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HIGH PREVALENCE OF CEREBRAL ENLARGED PERIVASCULAR SPACE IN AMYOTROPHIC LATERAL SCLEROSIS CAUSING BY ACCUMULATION OF MISFOLDED PROTEIN
Li-Kai Tsaiand 2 co-authors
National Taiwan University Hospital
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS05-09AM-244
Presentation
Date TBA
Board: PS05-09AM-244
Event Information
Poster Board
PS05-09AM-244
Poster
View posterAbstract
Enlarged perivascular space (EPVS) is an indicator of glymphatic system dysfunction. This study aims to analyze the prevalence, significance, and mechanism of EPVS in patients and model mice of amyotrophic lateral sclerosis (ALS). Data of consecutive patients with ALS (n = 114) and controls (n = 119) were analyzed. MRI-visible perivascular spaces (PVSs) were evaluated on T2-weighted imaging and high-degree EPVS was defined as >20 visible PVSs. The width of cerebral PVS was analyzed in a mouse model of ALS with human SOD1/G93A transgenes. High-degree EPVS in centrum semiovale (CSO) was more prevalent in ALS patients than in controls (49.1% vs. 15.1%, p <0.001). Age (odds ratio (OR) 1.59; 95% confidence interval (CI) 1.18-2.15), male sex (OR 2.16; CI 1.13-4.12) and ALS diagnosis (OR 6.95; CI 3.48-13.88) were major predictive factors for developing high-degree CSO-EPVS. Patients with ALS who had high-degree CSO-EPVS were older at disease onset and MRI-acquisition than those without high-degree CSO-EPVS, but both groups had similar disease severity and aggressiveness. ALS mice at age 5 months showed larger PVS width than wild-type littermates and ALS mice at age 3 months (0.72 ± 0.04 vs. 0.41 ± 0.14 and 0.36 ± 0.14 µm, p = 0.0286). Cervical lymphatic vessel ligation enhanced misfolded SOD1 accumulation in motor neurons and cerebral vessels along with increases in PVS width but without influence in functional behavior. In conclusion, about half of ALS patients exhibit high-degree CSO-EPVS, which is not associated with disease aggressiveness and likely caused by accumulation of misfolded protein.
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