Pathological drivers of neurodegeneration in suspected non-Alzheimer’s disease pathophysiology

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Pathological drivers of neurodegeneration in suspected non-Alzheimer’s disease pathophysiology. / Wisse, L. E.M.; de Flores, R.; Xie, L.; Das, S. R.; McMillan, C. T.; Trojanowski, J. Q.; Grossman, M.; Lee, E. B.; Irwin, D.; Yushkevich, P. A.; Wolk, D. A.; Alzheimer's Disease Neuroimaging Initiative.

I: Alzheimer's Research and Therapy, Vol. 13, 100, 12.2021.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

Harvard

Wisse, LEM, de Flores, R, Xie, L, Das, SR, McMillan, CT, Trojanowski, JQ, Grossman, M, Lee, EB, Irwin, D, Yushkevich, PA, Wolk, DA & Alzheimer's Disease Neuroimaging Initiative 2021, 'Pathological drivers of neurodegeneration in suspected non-Alzheimer’s disease pathophysiology', Alzheimer's Research and Therapy, vol. 13, 100. https://doi.org/10.1186/s13195-021-00835-2

APA

Wisse, L. E. M., de Flores, R., Xie, L., Das, S. R., McMillan, C. T., Trojanowski, J. Q., Grossman, M., Lee, E. B., Irwin, D., Yushkevich, P. A., Wolk, D. A., & Alzheimer's Disease Neuroimaging Initiative (2021). Pathological drivers of neurodegeneration in suspected non-Alzheimer’s disease pathophysiology. Alzheimer's Research and Therapy, 13, [100]. https://doi.org/10.1186/s13195-021-00835-2

CBE

Wisse LEM, de Flores R, Xie L, Das SR, McMillan CT, Trojanowski JQ, Grossman M, Lee EB, Irwin D, Yushkevich PA, Wolk DA, Alzheimer's Disease Neuroimaging Initiative. 2021. Pathological drivers of neurodegeneration in suspected non-Alzheimer’s disease pathophysiology. Alzheimer's Research and Therapy. 13:Article 100. https://doi.org/10.1186/s13195-021-00835-2

MLA

Vancouver

Author

Wisse, L. E.M. ; de Flores, R. ; Xie, L. ; Das, S. R. ; McMillan, C. T. ; Trojanowski, J. Q. ; Grossman, M. ; Lee, E. B. ; Irwin, D. ; Yushkevich, P. A. ; Wolk, D. A. ; Alzheimer's Disease Neuroimaging Initiative. / Pathological drivers of neurodegeneration in suspected non-Alzheimer’s disease pathophysiology. I: Alzheimer's Research and Therapy. 2021 ; Vol. 13.

RIS

TY - JOUR

T1 - Pathological drivers of neurodegeneration in suspected non-Alzheimer’s disease pathophysiology

AU - Wisse, L. E.M.

AU - de Flores, R.

AU - Xie, L.

AU - Das, S. R.

AU - McMillan, C. T.

AU - Trojanowski, J. Q.

AU - Grossman, M.

AU - Lee, E. B.

AU - Irwin, D.

AU - Yushkevich, P. A.

AU - Wolk, D. A.

AU - Alzheimer's Disease Neuroimaging Initiative

PY - 2021/12

Y1 - 2021/12

N2 - Background: Little is known about the heterogeneous etiology of suspected non-Alzheimer’s pathophysiology (SNAP), a group of subjects with neurodegeneration in the absence of β-amyloid. Using antemortem MRI and pathological data, we investigated the etiology of SNAP and the association of neurodegenerative pathologies with structural medial temporal lobe (MTL) measures in β-amyloid-negative subjects. Methods: Subjects with antemortem MRI and autopsy data were selected from ADNI (n=63) and the University of Pennsylvania (n=156). Pathological diagnoses and semi-quantitative scores of MTL tau, neuritic plaques, α-synuclein, and TDP-43 pathology and MTL structural MRI measures from antemortem T1-weighted MRI scans were obtained. β-amyloid status (A+/A−) was determined by CERAD score and neurodegeneration status (N+/N−) by hippocampal volume. Results: SNAP reflects a heterogeneous group of pathological diagnoses. In ADNI, SNAP (A−N+) had significantly more neuropathological diagnoses than A+N+. In the A− group, tau pathology was associated with hippocampal, entorhinal cortex, and Brodmann area 35 volume/thickness and TDP-43 pathology with hippocampal volume. Conclusion: SNAP had a heterogeneous profile with more mixed pathologies than A+N+. Moreover, a role for TDP-43 and tau pathology in driving MTL neurodegeneration in the absence of β-amyloid was supported.

AB - Background: Little is known about the heterogeneous etiology of suspected non-Alzheimer’s pathophysiology (SNAP), a group of subjects with neurodegeneration in the absence of β-amyloid. Using antemortem MRI and pathological data, we investigated the etiology of SNAP and the association of neurodegenerative pathologies with structural medial temporal lobe (MTL) measures in β-amyloid-negative subjects. Methods: Subjects with antemortem MRI and autopsy data were selected from ADNI (n=63) and the University of Pennsylvania (n=156). Pathological diagnoses and semi-quantitative scores of MTL tau, neuritic plaques, α-synuclein, and TDP-43 pathology and MTL structural MRI measures from antemortem T1-weighted MRI scans were obtained. β-amyloid status (A+/A−) was determined by CERAD score and neurodegeneration status (N+/N−) by hippocampal volume. Results: SNAP reflects a heterogeneous group of pathological diagnoses. In ADNI, SNAP (A−N+) had significantly more neuropathological diagnoses than A+N+. In the A− group, tau pathology was associated with hippocampal, entorhinal cortex, and Brodmann area 35 volume/thickness and TDP-43 pathology with hippocampal volume. Conclusion: SNAP had a heterogeneous profile with more mixed pathologies than A+N+. Moreover, a role for TDP-43 and tau pathology in driving MTL neurodegeneration in the absence of β-amyloid was supported.

KW - Hippocampus

KW - Limbic-predominant age-related TDP-43 encephalopathy

KW - Medial temporal lobe

KW - Neurodegeneration

KW - Neurodegenerative pathologies

KW - Neuropathologies diagnosis

KW - Primary age-related tauopathy

KW - Suspected non-Alzheimer’s pathophysiology

U2 - 10.1186/s13195-021-00835-2

DO - 10.1186/s13195-021-00835-2

M3 - Article

C2 - 33990226

AN - SCOPUS:85105963749

VL - 13

JO - Alzheimer's Research & Therapy

JF - Alzheimer's Research & Therapy

SN - 1758-9193

M1 - 100

ER -