11C-CFT-PET in Presymptomatic FTDP-17: A Potential Biomarker Predicting Onset

Wu, Liyong; Liu, Jia; Feng, Xueyan; Dong, Jing; Qin, Wei; Liu, Yang; Wang, Jingjuan; Liu, Jie; Chen, Kewei; Wang, Yuping; Jia, Jianping

doi:10.3233/jad-170561

Cited by 11 publications

(10 citation statements)

References 17 publications

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“…9 This is the first study based on Chinese FTDP-17 pedigree of Han nationality. 10 Through the comparisons with control patients and patients with PD, significant sleep structure changes of FTDP-17 were found in TST, sleep efficiency, percentage of stage N1 sleep, and percentage of stage R sleep. In comparison with patients carrying a presymptomatic mutation, TST and sleep efficiency in symptomatic patients were drastically changed and seemed to be associated with disease progression.…”

Section: Discussionmentioning

confidence: 96%

“…13,14 Interestingly, FTDP-17 was previously known as pallidopontonigral degeneration before gene era, according to neuropathological features, 1 in which striatum and brainstem are the main pathological lesions. In our previous study of C11-CFT-PET, striatal dopaminergic dysfunction can be seen in presymptomatic FTDP-17 and is a potential biomarker predicting onset, 10 which may be also involved in the sleep disorders. In contrast, PD is generally characterized by RBD, which is associated with neuronal network dysfunction in the brainstem.…”

Section: Discussionmentioning

confidence: 97%

“…In this study, five members with N279K mutation in MAPT (two symptomatic patients and three with a presymptomatic mutation) were analyzed, 10 in comparison with 9 patients with PD and 11 controls. Parkinsonism was the first-onset symptom for the two symptomatic patients.…”

Section: R Esu Lt Smentioning

confidence: 99%

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Sleep Architecture Changed Without RBD in Patients With FTDP-17

Liu

Zhan

Huang

et al. 2018

Journal of Clinical Sleep Medicine

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The aim of this study is to detect the features of sleep disorder via polysomnography (PSG) based on Chinese pedigree of frontotemporal dementia with parkinsonism linked to chromosome 17 . Methods: Five members (two symptomatic patients and three patients with a presymptomatic mutation) from the FTDP-17 pedigree were enrolled, in comparison with 9 patients with Parkinson disease (PD) and 11 control patients. Each patient underwent standard PSG and hypnogram analysis. Results: Sleep architecture is affected in the presymptomatic stage of FTDP-17, including total sleep time and sleep efficiency. However, rapid eye movement sleep behavior disorder seems to be exempt from FTDP-17. In hypnogram analysis, five individuals with FTDP-17 exhibited decreased sleep efficiency and disruption of the normal cyclic sleep organization. Conclusions: In FTDP-17, striatum and brainstem are the pathological lesions, which may be involved in the pathophysiology of the alterations in sleep architecture. The concrete mechanisms need further investigation.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 97%

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Sleep Architecture Changed Without RBD in Patients With FTDP-17

Liu

Zhan

Huang

et al. 2018

Journal of Clinical Sleep Medicine

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“…We did not classify MCI into vascular MCI and amnestic MCI (aMCI), for the overlap of the early stage of those pathological process were not further estimated by the molecular dementia biomarkers either in imaging or in CSF. 20 Even most studies follow the routine to classify the patients into distinct pathologies; most of the diagnosis was based on symptom and clinical characteristics instead of hard proof of the pathology or molecular basis. 21 Thus, the functional decay mechanism in dementia in different stages could bring a more systematic and unbiased view of the dementia process.…”

Section: Discussionmentioning

confidence: 99%

Spectrum-specific encephalography standardized low-resolution brain electromagnetic tomography network and gray matter correlations in vascular dementia patients

