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Walker, Rod

0000-0002-8464-9805

Mayo Clinic

Kaiser Permanente Washington Health Research Institute

Citations 1

The prevalence of Lewy body pathology across nine international community-based cohorts
Gibson, Lucy L. , Suemoto, Claudia K, Corrada, Maria M, Gómez-Isaza, Laura , Grinberg, Lea T, Kapasi, Alifiya , Jicha, Gregory A, Keene, C Dirk, Latimer, Caitlin S, Leite, Renata E P, Montine, Thomas, Neltner, Allison M. , Troncoso, Juan, Walker, Keenan A, Wang, Shih-Hsiu J, Aarsland, Dag, Nelson, Peter T, Suemoto, Cláudia Kimie , Suemoto, Claudia Kimie , Kapasi, Alifiya , Kovacs, Gabor G , Myllykangas, Liisa , Walker, Rod , Attems, Johannes , Abner, Erin L. , Corrada, María M. , Grinberg, Lea T. , Jicha, Gregory A. , Kawas, Claudia H. , Kovács, Gábor G. , Latimer, Caitlin S. , Leite, Renata Elaine Paraizo , Myllykangas, Liisa , Troncoso, Juan C. , Walker, Keenan A. , Aarsland, Dag , Nelson, Peter T.

Brain | March 25, 2026 | Volume: No volume available | Issue: No issue available | Pages: No page available

10.1093/brain/awag112 Get It

Abstract Reported prevalence estimates of Lewy body pathology (LBP) vary widely, often without considering brain regional distributions or demographic influences. Large, population-representative autopsy cohorts are needed to provide estimates and clarify the distribution and clinical implications of LBP. Neuropathological, genetic, and clinical data were pooled from nine community- or population-based brain autopsy cohorts in the USA (n=6), Brazil, Austria, and Finland (n=7309 total; 59% women; mean age of death 84.2 years). Cognitive status was available for 6166 participants: dementia (38.5%), mild cognitive impairment (14.8%), and cognitively unimpaired (47.0%). Frequency of LBP was examined by anatomical distribution (neocortical, limbic, brainstem, amygdala, olfactory) and stratified by covariates. Prevalence was calculated in meta-analysis, and mixed-effect logistic regression examined associations with sex, cognitive status, Alzheimer’s disease neuropathological change (ADNC), and limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) co-pathology. Overall, 27.3% of participants had LBP: neocortical 8.4%, limbic 6.8%, brainstem 4.8%, amygdala 3.7%, and olfactory 3.6%. Neocortical LBP was associated with dementia (present in 15%; OR=4.06 [95%CI 3.24-5.10]) and with increased odds of ADNC (OR=2.30 [95%CI 1.88–2.81]) and LATE-NC (OR=2.03 [95%CI 1.69-2.44]). Sex differences were not observed in the frequencies of neocortical or limbic LBP. However, amygdala-predominant LBP was more frequent in women (OR=1.53 [95%CI 1.06-2.21]) whereas brainstem-predominant LBP was more common in men (OR=0.64 [95%CI 0.49-0.84]). Additionally, amygdala-predominant LBP was associated with increased odds of comorbid ADNC (OR=12.7 [95%CI 5.30–30.6]) while brainstem-predominant LBP was not associated with greater odds of ADNC co-pathology (OR=0.88 [95%CI 0.67–1.16]). Pooling data from large, international community-based autopsy cohorts allows for more robust estimates of region-specific LBP prevalence and their associations with cognitive status. The observed sex- and co-pathology–specific differences in brainstem and amygdala-predominant LBP highlight potential biological heterogeneity and suggest that distinct disease pathways may underlie these patterns.