Clarifying the association of CSF Aβ, tau, BACE1, and neurogranin with AT(N) stages in Alzheimer disease

The early transition to an A + phenotype (A + T-N-) primarily impacts synaptic function. The appearance of T + and then N + is associated with a significant and progressive increase in pathological Alzheimer's disease biomarkers. Our main finding is that CSF pTau181 is an indicator of N + rather than T + , and that N + is associated with elevated levels of BACE1 protein and beta-amyloid peptides. This increase may potentially fuel the amyloid cascade in a positive feedback loop. Overall, our data provide further insights into understanding the interconnected pathological processes of amyloid, tau, and neurodegeneration underlying Alzheimer's disease.

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Publication Details

Journal
Molecular Neurodegeneration
Published
2024-10-08
DOI
https://doi.org/10.1186/s13024-024-00755-3
Citations
15
Primary Topic
Alzheimer's disease research and treatments
Type
article
Field-Weighted Citation Impact
4.90
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article

Clarifying the association of CSF Aβ, tau, BACE1, and neurogranin with AT(N) stages in Alzheimer disease

Olivier Hanon, Susanna Schraen‐Maschke, Audrey Gabelle, Bernadette Allinquant et al.
15 citations
Molecular Neurodegeneration
Alzheimer's disease research and treatments
4.90
article

Clarifying the association of CSF Aβ, tau, BACE1, and neurogranin with AT(N) stages in Alzheimer disease

Olivier Hanon, Susanna Schraen‐Maschke, Audrey Gabelle, Bernadette Allinquant, Sylvain Lehmann, Christophe Hirtz, Jean‐Sébastien Vidal, Luc Buée, Constance Delaby, Stéphanie Bombois, Claire Paquet, ‪Frederic Blanc‬
article en
15 citations

Abstract

The early transition to an A + phenotype (A + T-N-) primarily impacts synaptic function. The appearance of T + and then N + is associated with a significant and progressive increase in pathological Alzheimer's disease biomarkers. Our main finding is that CSF pTau181 is an indicator of N + rather than T + , and that N + is associated with elevated levels of BACE1 protein and beta-amyloid peptides. This increase may potentially fuel the amyloid cascade in a positive feedback loop. Overall, our data provide further insights into understanding the interconnected pathological processes of amyloid, tau, and neurodegeneration underlying Alzheimer's disease.

Molecular NeurodegenerationVol. 19(1)
Universitat Autònoma de Barcelona (ES), Centre National de la Recherche Scientifique (FR), Inserm (FR), Université de Montpellier (FR), Université Paris Cité (FR), Université de Lille (FR), Hospital de Sant Pau (ES), Centre Hospitalier Universitaire de Lille (FR), Sorbonne Université (FR), Sorbonne Paris Cité (FR), Centre Hospitalier Universitaire de Montpellier (FR), Institute for Regenerative Medicine & Biotherapy (FR), Assistance Publique – Hôpitaux de Paris (FR), Centre de Recherche Jean Pierre Aubert (FR), Laboratoire des Sciences de l'Ingénieur, de l'Informatique et de l'Imagerie (FR), Hôpital Broca (FR), Hôpital Fernand-Widal (FR), Pitié-Salpêtrière Hospital (FR), Institut des Sciences Cognitives Marc Jeannerod (FR), Institut de Psychiatrie et Neurosciences de Paris (FR), Institute for Neurosciences of Montpellier (FR), Hôpital Saint Eloi (FR), Hôpitaux Universitaires de Strasbourg (FR), Lille Neurosciences & Cognition (FR), Maladie d'Alzheimer : marqueurs génétiques et vasculaires, neuropsychologie (FR), Université de Strasbourg (FR)
Good health and well-being
Openalex Percentile: Top 4%
Alzheimer's disease research and treatments
4.90
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