Amyloid-β predominant Alzheimer's disease neuropathologic change

Gabor G. Kovacs; Yuriko Katsumata; Xian Wu; Khine Zin Aung; David W. Fardo; Shelley L. Forrest; Peter T. Nelson

doi:10.1093/brain/awae325

Amyloid-β predominant Alzheimer's disease neuropathologic change

Gabor G. Kovacs, Yuriko Katsumata, Xian Wu, Khine Zin Aung, David W. Fardo, Shelley L. Forrest, Peter T. Nelson

Research output: Contribution to journal › Article › peer-review

1 Scopus citations

Abstract

Different subsets of Alzheimer's disease neuropathologic change (ADNC), including the intriguing set of individuals with severe/widespread amyloid-β (Aβ) plaques but no/mild tau tangles [Aβ-predominant (AP)-ADNC], may have distinct genetic and clinical features. Analysing National Alzheimer's Coordinating Center data, we stratified 1187 participants into AP-ADNC (n = 95), low Braak primary age-related tauopathy (PART; n = 185), typical-ADNC (n = 832) and high-Braak PART (n = 75). AP-ADNC differed in some clinical features and genetic polymorphisms in the APOE, SNX1, WNT3/MAPT and IGH genes. We conclude that AP-ADNC differs from classical ADNC with implications for in vivo studies.

Original language	English
Pages (from-to)	401-407
Number of pages	7
Journal	Brain
Volume	148
Issue number	2
DOIs	https://doi.org/10.1093/brain/awae325
State	Published - Feb 1 2025

Bibliographical note

Publisher Copyright:
© 2024 The Author(s). Published by Oxford University Press on behalf of the Guarantors of Brain.

Keywords

ADGC
NACC
amyloid-β
biomarker
diffuse plaques

ASJC Scopus subject areas

Clinical Neurology

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10.1093/brain/awae325

Cite this

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title = "Amyloid-β predominant Alzheimer's disease neuropathologic change",

abstract = "Different subsets of Alzheimer's disease neuropathologic change (ADNC), including the intriguing set of individuals with severe/widespread amyloid-β (Aβ) plaques but no/mild tau tangles [Aβ-predominant (AP)-ADNC], may have distinct genetic and clinical features. Analysing National Alzheimer's Coordinating Center data, we stratified 1187 participants into AP-ADNC (n = 95), low Braak primary age-related tauopathy (PART; n = 185), typical-ADNC (n = 832) and high-Braak PART (n = 75). AP-ADNC differed in some clinical features and genetic polymorphisms in the APOE, SNX1, WNT3/MAPT and IGH genes. We conclude that AP-ADNC differs from classical ADNC with implications for in vivo studies.",

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AU - Kovacs, Gabor G.

AU - Katsumata, Yuriko

AU - Wu, Xian

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AU - Fardo, David W.

AU - Forrest, Shelley L.

AU - Nelson, Peter T.

PY - 2025/2/1

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N2 - Different subsets of Alzheimer's disease neuropathologic change (ADNC), including the intriguing set of individuals with severe/widespread amyloid-β (Aβ) plaques but no/mild tau tangles [Aβ-predominant (AP)-ADNC], may have distinct genetic and clinical features. Analysing National Alzheimer's Coordinating Center data, we stratified 1187 participants into AP-ADNC (n = 95), low Braak primary age-related tauopathy (PART; n = 185), typical-ADNC (n = 832) and high-Braak PART (n = 75). AP-ADNC differed in some clinical features and genetic polymorphisms in the APOE, SNX1, WNT3/MAPT and IGH genes. We conclude that AP-ADNC differs from classical ADNC with implications for in vivo studies.

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KW - NACC

KW - amyloid-β

KW - biomarker

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Amyloid-β predominant Alzheimer's disease neuropathologic change

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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