Related Experiment Video
Updated: Jul 16, 2026
09:24
Expanding the Toolkit for In Vivo Imaging of Axonal Transport
Published on: December 23, 2021
In vivo axonal transport rates decrease in a mouse model of Alzheimer's disease.
Karen Dell Brown Smith1, Verena Kallhoff, Hui Zheng
1Department of Molecular Physiology and Biophysics, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Neuroimage
|March 21, 2007
Summary
Axonal transport slows before plaque formation in Alzheimer's disease (AD) models. This finding, using Manganese-Enhanced MRI (MEMRI), offers new insights into early AD progression and axonal damage.
Area of Science:
- Neuroscience
- Biomedical Imaging
- Neurodegenerative Diseases
Background:
- Axonopathy is a key feature of neurodegenerative diseases like Alzheimer's disease (AD).
- Axonal swellings and degeneration are common in AD, potentially causing dementia symptoms.
- Current methods to study axonal damage in AD are invasive and lack temporal resolution.
Purpose of the Study:
- To develop and utilize Manganese-Enhanced MRI (MEMRI) for assessing in vivo axonal transport rates.
- To investigate the temporal relationship between axonal transport deficits and amyloid-beta (Abeta) deposition in an AD mouse model.
Main Methods:
- Manganese-Enhanced MRI (MEMRI) was employed to measure axonal transport rates in Tg2576 mice, a model for AD.
- Axonal transport rates were compared between Tg2576 mice and control groups at different stages of Abeta pathology.
Main Results:
- Axonal transport rates were normal in Tg2576 mice before amyloid-beta (Abeta) deposition.
- A significant decrease in axonal transport rates was observed as Abeta levels increased, preceding plaque formation.
- Axonal transport decline became more pronounced after the formation of amyloid plaques.
Conclusions:
- In vivo axonal transport rates decrease in the Tg2576 mouse model of AD prior to plaque formation.
- MEMRI is a valuable tool for detecting early axonal transport deficits in AD.
- These findings suggest that axonal transport impairment is an early event in AD pathogenesis.
