Abstract
There is an increasing role for biological markers (biomarkers) in the understanding and diagnosis of neurodegenerative disorders. The application of imaging biomarkers specifically for the in vivo investigation of neurodegenerative disorders has increased substantially over the past decades and continues to provide further benefits both to the diagnosis and understanding of these diseases. This review forms part of a series of articles which stem from the University College London/University of Gothenburg course “Biomarkers in neurodegenerative diseases”. In this review, we focus on neuroimaging, specifically positron emission tomography (PET) and magnetic resonance imaging (MRI), giving an overview of the current established practices clinically and in research as well as new techniques being developed. We will also discuss the use of machine learning (ML) techniques within these fields to provide additional insights to early diagnosis and multimodal analysis.
Highlights
Neurodegenerative diseases, including Alzheimer’s disease (AD), are recognised to start years before symptoms appear [1]
Studies of the genetically caused familial AD have proposed a sequence of pathologic events, starting with build-up and accumulation of amyloid-β (Aβ), that can be measured in the brain (using positron emission tomography (PET) imaging) and in cerebrospinal fluid and ending with cognitive deficits and dementia [2]
This vulnerability of brain regions for tau pathology overlaps with brain regions underlying the different clinical phenotypes in typical and atypical AD dementia and correlates with atrophy and reduced glucose metabolism in those regions, a relationship that is not found with Aβ [66, 67]
Summary
Neurodegenerative diseases, including Alzheimer’s disease (AD), are recognised to start years before symptoms appear [1]. In AD, tau PET imaging studies have demonstrated that tau deposition seems to follow the staging pattern revealed by Braak and Braak, suggesting tau spreads from the entorhinal cortex (Braak I/II) to the inferolateral temporal and medial parietal lobes (Braak III/IV) and the neocortex (Braak V/VI) [63,64,65] This vulnerability of brain regions for tau pathology overlaps with brain regions underlying the different clinical phenotypes in typical and atypical AD dementia and correlates with atrophy and reduced glucose metabolism in those regions, a relationship that is not found with Aβ [66, 67]. Research key aims include improving early diagnosis and tracking disease progression
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