Abstract
A compelling need in the field of neurodegenerative diseases is the development and validation of biomarkers for early identification and differential diagnosis. The availability of positron emission tomography (PET) neuroimaging tools for the assessment of molecular biology and neuropathology has opened new venues in the diagnostic design and the conduction of new clinical trials. PET techniques, allowing the in vivo assessment of brain function and pathology changes, are increasingly showing great potential in supporting clinical diagnosis also in the early and even preclinical phases of dementia. This review will summarize the most recent evidence on fluorine-18 fluorodeoxyglucose-, amyloid -, tau -, and neuroinflammation - PET tools, highlighting strengths and limitations and possible new perspectives in research and clinical applications. Appropriate use of PET tools is crucial for a prompt diagnosis and target evaluation of new developed drugs aimed at slowing or preventing dementia.
Highlights
The last decades have progressively witnessed a shift from a solely clinical diagnosis to a biomarker-supported diagnosis, and molecular neuroimaging techniques such as positron emission tomography (PET) have played a leading role in the dementia diagnostic work-up[1,2,3,4,5,6,7,8]
Given the recent advances in neuroimaging techniques, it is likely that the multi-modal integration of pathological and functional biomarkers will be the key proxy to the most accurate identification of both underlying pathology and phenotypic syndrome, leading to the tailoring of the most appropriate care plan and prognosis
The increasing availability of PET in vivo pathology markers will likely favor the implementation of a spectrumbased research framework
Summary
The last decades have progressively witnessed a shift from a solely clinical diagnosis to a biomarker-supported diagnosis, and molecular neuroimaging techniques such as positron emission tomography (PET) have played a leading role in the dementia diagnostic work-up[1,2,3,4,5,6,7,8]. The topographical specificity of tau-PET uptake distribution especially emerged for the AD variants, such as posterior cortical atrophy and the logopenic variant of primary progressive aphasia, which are known to be associated with phenotype-specific patterns of neurodegeneration and cognitive deficits[124] These studies showed a consistent spatial correspondence between in vivo tau burden, neurodegeneration, and clinical syndromes, at group and singlesubject levels[83,119,125,126,127]. Several non-TSPO new targets to measure microglia activation with PET-based techniques, including but not limited to purinergic and cannabinoid receptors, are currently under evaluation[188] The development of these new radioligands is linked to the attempt of overcoming TSPO intrinsic limits (see above) and aims at the detection of specific microglial functional phenotypes[188]. The development of PET tracers addressing phenotype-specific microglia activation will hopefully allow novel insights into how neuroinflammation responses could be contributing to neurodegeneration
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