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Academic Year 2018-2019 the in Vivo Quantification of Iron Deposition In

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Academic Year 2018-2019 the in Vivo Quantification of Iron Deposition In Academic Year 2018-2019 Faculty Pharmaceutical, Biomedical and Veterinary Sciences Biomedical Sciences The in vivo quantification of iron deposition in the brain and its relation to pathological hallmarks of Alzheimer’s disease By: Wachtelaer, Eva Master Thesis in partial fulfillment of the requirements for the degree Master in Biomedical Sciences Promoter: Prof. Dr. Pedro Rosa-Neto Co-promoter: Prof. Dr. Sebastiaan Engelborghs Douglas Mental Health University Institute 6875 LaSalle Boulevard Montreal, Quebec H4H 1R3 Canada 1 Table of contents Table of contents .................................................................................................................................................... 2 Abstract ................................................................................................................................................................... 4 Samenvatting .......................................................................................................................................................... 6 Introduction ............................................................................................................................................................ 8 1. General overview ............................................................................................................................................. 8 2. Properties of iron in humans ............................................................................................................................ 9 a) The iron element ......................................................................................................................................... 9 b) Iron metabolism ......................................................................................................................................... 9 c) Iron in the brain ....................................................................................................................................... 10 d) Brain iron regulation ............................................................................................................................... 12 e) Role of iron in neurological function in humans ..................................................................................... 13 f) Iron related to pathology: neurodegeneration with brain iron accumulation ......................................... 13 g) Magnetic properties of iron and its effects on magnetic resonance imaging .......................................... 14 h) The contribution of different iron forms to the MRI signal ...................................................................... 16 3. Current knowledge of the involvement of iron in healthy aging ................................................................... 18 4. Current knowledge of the involvement of iron in Alzheimer’s disease ........................................................ 18 a) Relation between iron and oxidative stress .............................................................................................. 18 b) Gender differences in susceptibility to Alzheimer’s disease .................................................................... 22 c) b-Amyloid neuropathology ...................................................................................................................... 22 d) Tau neuropathology ................................................................................................................................. 24 e) Genetic findings ....................................................................................................................................... 24 f) Knowledge from drugs ............................................................................................................................. 25 g) Knowledge from diet ................................................................................................................................ 25 5. Conclusion ..................................................................................................................................................... 26 Materials and method .......................................................................................................................................... 28 1. Study design ................................................................................................................................................... 28 2. Magnetic resonance acquisition and processing protocols ............................................................................ 28 3. Positron emission tomography acquisition and processing protocols ........................................................... 29 4. Mini-mental state eXamination ...................................................................................................................... 29 5. Genetic analysis ............................................................................................................................................. 30 6. Statistical analysis .......................................................................................................................................... 30 Results ................................................................................................................................................................... 32 1. The site of acquisition affects brain iron quantification ................................................................................ 32 2. The brain does not show seX differences in iron values ................................................................................ 33 3. Iron tends to accumulate in the healthy aging brain ...................................................................................... 33 4. Alzheimer’s disease patients show differences in iron load compared to controls ....................................... 35 5. Iron load is not related to b-amyloid deposition ............................................................................................ 38 6. Iron load relates to global tau load ................................................................................................................ 38 7. Iron values relate to MMSE scores ................................................................................................................ 39 8. Iron values differ for varying APOE e4 variants ........................................................................................... 39 Discussion .............................................................................................................................................................. 44 1. Strengths and limitations ............................................................................................................................... 47 2. Future perspectives ........................................................................................................................................ 50 Conclusion ............................................................................................................................................................. 54 Acknowledgements ............................................................................................................................................... 56 References ............................................................................................................................................................. 58 Supplementary material ...................................................................................................................................... 68 2 3 Abstract Background: Alzheimer’s disease (AD), the most common cause of dementia, affects millions of people worldwide. Its increasing incidence and the lack of disease-modifying drugs is of major concern to our society. An improved understanding of the pathophysiology of the disease and the discovery of novel therapeutic targets are strongly desired. Iron dyshomeostasis has been found to damage the brain by inducing oxidative stress and has been associated with the pathological hallmarks of AD. Investigating the role of iron can contribute to an improvement of the understanding of the disease and might provide insight into new therapeutic options. We hypothesize that brain iron dyshomeostasis is related to the development and progression of AD. In addition, we hypothesize a relation between abnormal brain iron levels and the pathological hallmarks characterizing AD. Objective: This study investigates the role of brain iron dyshomeostasis in healthy aging and the pathophysiology of AD. Material and methods: A cross-sectional study was performed to analyse brain iron load across clinical populations. In total, 180 subjects participated in this study, including 127 controls (22 young and 105 elder) and 53 patients (21 diagnosed with mild cognitive impairment (MCI) and 32 with AD). MRI T2* relaxometry was performed to assess iron load in the brain grey matter. R2* (1/T2*) values were calculated by applying a voxel-wise mono- exponential fit. PET imaging provided estimates of b-amyloid and tau deposition using the [18F]AZD4694 and [18F]MK6240 standardized uptake value ratio (SUVR), respectively. Cognitive function was evaluated by MMSE. APOE genotyping was carried out using the polymerase chain reaction. Multiple least squared linear regression models were applied for the statistical
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