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Related Experiment Video

Updated: Apr 13, 2026

Fractionation for Resolution of Soluble and Insoluble Huntingtin Species

Fractionation for Resolution of Soluble and Insoluble Huntingtin Species

Published on: February 27, 2018

Presymptomatic Targeted Circuit Manipulation for Ameliorating Huntington's Disease Pathogenesis.

Ebenezer C Ikefuama¹, Ashley N Slaviero², Raegan Schalau¹

¹Program in Neuroscience, Central Michigan University, Mount Pleasant, MI 48859, USA.

Biorxiv : the Preprint Server for Biology

|August 2, 2024

Summary

Targeting early Huntington

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Efficient and Scalable Production of Full-length Human Huntingtin Variants in Mammalian Cells using a Transient Expression System

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Efficient and Scalable Production of Full-length Human Huntingtin Variants in Mammalian Cells using a Transient Expression System

Efficient and Scalable Production of Full-length Human Huntingtin Variants in Mammalian Cells using a Transient Expression System

Published on: December 10, 2021

Area of Science:

Neuroscience
Neurodegenerative Disorders
Molecular and Cellular Neuroscience

Background:

Early Huntington's disease (HD) exhibits cortical excitatory/inhibitory (E/I) imbalance before motor and cognitive symptoms.
This pre-symptomatic window offers a therapeutic opportunity to restore E/I balance and potentially slow disease progression.

Purpose of the Study:

To investigate the impact of pre-symptomatic, cell-type-specific modulation of M1 motor cortex activity on HD progression.
Specifically, examining the effects of altering pyramidal neuron and parvalbumin interneuron activity in the R6/2 HD mouse model.

Main Methods:

Presymptomatic R6/2 HD mice underwent daily, cell-type-specific manipulation of M1 motor cortex activity for three weeks.
Methods included dampening Emx1 pyramidal neuron excitation and increasing parvalbumin interneuron activity.

Main Results:

Cell-type-specific modulation significantly alleviated HD-related motor coordination deficits.
Dampening pyramidal neuron excitation or increasing interneuron activity improved motor function in pre-symptomatic HD mice.

Conclusions:

Cell-type-specific modulation of cortical output represents a promising therapeutic strategy for Huntington's disease.
Normalizing E/I balance in the cortex may offer a viable approach for treating HD and other neurodegenerative conditions.