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Updated: Dec 30, 2025
Positron Emission Tomography Imaging for In Vivo Measuring of Myelin Content in the Lysolecithin Rat Model of Multiple Sclerosis
Published on: February 28, 2021
Imaging Biomarkers of Alzheimer Disease in Multiple Sclerosis
Burcu Zeydan1,2,3, Val J Lowe1, Ross R Reichard4
1Department of Radiology, Mayo Clinic, Rochester, MN.
Objective:
To investigate β-amyloid and tau depositions using Pittsburgh compound B (PiB) positron emission tomography (PET) and AV1451 tau PET imaging in aging multiple sclerosis (MS) patients.
Methods:
Patients with MS (n = 16) and controls (n = 80) matched for age, sex, and APOE ε4 status from the population-based Mayo Clinic Study of Aging who underwent PiB PET imaging were studied. Of these individuals, 12 patients with MS and 60 matching controls also underwent AV1451 tau PET. Cortical PiB and AV1451 standard uptake value ratios (SUVrs) from the entire cortex and previously determined Alzheimer disease (AD) signature regions in the same population were calculated for group comparisons and testing for associations with age.
Results:
AD signature PiB SUVr (odds ratio [OR] [95% confidence interval (CI)] = 0.52 [0.27-0.98], p = 0.044), total cortical PiB SUVr (OR [95% CI] = 0.52 [0.28-0.99], p = 0.048), and the frequency of abnormal PiB SUVrs (OR [95% CI] = 0.10 [0.01-0.90], p = 0.040) were lower in MS than controls. Although AD-signature and total cortical AV1451 SUVrs were not different between the groups, the frequency of abnormal AV1451 SUVrs was higher (OR [95% CI] = 10.65 [1.10-103.35], p = 0.041) in MS than controls. The association of AD signature PiB SUVr with age was steeper in the controls compared to patients with MS (estimate [95% CI] = -0.14 [-0.023 to -0.006], p = 0.002). Similarly, the association of total cortical PiB SUVr with age was steeper in the controls compared to patients with MS (estimate [95% CI] = -0.13 [-0.021 to -0.005], p = 0.002). There was no difference in the association of AV1451 SUVr findings with age between the MS patients and controls.
Interpretation:
Although both β-amyloid and tau are biomarkers of cognitive aging and AD, cortical β-amyloid deposition was lower in MS than age-matched controls, suggesting that some aspect of MS pathobiology retards the accumulation of β-amyloid but not the accumulation of tau. ANN NEUROL 2020;87:556-567.
Insights
Multiple sclerosis patients show reduced beta-amyloid deposition but increased tau accumulation compared to controls. This suggests MS pathology may slow beta-amyloid buildup but not tau, impacting cognitive aging biomarkers.
Area of Science:
- Neuroimaging
- Neurology
- Biomarkers of Cognitive Aging
Background:
- Beta-amyloid and tau are key biomarkers for Alzheimer's disease (AD) and cognitive aging.
- Multiple sclerosis (MS) is a chronic inflammatory disease affecting the central nervous system.
- The relationship between MS pathology and the deposition of AD biomarkers is not fully understood.
Purpose of the Study:
- To investigate beta-amyloid and tau depositions in aging multiple sclerosis (MS) patients.
- To compare positron emission tomography (PET) imaging findings between MS patients and age-matched controls.
- To examine the association of these biomarkers with age in both groups.
Main Methods:
- Utilized Pittsburgh Compound B (PiB) PET and AV1451 tau PET imaging.
- Studied 16 MS patients and 80 matched controls from the Mayo Clinic Study of Aging.
- Calculated cortical PiB and AV1451 standard uptake value ratios (SUVrs) for group comparisons and age associations.
Main Results:
- MS patients exhibited lower cortical beta-amyloid (PiB) deposition compared to controls.
- No significant difference in AD-signature or total cortical tau (AV1451) SUVrs between groups.
- Frequency of abnormal tau (AV1451) deposition was higher in MS patients than controls.
Conclusions:
- Cortical beta-amyloid deposition is reduced in MS patients relative to age-matched controls.
- MS pathobiology may retard beta-amyloid accumulation but not tau accumulation.
- Findings suggest differential effects of MS on key biomarkers of cognitive aging and AD.
