ApoE4 lowers age at onset in patients with frontotemporal dementia and tauopathy independent of amyloid‐β copathology

Koriath, Carolin, Lashley, Tammaryn, Taylor, William, Druyeh, Ronald, Dimitriadis, Athanasios, Denning, Nicola, Williams, Julie ORCID: https://orcid.org/0000-0002-4069-0259, Warren, Jason D., Fox, Nick C., Schott, Jonathan M., Rowe, James B., Collinge, John, Rohrer, Jonathan D. and Mead, Simon 2019. ApoE4 lowers age at onset in patients with frontotemporal dementia and tauopathy independent of amyloid‐β copathology. Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring 11 (1) , pp. 277-280. 10.1016/j.dadm.2019.01.010

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Abstract

Introduction Apolipoprotein E (ApoE) is the most important genetic risk factor for Alzheimer's disease (AD), with ApoE4 thought to enhance and accelerate amyloid‐β (Aβ) pathology. ApoE4 has recently been described to increase neurodegeneration in a mouse model of frontotemporal dementia (FTD), in vitro, and in patients, demonstrating that ApoE4 modifies tauopathy independently of Aβ. This raises the question whether ApoE genotype also modifies the clinical phenotype in patients with FTD with tau pathology. Methods We analyzed 704 patients with FTD, including a genetically and neuropathologically confirmed subset, and 452 healthy elderly controls. We compared ApoE4 genotype frequency and age at onset in tau+ or TDP43+ FTD patients with or without Aβ copathology. Results The ApoE4 genotype lowered age at onset in patients with FTD and tau pathology, particularly once accounting for confounding effects of Aβ pathology. Discussion We conclude that ApoE4 accelerates neurodegeneration in FTD patients with MAPT mutations or FTLD‐tau pathology, independent of Aβ.

Item Type:	Article
Date Type:	Published Online
Status:	Published
Schools:	Medicine
Publisher:	Elsevier
ISSN:	2352-8729
Date of First Compliant Deposit:	26 October 2020
Last Modified:	05 May 2023 12:37
URI:	https://orca.cardiff.ac.uk/id/eprint/135937

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