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Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice

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Default-mode network changes in preclinical Huntington's disease.

Robert Christian Wolf¹, Fabio Sambataro, Nenad Vasic

¹Center for Psychosocial Medicine, Department of General Psychiatry, University of Heidelberg, Germany. christian.wolf@med.uni-heidelberg.de

Experimental Neurology

|June 30, 2012

Summary

This summary is machine-generated.

Altered default-mode network (DMN) connectivity is seen in individuals at risk for Huntington's disease (preHD). Lower DMN connectivity in preHD may help maintain cognitive performance during attention tasks.

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Area of Science:

Neuroscience
Cognitive Neuroscience
Neuroimaging

Background:

The default-mode network (DMN) is crucial for cognitive function and its alteration is linked to neurodegeneration.
Huntington's disease (HD) is an inherited neurodegenerative disorder with known cognitive impacts.
Previous studies show altered brain activation in preclinical HD gene carriers (preHD), but DMN functional connectivity remains unexamined.

Purpose of the Study:

To investigate the functional connectivity of the DMN in preHD individuals compared to healthy controls.
To explore the relationship between DMN functional connectivity and cognitive performance in preHD.

Main Methods:

Functional magnetic resonance imaging (fMRI) was used to assess DMN connectivity.
18 preHD individuals and 18 healthy controls participated in the study during an attention task.
Group independent component analysis (ICA) was employed to identify DMN subsystems and their connectivity patterns.

Main Results:

Spatial distribution of DMN subsystems was similar between preHD and controls.
PreHD individuals exhibited reduced subsystem-specific connectivity in key regions: anterior medial prefrontal cortex, left inferior parietal cortex, and posterior cingulate cortex.
Increased connectivity between the two DMN subsystems was observed in preHD.
Lower functional connectivity in the left inferior parietal cortex correlated with faster reaction times in the attention task for preHD individuals.

Conclusions:

Preclinical Huntington's disease is associated with altered DMN functional connectivity.
Compromised DMN connectivity in specific regions may necessitate compensatory mechanisms to maintain cognitive function in preHD.
These findings highlight the potential for DMN alterations to serve as biomarkers for cognitive changes in preHD.