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

Publication: Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring

Carolin Koriath, Tammaryn Lashley, William Taylor, Ronald Druyeh, Athanasios Dimitriadis, Nicola Denning, Julie Williams, Jason D. Warren, Nick C. Fox, Jonathan M. Schott, James B. Rowe, John Collinge, Jonathan D. Rohrer, Simon Mead

19 March 2019


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.

The ApoE4 genotype lowered age at onset in patients with FTD and tau pathology, particularly once accounting for confounding effects of Aβ pathology.

The researchers conclude that ApoE4 accelerates neurodegeneration in FTD patients with MAPT mutations or FTLD‐tau pathology, independent of Aβ.

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