According to new research, an advanced type of diffusion MRI scan called soma and neurite density imaging (Sandi) can detect cellular damage in the living brains of people with Huntington’s disease, matching abnormalities previously identified only through postmortem tissue analysis. The technique estimates apparent cell-body size and density, providing a potential non-invasive biomarker to track disease progression and evaluate emerging gene therapies.
How Soma and Neurite Density Imaging Works
Standard brain scans show overall tissue shrinkage, but they offer little insight into cellular-level changes. Because surrounding cellular structures alter water movement, the method generates indirect estimates of cell-body size and density.
During the study, investigators scanned 56 people with Huntington’s disease alongside 57 healthy volunteers of a similar age and sex using a strong-gradient MRI scanner. They focused specifically on the basal ganglia, where the inherited condition typically causes neuronal loss, while using the nearby thalamus—a region spared during early stages—as a comparison.
Did you know? About 8,000 people in the UK live with Huntington’s disease, an inherited condition caused by a faulty gene that typically manifests its effects between the ages of 30 and 50.
Detecting Cellular Changes in the Living Brain
The scan results revealed distinct differences in the basal ganglia of participants with Huntington’s disease compared to healthy controls. Researchers found lower estimates of apparent cell-body density, larger estimates of apparent cell-body size, and increased space between cells. Conversely, the thalamus showed no such pattern.
These living-brain measurements closely mirror postmortem studies, which show that Huntington’s destroys specific striatal neurons that send signals through the nervous system. At the same time, glial cells swell and become active to protect damaged tissue, altering the environment around surviving neurons. According to the research team, these biological shifts correlate with disease severity and poorer motor control performance on finger-tapping tests.
Implications for Future Huntington’s Disease Treatments
In certain regions of the striatum, researchers found that cell-size and density estimates, combined with a patient’s age, accounted for up to 63% of observed brain shrinkage. This suggests the technique successfully captures the underlying biological drivers of tissue loss.
While new cell and gene therapies are currently in development, clinical trials require reliable ways to measure whether a treatment successfully protects brain cells in a living person. Although the current study relied on a single snapshot in time rather than tracking progression over months or years, future longitudinal studies could validate Sandi for clinical trials. Because cell loss also drives conditions like Alzheimer’s and Parkinson’s disease, the imaging approach may eventually extend beyond Huntington’s.
Frequently Asked Questions
What causes Huntington’s disease?
Huntington’s disease is an inherited condition caused by a faulty gene that leads to the gradual loss of neuronal cells in the striatum, affecting movement, thinking, and mood.
How does Sandi differ from a standard MRI?
While a conventional MRI reveals general brain shrinkage, Sandi analyzes diffusion MRI data to provide indirect estimates of cellular properties, such as cell-body size, density, and spacing.
Can Sandi currently track disease progression?
Not yet. The initial study was a single-point snapshot; researchers state that larger, longitudinal studies tracking patients over time are required to prove the technique can monitor disease progression or treatment efficacy.
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