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High baseline perivascular space volume in basal ganglia is associated with attention and executive function decline in Parkinsons disease.

Authors :
Foreman, Ryan
Foreman, Ryan
Donahue, Erin
Duran, Jared
Schiehser, Dawn
Petkus, Andrew
ONeill, Joseph
Holschneider, Daniel
Choupan, Jeiran
Van Horn, John
Bayram, Ece
Litvan, Irene
Jakowec, Michael
Petzinger, Giselle
Foreman, Ryan
Foreman, Ryan
Donahue, Erin
Duran, Jared
Schiehser, Dawn
Petkus, Andrew
ONeill, Joseph
Holschneider, Daniel
Choupan, Jeiran
Van Horn, John
Bayram, Ece
Litvan, Irene
Jakowec, Michael
Petzinger, Giselle
Source :
Brain and Behavior; vol 14, iss 7
Publication Year :
2024

Abstract

BACKGROUND: Pathologic perivascular spaces (PVS), the fluid-filled compartments surrounding brain vasculature, may underlie cognitive decline in Parkinsons disease (PD). However, whether this impacts specific cognitive domains has not been investigated. OBJECTIVES: This study examined the relationship of PVS volume at baseline with domain-specific and global cognitive change over 2 years in PD individuals. METHODS: A total of 39 individuals with PD underwent 3T T1w magnetic resonance imaging to determine PVS volume fraction (PVS volume normalized to total regional volume) within (i) centrum semiovale, (ii) prefrontal white matter (medial orbitofrontal, rostral middle frontal, and superior frontal), and (iii) basal ganglia. A neuropsychological battery included assessment of cognitive domains and global cognitive function at baseline and after 2 years. RESULTS: Higher basal ganglia PVS at baseline was associated with greater decline in attention, executive function, and global cognition scores. CONCLUSIONS: While previous reports have associated elevated PVS volume in the basal ganglia with decline in global cognition in PD, our findings show such decline may affect the attention and executive function domains.

Details

Database :
OAIster
Journal :
Brain and Behavior; vol 14, iss 7
Notes :
application/pdf, Brain and Behavior vol 14, iss 7
Publication Type :
Electronic Resource
Accession number :
edsoai.on1452695877
Document Type :
Electronic Resource