Abstract
Abnormal accumulation of Tau protein is closely associated with neurodegeneration and cognitive impairment and it is a biomarker of neurodegeneration in the dementia field, especially in Alzheimer’s disease (AD); therefore, it is crucial to be able to assess the Tau deposits in vivo. Beyond the fluid biomarkers of tauopathy described in this review in relationship with the brain glucose metabolic patterns, this review aims to focus on tauopathy assessment by using Tau PET imaging. In recent years, several first-generation Tau PET tracers have been developed and applied in the dementia field. Common limitations of first-generation tracers include off-target binding and subcortical white-matter uptake; therefore, several institutions are working on developing second-generation Tau tracers. The increasing knowledge about the distribution of first- and second-generation Tau PET tracers in the brain may support physicians with Tau PET data interpretation, both in the research and in the clinical field, but an updated description of differences in distribution patterns among different Tau tracers, and in different clinical conditions, has not been reported yet. We provide an overview of first- and second-generation tracers used in ongoing clinical trials, also describing the differences and the properties of novel tracers, with a special focus on the distribution patterns of different Tau tracers. We also describe the distribution patterns of Tau tracers in AD, in atypical AD, and further neurodegenerative diseases in the dementia field.
Highlights
The erroneous folding of some structural proteins of neurons is associated with several neurodegenerative diseases
To develop targeted intervention strategies for Alzheimer’s disease (AD) treatment, we first need to focus our resources on finding early markers of brain changes that happen before the onset of cognitive impairment
We focus on the usage of Positron Emission Tomography (PET) imaging in the assessment of tauopathy
Summary
The erroneous folding of some structural proteins of neurons is associated with several neurodegenerative diseases These are progressive and irreversible processes with variable neurological disturbances (e.g., language, visuospatial orientation and problemsolving skills’ impairment, loss of memory, changes in behavior) responsible for cognitive impairment and dementia, such as Alzheimer’s disease, tauopathies, synucleinopathies and prionopathies [1,2,3]. In 2020, there were over 50 million people living with AD worldwide and epidemiologic data from the last decade show a sharp growth of AD incidence, owing to the older population’s constant growth in size. Both genetic and environmental risk factors play a role in AD, but age is the greatest contributor. To develop targeted intervention strategies for AD treatment, we first need to focus our resources on finding early markers of brain changes that happen before the onset of cognitive impairment
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