Chen

Sui

et al. 2020

International Journal of Distributed Sensor Networks

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Vascular dementia, secondary to Alzheimer’s dementia, ranks as one of the most frequent dementia types. The process of vascular dementia is divergent with other neurodegenerative dementias and thus reversible at the early cognitive disorder or mild dementia stages. The encephalography and neuroimaging data mining at different stages would bring neuromodulation strategies in practice; 15 mild cognitive impairment patients and 16 mild vascular dementia patients as well as 17 cognitive healthy controls were screened in this study. Cognitive tests such as Mini-Mental State Examination, Montreal cognitive assessment, voxel-based morphometry, electroencephalography, and standardized low-resolution brain electromagnetic tomography connectivity network were conducted. Compared with healthy group, voxel-based morphometry analysis showed a decrease in gray/cerebrospinal fluid ratio ( p < .05) in mild dementia group; the energy power of gamma band decreased ( p < .05) in mild dementia group; and electroencephalography standardized low-resolution brain electromagnetic tomography analysis showed wider frontal and temporal lobe involvement in mild dementia patients ( p < .05). Network topological analysis screened top 10 key Brodmann areas (44R, 7R, 8L, 22L, 47L, 27L, 1L, 1R, 7R, 43L), which could be underlying neuromodulators for dementia patients. Electroencephalography as well as structural magnetic resonance imaging could be used for the evaluation of cognitive disorder patients. The spectrum-specific standardized low-resolution brain electromagnetic tomography analysis and connectivity network analysis could shed light on the neuromodulator targets in the early phase of dementia.

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“…Tracers associated with dopaminergic function were applied in MAPT mutation carriers, especially in the N279K mutation type, which may present with parkinsonism as the first symptom. Dopaminergic dysfunction was shown early in asymptomatic MAPT N279K mutation carriers via 2b-carbomethoxy-3b-(4trmethylstannylphenyl) tropane (11C-CFT)-PET (34,98). Glial activity was elevated in the frontal cortex, the posterior cingulate cortex, and the occipital cortex of asymptomatic MAPT mutation carriers on [ 11 C] DAA1106 PET, and acetylcholinesterase activity was reduced in the temporo-parietal cortex using [ 11 C] Nmethylpiperidin-4-yl acetate PET in three asymptomatic MAPT mutation carriers (34).…”

Section: Mapt_petmentioning

confidence: 99%

Imaging Biomarkers for Neurodegeneration in Presymptomatic Familial Frontotemporal Lobar Degeneration

Chen

Kantarci

2020

Front. Neurol.

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Frontotemporal lobar degeneration (FTLD) is a neurodegenerative disorder characterized by behavioral changes, language abnormality, as well as executive function deficits and motor impairment. In about 30-50% of FTLD patients, an autosomal dominant pattern of inheritance was found with major mutations in the MAPT, GRN, and the C9orf72 repeat expansion. These mutations could lead to neurodegenerative pathology years before clinical symptoms onset. With potential disease-modifying treatments that are under development, non-invasive biomarkers that help determine the early brain changes in presymptomatic FTLD patients will be critical for tracking disease progression and enrolling the right participants into the clinical trials at the right time during the disease course. In recent years, there is increasing evidence that a number of imaging biomarkers show the abnormalities during the presymptomatic stage. Imaging biomarkers of presymptomatic familial FTLD may provide insight into the underlying neurodegenerative process years before symptom onset. Structural magnetic resonance imaging (MRI) has demonstrated cortical degeneration with a mutation-specific neurodegeneration pattern years before onset of clinical symptoms in presymptomatic familial FTLD mutation carriers. In addition, diffusion tensor imaging (DTI) has shown the loss of white matter microstructural integrity in the presymptomatic stage of familial FTLD. Furthermore, proton magnetic resonance spectroscopy ( 1 H MRS), which provides a non-invasive measurement of brain biochemistry, has identified early neurochemical abnormalities in presymptomatic MAPT mutation carriers. Positron emission tomography (PET) imaging with [ 18 F]-fluorodeoxyglucose (FDG) has demonstrated the glucose hypometabolism in the presymptomatic stage of familial FTLD. Also, a novel PET ligand, 18 F-AV-1451, has been used in this group to evaluate tau deposition in the brain. Promising imaging biomarkers for presymptomatic familial FTLD have been identified and assessed for specificity and sensitivity for accurate prediction of symptom onset and tracking disease progression during the presymptomatic stage when clinical measures are not useful. Furthermore, identifying imaging biomarkers for the presymptomatic stage is important for the design of disease-modifying trials. We review the recent progress in imaging biomarkers of the presymptomatic phase of familial FTLD and discuss the imaging techniques and analysis methods, with a focus on the potential implication of these imaging techniques and their utility in specific mutation types.

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11C-CFT-PET in Presymptomatic FTDP-17: A Potential Biomarker Predicting Onset

Cited by 11 publications

References 17 publications

Sleep Architecture Changed Without RBD in Patients With FTDP-17

Sleep Architecture Changed Without RBD in Patients With FTDP-17

Spectrum-specific encephalography standardized low-resolution brain electromagnetic tomography network and gray matter correlations in vascular dementia patients

Imaging Biomarkers for Neurodegeneration in Presymptomatic Familial Frontotemporal Lobar Degeneration

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