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Prognostic importance of apathy in syndromes associated with frontotemporal lobar degeneration

Publication: Neurology

Claire J. Lansdall, Ian T.S. Coyle-Gilchrist, Patricia Vázquez Rodríguez, Alicia Wilcox, Eileen Wehmann, Trevor W. Robbins, James B. Rowe

12 April 2019

This research determined the influence of apathy, impulsivity, and behavioral change on survival in patients with frontotemporal dementia, progressive supranuclear palsy, and corticobasal syndrome.

The relationship between apathy and survival highlights the need to develop more effective and targeted measurement tools to improve its recognition and facilitate treatment. The prognostic importance of apathy suggests that neurobehavioral features might be useful to predict survival and stratify patients for interventional trials.

Effective symptomatic interventions targeting the neurobiology of apathy might ultimately also improve prognosis.

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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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Proximity extension assay testing reveals novel diagnostic biomarkers of atypical parkinsonian syndromes

Publication: Journal of Neurology Neurosurgery and Psychiatry

Edwin Jabbari, John Woodside, Tong Guo, Nadia K Magdalinou, Viorica Chelban, Dilan Athauda, Andrew J Lees, Thomas Foltynie, Henry Houlden, Alistair Church, Michele TM Hu, James B Rowe, Henrik Zetterberg, Huw R Morris

13 March 2019

The high degree of clinical overlap between atypical parkinsonian syndromes (APS) and Parkinson’s disease (PD) makes diagnosis challenging. The researchers aimed to identify novel diagnostic protein biomarkers of APS using multiplex proximity extension assay (PEA) testing.

The biological processes regulated by the significant proteins include cell differentiation and immune cell migration. Delta and notch-like epidermal growth factor-related receptor (DNER) had the strongest effect size in APS versus controls and APS versus PD analyses. DNER is highly expressed in substantia nigra and is an activator of the NOTCH1 pathway which has been implicated in the aetiology of other neurodegenerative disorders including Alzheimer’s disease.

PEA testing has identified potential novel diagnostic biomarkers of APS.

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In vivo evidence for pre-symptomatic neuroinflammation ina MAPT mutation carrier

Publication: Annals of Clinical and Translational Neurology

W. Richard Bevan-Jones, Thomas E. Cope, P. Simon Jones, Luca Passamonti, Young T. Hong, Tim Fryer, Robert Arnold, Jonathan P. Coles, Franklin I. Aigbirhio, John T. O’Brien, James B. Rowe

1 March 2019

Neuroinflammation occurs in frontotemporal dementia, however its timing relative to protein aggregation and neuronal loss is unknown.

Using positron emission tomography and magnetic resonance imaging to quantify these processes in a pre‐symptomatic carrier of the 10 + 16 MAPT mutation, the researchers show microglial activation in frontotemporal regions, despite a lack of protein aggregation or atrophy in these areas.

The distribution of microglial activation better discriminated the carrier from controls than did protein aggregation at this pre‐symptomatic disease stage. The findings suggest an early role for microglial activation in frontotemporal dementia. Longitudinal studies are needed to explore the causality of this pathophysiological association.

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