Amyloid-β predominant Alzheimer's disease neuropathologic change

Brain. 2025 Feb 3;148(2):401-407. doi: 10.1093/brain/awae325.

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.

Keywords: ADGC; NACC; amyloid-β; biomarker; diffuse plaques.

MeSH terms

  • Aged
  • Aged, 80 and over
  • Alzheimer Disease* / genetics
  • Alzheimer Disease* / metabolism
  • Alzheimer Disease* / pathology
  • Amyloid beta-Peptides* / metabolism
  • Apolipoproteins E / genetics
  • Brain* / metabolism
  • Brain* / pathology
  • Female
  • Humans
  • Male
  • Middle Aged
  • Neurofibrillary Tangles / pathology
  • Plaque, Amyloid / pathology
  • Sorting Nexins / genetics
  • Tauopathies / genetics
  • Tauopathies / pathology
  • tau Proteins / genetics
  • tau Proteins / metabolism

Substances

  • Amyloid beta-Peptides
  • tau Proteins
  • Apolipoproteins E
  • Sorting Nexins
  • MAPT protein, human

Grants and funding