TY - JOUR
T1 - The influence of limbic-predominant age-related TDP-43 encephalopathy on argyrophilic grain disease
T2 - A voxel-based morphometry analysis of pathologically confirmed cases
AU - Inui, Shohei
AU - Kaneda, Daita
AU - Sakurai, Keita
AU - Morimoto, Satoru
AU - Uchida, Yuto
AU - Abe, Osamu
AU - Hashizume, Yoshio
N1 - Publisher Copyright:
© 2024 Elsevier B.V.
PY - 2024/2/15
Y1 - 2024/2/15
N2 - Background: The influence of limbic-predominant age-related TAR DNA-binding protein of 43 kDa encephalopathy neuropathological change (LATE-NC) on structural alterations in argyrophilic grain disease (AGD) have not been documented. This study aimed to investigate the morphological impact of LATE-NC on AGD through voxel-based morphometry (VBM) technique. Materials and methods: Fifteen individuals with pathologically verified AGD, comprising 6 with LATE-NC (comorbid AGD [cAGD]) and 9 without LATE-NC (pure AGD [pAGD]), along with 10 healthy controls (HC) were enrolled. Whole-brain 3D-T1-weighted images were captured and preprocessed utilizing the Computational Anatomy Toolbox 12. VBM was employed to compare gray matter volume among (i) pAGD and HC, (ii) cAGD and HC, and (iii) pAGD and cAGD. Results: In comparison to HC, the pAGD group exhibited slightly asymmetric gray matter volume loss, particularly in the ambient gyrus, amygdala, hippocampus, anterior cingulate gyrus, and insula. Alternatively, the cAGD group exhibited greater gray matter volume loss, with a predominant focus on the inferolateral regions encompassing the ambient gyrus, amygdala, hippocampus, and the inferior temporal area, including the anterior temporal pole. The atrophy of the bilateral anterior temporal pole and right inferior temporal gyrus persisted when contrasting the pAGD and cAGD groups. Conclusion: Comorbidity with LATE-NC is linked to different atrophic distribution, particularly affecting the inferolateral regions in AGD. Consequently, the consideration of comorbid LATE-NC is crucial in individuals with AGD exhibiting more widespread temporal atrophy.
AB - Background: The influence of limbic-predominant age-related TAR DNA-binding protein of 43 kDa encephalopathy neuropathological change (LATE-NC) on structural alterations in argyrophilic grain disease (AGD) have not been documented. This study aimed to investigate the morphological impact of LATE-NC on AGD through voxel-based morphometry (VBM) technique. Materials and methods: Fifteen individuals with pathologically verified AGD, comprising 6 with LATE-NC (comorbid AGD [cAGD]) and 9 without LATE-NC (pure AGD [pAGD]), along with 10 healthy controls (HC) were enrolled. Whole-brain 3D-T1-weighted images were captured and preprocessed utilizing the Computational Anatomy Toolbox 12. VBM was employed to compare gray matter volume among (i) pAGD and HC, (ii) cAGD and HC, and (iii) pAGD and cAGD. Results: In comparison to HC, the pAGD group exhibited slightly asymmetric gray matter volume loss, particularly in the ambient gyrus, amygdala, hippocampus, anterior cingulate gyrus, and insula. Alternatively, the cAGD group exhibited greater gray matter volume loss, with a predominant focus on the inferolateral regions encompassing the ambient gyrus, amygdala, hippocampus, and the inferior temporal area, including the anterior temporal pole. The atrophy of the bilateral anterior temporal pole and right inferior temporal gyrus persisted when contrasting the pAGD and cAGD groups. Conclusion: Comorbidity with LATE-NC is linked to different atrophic distribution, particularly affecting the inferolateral regions in AGD. Consequently, the consideration of comorbid LATE-NC is crucial in individuals with AGD exhibiting more widespread temporal atrophy.
KW - 3D T1-weighted image
KW - Argyrophilic grain disease (AGD)
KW - Limbic-predominant age-related TDP-43 encephalopathy neuropathological change (LATE-NC)
KW - Voxel-based morphometry (VBM)
UR - https://www.scopus.com/pages/publications/85183662347
UR - https://www.scopus.com/pages/publications/85183662347#tab=citedBy
U2 - 10.1016/j.jns.2024.122894
DO - 10.1016/j.jns.2024.122894
M3 - Article
C2 - 38266517
AN - SCOPUS:85183662347
SN - 0022-510X
VL - 457
JO - Journal of the Neurological Sciences
JF - Journal of the Neurological Sciences
M1 - 122894
ER -