PET Neuroimaging in Dementia Conditions

Perani, Daniela; Caminiti, Silvia Paola; Carli, Giulia; Tondo, Giacomo

doi:10.1007/978-3-030-53168-3_9

Cited by 14 publications

(16 citation statements)

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“…The potential of possible future interventions justifies the massive effort of in vivo molecular research to identify early abnormalities, even years before the clinical onset [ 12 ]. PET imaging is today a valuable tool in supporting the diagnosis of neurodegenerative conditions in both clinical and research settings [ 1 ]. Moreover, PET imaging may represent a useful tool in screening candidates for clinical trials and may serve as a marker of disease activity in monitoring disease progression [ 2 ].…”

Section: The Role Of Pet Imaging In Neurodegenerative Conditionsmentioning

confidence: 99%

“…Additionally worth noting is that amyloid-PET positivity may also be present in neurodegenerative dementia other than AD, including FTLD and dementia with Lewy bodies (DLB) [ 26 , 27 ]. For all these reasons, using amyloid-PET imaging for screening candidates in clinical trials has been criticized, while the employment of multiple, more specific neurodegeneration biomarkers should be encouraged [ 1 ].…”

Section: The Role Of Pet Imaging In Neurodegenerative Conditionsmentioning

confidence: 99%

“…As discussed above, progressive neuronal loss and local changes detected by regional hypometabolism or neurotransmission deficits are well-known hallmarks of neurodegenerative disorders [ 1 , 35 ]. Neurodegeneration affects molecular pathways, local circuits in specific brain regions, and higher-order neural networks [ 5 , 38 ].…”

Section: The Viewpoint Of Network Dysfunction In Neurodegenerative Diseasesmentioning

confidence: 99%

“…Positron emission tomography (PET) plays a relevant role as a tool able to provide in vivo biomarkers for neurodegenerative diseases, crucial in the diagnosis process [ 1 ]. PET measures different molecular processes underlying the pathophysiology of neurodegenerative diseases [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

“…PET measures different molecular processes underlying the pathophysiology of neurodegenerative diseases [ 2 ]. These targets include glucose metabolism of cells throughout the well-established radiotracer [18F] 2-fluoro-2-deoxy-D-glucose (FDG), and a broad range of biological and pathological processes, from neurotransmission to amyloid and tau pathology, with corresponding tracers [ 1 ].…”

Section: Introductionmentioning

confidence: 99%

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Brain Molecular Connectivity in Neurodegenerative Conditions

et al. 2021

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Positron emission tomography (PET) allows for the in vivo assessment of early brain functional and molecular changes in neurodegenerative conditions, representing a unique tool in the diagnostic workup. The increased use of multivariate PET imaging analysis approaches has provided the chance to investigate regional molecular processes and long-distance brain circuit functional interactions in the last decade. PET metabolic and neurotransmission connectome can reveal brain region interactions. This review is an overview of concepts and methods for PET molecular and metabolic covariance assessment with evidence in neurodegenerative conditions, including Alzheimer’s disease and Lewy bodies disease spectrum. We highlight the effects of environmental and biological factors on brain network organization. All of the above might contribute to innovative diagnostic tools and potential disease-modifying interventions.

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Section: The Role Of Pet Imaging In Neurodegenerative Conditionsmentioning

confidence: 99%

Section: The Role Of Pet Imaging In Neurodegenerative Conditionsmentioning

confidence: 99%

Section: The Viewpoint Of Network Dysfunction In Neurodegenerative Diseasesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Brain Molecular Connectivity in Neurodegenerative Conditions

et al. 2021

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The diagnostic and prognostic value of tau‐PET in amnestic MCI with different FDG‐PET subtypes

Boccalini,

Caminiti,

Chiti

et al. 2024

Ann Clin Transl Neurol

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ObjectivesMild cognitive impairment presenting with an amnestic syndrome (aMCI) and amyloid positivity is considered due to AD. Many subjects, however, can show an overall very slow progression relevant for differential diagnosis, prognosis, and treatment. This study assessed PET biomarkers, including brain glucose metabolism, tau, and amyloid load, in a series of comparable aMCI at baseline, clinically evaluated at follow‐up.MethodsWe included 72 aMCI subjects from Geneva Memory Center (N = 31) and ADNI cohorts (N = 41), selected based on available FDG‐PET, tau‐PET, amyloid‐PET, and clinical follow‐up (2.3 years ± 1.2). A data‐driven algorithm classified brain metabolic patterns into subtypes that were then compared for clinical and PET biomarker measures and cognitive decline. Voxel‐wise comparisons were performed both with FDG‐PET and tau‐PET data.ResultsThe algorithm classified three metabolic subtypes, namely “Hippocampal‐sparing with cortical hypometabolism” (Type1; N = 27), “Hippocampal and cortical hypometabolism” (Type 2; N = 23), and “Medial temporal hypometabolism” (Type 3; N = 22). Amyloid positivity and tau accumulation in the medial temporal and neocortical regions characterized Type 1 and Type 2, whereas Type 3 showed no significant tau pathology, variable amyloid positivity, and stability at follow‐up. All tau‐positive patients, independently of the FDG‐based subtype, showed faster cognitive decline.InterpretationaMCI subjects can differ in metabolic patterns, tau and amyloid pathology, and clinical progression. Here, we complemented with PET tau biomarker the specific brain hypometabolic patterns at the individual level in the prodromal phase, contributing to the patient's classification. Tau PET is the most accurate biomarker in supporting or excluding the AD diagnosis in aMCI across metabolic subtypes and also predicting the risk of decline.

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The impact of tau deposition and hypometabolism on cognitive impairment and longitudinal cognitive decline

Boccalini

Ribaldi

Hristovska

et al. 2023

Alzheimer's & Dementia

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INTRODUCTIONTau and neurodegeneration strongly correlate with cognitive impairment, as compared to amyloid. However, their contribution in explaining cognition and predicting cognitive decline in memory clinics remains unclarified.METHODSWe included 94 participants with Mini‐Mental State Examination (MMSE), tau positron emission tomography (PET), amyloidPET, fluorodeoxyglucose (FDG)PET, and MRI scans from Geneva Memory Center. Linear regression and mediation analyses tested the independent and combined association between biomarkers, cognitive performance, and decline. Linear mixed‐effects and Cox proportional hazards models assessed biomarkers’ prognostic values.RESULTSMetabolism had the strongest association with cognition (r = 0.712; p < 0.001), followed by tau (r = ‐0.682; p < 0.001). Neocortical tau showed the strongest association with cognitive decline (r = ‐0.677; p < 0.001). Metabolism mediated the association between tau and cognition and marginally mediated the one with decline. Tau positivity represented the strongest risk factor for decline (hazard ratio = 32).DISCUSSIONTau and neurodegeneration synergistically contribute to global cognitive impairment while tau drives decline. The tauPET superior prognostic value supports its implementation in memory clinics.HIGHLIGHTS Hypometabolism has the strongest association with concurrent cognitive impairment. Neocortical tau pathology is the main determinant of cognitive decline over time. FDG‐PET has a superior value compared to MRI as a measure of neurodegeneration. The prognostic value of tau‐PET exceeded all other neuroimaging modalities.

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PET Neuroimaging in Dementia Conditions

Cited by 14 publications

References 474 publications

Brain Molecular Connectivity in Neurodegenerative Conditions

Brain Molecular Connectivity in Neurodegenerative Conditions

The diagnostic and prognostic value of tau‐PET in amnestic MCI with different FDG‐PET subtypes

The impact of tau deposition and hypometabolism on cognitive impairment and longitudinal cognitive decline

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