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Neuroimaging of Inflammation in Memory and Related Other Disorders (NIMROD) study protocol: a deep phenotyping cohort study of the role of brain inflammation in dementia, depression and other neurological illnesses

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Bevan Jones, RW 
Surendranathan, Ajenthan  ORCID logo
Vázquez Rodríguez, P 
Arnold, R 


Introduction Inflammation of the central nervous system is increasingly regarded as having a role in cognitive disorders such as dementia and depression, but it is not clear how such neuroinflammation relates to other aspects of neuropathology (e.g., tau and amyloid pathology) as well as to structural and functional changes in the brain and symptoms (as assessed via MRI and clinical and neuropsychological assessment). This study will explore these pathophysiological mechanisms using positron emission tomography (PET) which allows in vivo imaging of inflammation, amyloid and tau deposition, together with neuropsychological profiling, magnetic resonance imaging (MRI) and peripheral biomarker analysis.

'&' can not be used here\textit{Methods & analysis}\textit{Methods & analysis} Using PET imaging of the ligand [11C]PK11195 we will test for increased neuroinflammation in vivo in patients with Alzheimer’s disease, Lewy body dementia, frontotemporal dementia, progressive supranuclear palsy, late onset depression and mild cognitive impairment, when compared to healthy controls. We will assess whether areas of inflammatory change are associated with amyloid and tau deposition (assessed using 11C-labelled Pittsburgh Compound B ([11C]PiB) and 18F-labelled AV-1451 respectively), as well as structural and functional connectivity changes found on MRI. Inflammatory biomarker analysis and immune-phenotyping of peripheral blood monocytes will determine the correlation between central (i.e., neural) and peripheral inflammation. Finally, we will examine whether neuroinflammatory changes seen on PET imaging are associated with global and domain specific cognitive impairments, or predict cognitive decline over 12 months.

'&' can not be used here\textit{Ethics & dissemination}\textit{Ethics & dissemination} The study protocol was approved by the local ethics committee, East of England - Cambridge Central Research Ethics Committee (reference: 13/EE/0104). The study is also ARSAC approved as part of this process. Data will be disseminated by presentation at national and international conferences and by publication, predominantly in journals of neuroscience as well as clinical neurology and psychiatry.

Strengths Multimodal deep phenotyping Comparisons between diseases as well as with controls Longitudinal neuropsychology data Comparison of central and peripheral inflammation

Weaknesses Lack of longitudinal neuroimaging Not a prospective study, unable to assess causation



Neuroinflammation, Positron emission tomography, Tau, [11C]PK11195, [18F]AV-1451, Alzheimer Disease, Amyloid, Biomarkers, Cognitive Dysfunction, Cohort Studies, Cytokines, Dementia, Depression, Encephalitis, Frontotemporal Dementia, Humans, Late Onset Disorders, Lewy Body Disease, Magnetic Resonance Imaging, Middle Aged, Neuroimaging, Neuropsychological Tests, Phenotype, Positron-Emission Tomography, Research Design, Supranuclear Palsy, Progressive, T-Lymphocyte Subsets, tau Proteins

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BMJ Open

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BMJ Publishing Group
Wellcome Trust (103838/Z/14/Z)
PSP Association (unknown)
Medical Research Council (G0600986)
Medical Research Council (MR/K02308X/1)
Medical Research Council (MR/M009041/1)
Medical Research Council (MC_U105597119)
Medical Research Council (MR/M024873/1)
Medical Research Council (MC_UU_00005/12)
Medical Research Council (G0600986/1)
The study is funded by the UK National Institute of Health Research Cambridge Biomedical Research Unit in Dementia (Project 4 - RNAG/293). JBR is supported by the Wellcome Trust (103838). JPC is supported by the UK National Institute of Health Research Biomedical Research Centre at Cambridge. PVR is supported by the PSP Association.