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Articles by Roy Maimon
Multimodal spatial transcriptomics redefines cortical pathology in Huntington’s disease
Keywords multimodal spatial transcriptomics trinucleotide repeats Huntington’s disease protein aggregation neurodegeneration somatic repeat expansion Introduction Huntington's disease (HD) is a neurodegenerative disorder caused by a CAG expansion in the huntingtin gene (HTT), with more than 40 CAGs in exon 1 of HTT being fully penetrant.1,2 The expanded CAG tract encodes an elongated polyglutamine stretch that promotes mutant HTT misfolding and aggregation.1,2 Human HD brains show abundant...
Aberrant splicing in Huntington's disease via disrupted TDP-43 activity accompanied by altered m6A RNA modification.
Abstract Huntington?s disease (HD) is a neurodegenerative disorder caused by a CAG repeat expansion in the first exon of the HTT gene encoding huntingtin. Prior reports have established a correlation between CAG expanded HTT and altered gene expression. However, the mechanisms leading to disruption of RNA processing in HD remain unclear. Here, our analysis of the reported HTT protein interactome identifies interactions with known RNA-binding proteins (RBPs).
Therapeutically viable generation of neurons with antisense oligonucleotide suppression of PTB
Abstract Methods to enhance adult neurogenesis by reprogramming glial cells into neurons enable production of new neurons in the adult nervous system. Development of therapeutically viable approaches to induce new neurons is now required to bring this concept to clinical application.
Axonal Transport of Organelles in Motor Neuron Cultures using Microfluidic Chambers System
Neuroscience Fill out the form below to receive a free trial or learn more about access: Unable to load video. Please check your Internet connection and reload this page. If the problem continues, please let us know and we'll try to help. An unexpected error occurred. Please check your Internet connection and reload this page. If the problem continues, please let us know and we'll try to help. Summary Axonal transport is a crucial mechanism for motor neuron health.
A CRMP4‐dependent retrograde axon‐to‐soma death signal in amyotrophic lateral sclerosis
Abstract Amyotrophic lateral sclerosis (ALS) is a fatal non-cell-autonomous neurodegenerative disease characterized by the loss of motor neurons (MNs). Mutations in CRMP4 are associated with ALS in patients, and elevated levels of CRMP4 are suggested to affect MN health in the SOD1G93A-ALS mouse model. However, the mechanism by which CRMP4 mediates toxicity in ALS MNs is poorly understood.
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