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The Role of Neuroinflammation in Dementias

  • Neuroimaging (DJ Brooks, Section Editor)
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Abstract

The molecular mechanism of neuronal loss and synaptic damage in Alzheimer’s disease (AD), Parkinson’s disease dementia (PDD), frontotemporal dementia (FTD) and Lewy body dementia (LBD) is poorly understood and could differ among different types of neurodegenerative processes. However, the presence of neuroinflammation is a common feature of dementia. In this setting, reactive microgliosis, oxidative damage and mitochondrial dysfunction are associated with the pathogenesis of all types of neurodegenerative dementia. Moreover, an increased body of evidence suggests that microglia may play a central role in AD progression. In this paper, we review the scientific literature on neuroinflammation related to the most common neurodegenerative dementias (AD, PDD, FTD and LBD) focussing on the possible molecular mechanisms and the available clinical evidence. Furthermore, we discuss the neuroimaging techniques that are currently used for the study of neuroinflammation in human brain.

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Conflict of Interest

Giuseppe Pasqualetti received funding from University of Pisa and from PAIM (Pisa, Italy) and Italian Society of Pharmacology for research travel cost.

David J. Brooks was the chief medical officer for GE healthcare, and he has received consultancy fees/honoraria from the following: Acadia Pharmaceuticals Inc, Amsterdam Molecular Therapeuctics BV, AstraZeneca, BiogeIdec, NeuroNova AB, Eli Lilly and Company, Medtronic Inc, Shire Pharmaceuticals Inc, Synosia Therapeutics AG, GlaxoSmith Kline, UBC Biosciences Inc, Veralis (R&D) limited, Genentech Inc, Navidea.

Paul Edison received grant funding from Medical Research Council, UK; Alzheimer’s Research, UK; Alzheimer’s Society, UK; Novo Nordisk; GE Healthcare; and Piramal Life Science.

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This article does not contain any studies with human or animal subjects performed by any of the authors.

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Authors and Affiliations

  1. Division of Brain Sciences, Department of Medicine, Imperial College London, 1st Floor B Block, Du Cane Road, London, W12 0NN, UK

    Giuseppe Pasqualetti, David J. Brooks & Paul Edison

  2. Institute of Clinical Medicine, Aarhus University, Aarhus, Denmark

    David J. Brooks

  3. MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, UK

    Paul Edison

  4. Geriatrics Unit, University of Pisa, Pisa, Italy

    Giuseppe Pasqualetti

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  1. Giuseppe Pasqualetti
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Correspondence to Paul Edison.

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This article is part of the Topical Collection on Neuroimaging

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Pasqualetti, G., Brooks, D.J. & Edison, P. The Role of Neuroinflammation in Dementias. Curr Neurol Neurosci Rep 15, 17 (2015). https://doi.org/10.1007/s11910-015-0531-7

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