increasing Hsc70 levels can reverse this defect in a vertebrate synapse.

This paper introduces a CRISPR/Cas9 strategy to edit APP and manipulate the amyloid pathway in Alzheimer's disease by reducing β-cleavage and Aβ while increasing α-cleavage.

The paper shows that actin in axons moves via biased polymerization, not polymer-sliding, through dynamic hotspots and trails, explaining slow axonal transport.