TY - JOUR
T1 - Enlarged perivascular spaces and plasma Aβ42/Aβ40 ratio in older adults without dementia
AU - Kapoor, Arunima
AU - Gaubert, Aimée
AU - Yew, Belinda
AU - Jang, Jung Yun
AU - Dutt, Shubir
AU - Li, Yanrong
AU - Alitin, John Paul M.
AU - Nguyen, Amy
AU - Ho, Jean K.
AU - Blanken, Anna E.
AU - Sible, Isabel J.
AU - Marshall, Anisa
AU - Shenasa, Fatemah
AU - Rodgers, Kathleen E.
AU - Martini, Alessandra C.
AU - Head, Elizabeth
AU - Nation, Daniel A.
N1 - Publisher Copyright:
© 2023 The Authors
PY - 2023/8
Y1 - 2023/8
N2 - Dilation of perivascular spaces (PVS) in the brain may indicate poor fluid drainage due to the accumulation of perivascular cell debris, waste, and proteins, including amyloid-beta (Aβ). No prior study has assessed whether plasma Aβ levels are related to PVS in older adults without dementia. Independently living older adults (N = 56, mean age = 68.2 years; Standard deviation (SD) = 6.5; 30.4% male) free of dementia or clinical stroke were recruited from the community and underwent brain MRI and venipuncture. PVS were qualitatively scored and dichotomized to low PVS burden (scores 0–1,) or high PVS burden (score>1). Plasma was assayed using a Quanterix Simoa Kit to quantify Aβ42 and Aβ40 levels. A significant difference was observed in plasma Aβ42/Aβ40 ratio between low and high PVS burden, controlling for age (F[1, 53] = 5.59, p = 0.022, η2 = 0.10), with lower Aβ42/Aβ40 ratio in the high PVS burden group. Dilation of PVS is associated with a lower plasma Aβ42/Aβ40 ratio, which may indicate higher cortical amyloid deposition. Future longitudinal studies examining PVS changes, and the pathogenesis of AD are warranted.
AB - Dilation of perivascular spaces (PVS) in the brain may indicate poor fluid drainage due to the accumulation of perivascular cell debris, waste, and proteins, including amyloid-beta (Aβ). No prior study has assessed whether plasma Aβ levels are related to PVS in older adults without dementia. Independently living older adults (N = 56, mean age = 68.2 years; Standard deviation (SD) = 6.5; 30.4% male) free of dementia or clinical stroke were recruited from the community and underwent brain MRI and venipuncture. PVS were qualitatively scored and dichotomized to low PVS burden (scores 0–1,) or high PVS burden (score>1). Plasma was assayed using a Quanterix Simoa Kit to quantify Aβ42 and Aβ40 levels. A significant difference was observed in plasma Aβ42/Aβ40 ratio between low and high PVS burden, controlling for age (F[1, 53] = 5.59, p = 0.022, η2 = 0.10), with lower Aβ42/Aβ40 ratio in the high PVS burden group. Dilation of PVS is associated with a lower plasma Aβ42/Aβ40 ratio, which may indicate higher cortical amyloid deposition. Future longitudinal studies examining PVS changes, and the pathogenesis of AD are warranted.
KW - Alzheimer's disease
KW - Aβ42/Aβ40 Ratio
KW - Perivascular spaces
KW - Small vessel disease
KW - Vascular cognitive impairment
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U2 - 10.1016/j.neurobiolaging.2023.04.004
DO - 10.1016/j.neurobiolaging.2023.04.004
M3 - Article
C2 - 37156179
AN - SCOPUS:85156171085
SN - 0197-4580
VL - 128
SP - 43
EP - 48
JO - Neurobiology of Aging
JF - Neurobiology of Aging
ER -