In vivo evidence for pre-symptomatic neuroinflammation in a MAPT mutation carrier

被引：21

作者：

Bevan-Jones, W. Richard ^{[1
]}

Cope, Thomas E. ^{[2
]}

Jones, P. Simon ^{[2
]}

Passamonti, Luca ^{[2
]}

Hong, Young T. ^{[3
]}

Fryer, Tim ^{[3
]}

Arnold, Robert ^{[1
]}

Coles, Jonathan P. ^{[4
]}

Aigbirhio, Franklin I. ^{[3
]}

O'Brien, John T. ^{[1
]}

Rowe, James B. ^{[2
,5
]}

机构：

[1] Univ Cambridge, Dept Psychiat, Cambridge, England

[2] Univ Cambridge, Dept Clin Neurosci, Cambridge, England

[3] Univ Cambridge, Wolfson Brain Imaging Ctr, Cambridge, England

[4] Univ Cambridge, Div Anaesthesia, Cambridge, England

[5] MRC, Cognit & Brain Sci Unit, Cambridge, England

来源：

ANNALS OF CLINICAL AND TRANSLATIONAL NEUROLOGY | 2019年 / 6卷 / 02期

基金：

英国惠康基金;

关键词：

POSITRON-EMISSION-TOMOGRAPHY; GENETIC FRONTOTEMPORAL DEMENTIA; MICROGLIAL ACTIVATION; PET;

D O I：

10.1002/acn3.683

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

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, we 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. Our findings suggest an early role for microglial activation in frontotemporal dementia. Longitudinal studies are needed to explore the causality of this pathophysiological association.

引用

页码：373 / 378

页数：6

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