Nowadays,presynaptic dopaminergic positron emission tomography,which assesses deficiencies in dopamine synthesis,storage,and transport,is widely utilized for early diagnosis and differential diagnosis of parkinsonism....Nowadays,presynaptic dopaminergic positron emission tomography,which assesses deficiencies in dopamine synthesis,storage,and transport,is widely utilized for early diagnosis and differential diagnosis of parkinsonism.This review provides a comprehensive summary of the latest developments in the application of presynaptic dopaminergic positron emission tomography imaging in disorders that manifest parkinsonism.We conducted a thorough literature search using reputable databases such as PubMed and Web of Science.Selection criteria involved identifying peer-reviewed articles published within the last 5 years,with emphasis on their relevance to clinical applications.The findings from these studies highlight that presynaptic dopaminergic positron emission tomography has demonstrated potential not only in diagnosing and differentiating various Parkinsonian conditions but also in assessing disease severity and predicting prognosis.Moreover,when employed in conjunction with other imaging modalities and advanced analytical methods,presynaptic dopaminergic positron emission tomography has been validated as a reliable in vivo biomarker.This validation extends to screening and exploring potential neuropathological mechanisms associated with dopaminergic depletion.In summary,the insights gained from interpreting these studies are crucial for enhancing the effectiveness of preclinical investigations and clinical trials,ultimately advancing toward the goals of neuroregeneration in parkinsonian disorders.展开更多
While early-onset Parkinson’s disease(EOPD)caused by mutations in the parkin gene(PRKN)tends to have a relatively benign course compared to genetically undetermined(GU)-EOPD,the exact underlying mechanisms remain elu...While early-onset Parkinson’s disease(EOPD)caused by mutations in the parkin gene(PRKN)tends to have a relatively benign course compared to genetically undetermined(GU)-EOPD,the exact underlying mechanisms remain elusive.We aimed to search for the differences between PRKN-EOPD and GU-EOPD by dopamine transporter(DAT)and glucose metabolism positron-emission-tomography(PET)imaging.Twelve patients with PRKN-EOPD and 16 with GU-EOPD who accepted both ^(11)C-2b-carbomethoxy-3b-(4-trimethylstannylphenyl)tropane(^(11)C-CFT)and ^(18)F-fluorodeoxyglucose PET were enrolled.The ^(11)C-CFT uptake was analyzed on both regional and voxel levels,whereas glucose metabolism was assessed in a voxel-wise fashion.Correlations between DAT and glucose metabolism imaging,DAT imaging and clinical severity,as well as glucose metabolism imaging and clinical severity were explored.Both clinical symptoms and DAT-binding pat-terns in the posterior putamen were highly symmetrical in patients with PRKN-EOPD,and dopaminergic dysfunction in the ipsilateral putamen was severer in patients with PRKN-EOPD than GU-EOPD.Meanwhile,the DAT binding was associ-ated with the severity of motor dysfunction in patients with GU-EOPD only.Patients with PRKN-EOPD showed increased glucose metabolism in the contralateral medial frontal gyrus(supplementary motor area(SMA)),contralateral substantia nigra,contralateral thalamus,and contralateral cerebellum.Notably,glucose metabolic activity in the contralateral medial frontal gyrus was inversely associated with regional DAT binding in the bilateral putamen.Patients with PRKN-EOPD showed enhanced metabolic connectivity within the bilateral putamen,ipsilateral paracentral and precentral lobules,and the ipsilateral SMA.Collectively,compared to GU-EOPD,PRKN-EOPD is characterized by symmetrical,more severe dopaminergic dysfunction and relative increased glucose metabolism.Meanwhile,SMA with elevated glucose metabolism and enhanced connectivity may act as compensatory mechanisms in PRKN-EOPD.展开更多
基金supported by the Research Project of the Shanghai Health Commission,No.2020YJZX0111(to CZ)the National Natural Science Foundation of China,Nos.82021002(to CZ),82272039(to CZ),82171252(to FL)+1 种基金a grant from the National Health Commission of People’s Republic of China(PRC),No.Pro20211231084249000238(to JW)Medical Innovation Research Project of Shanghai Science and Technology Commission,No.21Y11903300(to JG).
文摘Nowadays,presynaptic dopaminergic positron emission tomography,which assesses deficiencies in dopamine synthesis,storage,and transport,is widely utilized for early diagnosis and differential diagnosis of parkinsonism.This review provides a comprehensive summary of the latest developments in the application of presynaptic dopaminergic positron emission tomography imaging in disorders that manifest parkinsonism.We conducted a thorough literature search using reputable databases such as PubMed and Web of Science.Selection criteria involved identifying peer-reviewed articles published within the last 5 years,with emphasis on their relevance to clinical applications.The findings from these studies highlight that presynaptic dopaminergic positron emission tomography has demonstrated potential not only in diagnosing and differentiating various Parkinsonian conditions but also in assessing disease severity and predicting prognosis.Moreover,when employed in conjunction with other imaging modalities and advanced analytical methods,presynaptic dopaminergic positron emission tomography has been validated as a reliable in vivo biomarker.This validation extends to screening and exploring potential neuropathological mechanisms associated with dopaminergic depletion.In summary,the insights gained from interpreting these studies are crucial for enhancing the effectiveness of preclinical investigations and clinical trials,ultimately advancing toward the goals of neuroregeneration in parkinsonian disorders.
基金the grants from Ministry of Science and Technology of China(No.2016YFC1306504)Shanghai Municipal Science and Technology Major Project(No.2018SHZDZX01)+7 种基金ZJLab,and National Nature Science Foundation of China(Nos.91949118,81771372)Chuan-Tao Zuo received the research funding from the National Natural Science Foundation of China(Nos.82021002,81971641,81671239,and 81361120393)Shanghai Municipal Science and Technology Major Project(No.2017SHZDZX01)Science and Technology Commission of Shanghai Municipality(Nos.19441903500 and 17JC1401600)Shanghai Aging and Maternal and Child Health Research Special Project(No.2020YJZX0111)Clinical Research Plan of Shanghai Hospital Development Center(No.SHDC2020CR1038B)Science and Technology Innovation 2030 Major Project(No.2022ZD0211600)Feng-Tao Liu received the grant of the National Nature Science Foundation of China(Nos.82171252,81701250).
文摘While early-onset Parkinson’s disease(EOPD)caused by mutations in the parkin gene(PRKN)tends to have a relatively benign course compared to genetically undetermined(GU)-EOPD,the exact underlying mechanisms remain elusive.We aimed to search for the differences between PRKN-EOPD and GU-EOPD by dopamine transporter(DAT)and glucose metabolism positron-emission-tomography(PET)imaging.Twelve patients with PRKN-EOPD and 16 with GU-EOPD who accepted both ^(11)C-2b-carbomethoxy-3b-(4-trimethylstannylphenyl)tropane(^(11)C-CFT)and ^(18)F-fluorodeoxyglucose PET were enrolled.The ^(11)C-CFT uptake was analyzed on both regional and voxel levels,whereas glucose metabolism was assessed in a voxel-wise fashion.Correlations between DAT and glucose metabolism imaging,DAT imaging and clinical severity,as well as glucose metabolism imaging and clinical severity were explored.Both clinical symptoms and DAT-binding pat-terns in the posterior putamen were highly symmetrical in patients with PRKN-EOPD,and dopaminergic dysfunction in the ipsilateral putamen was severer in patients with PRKN-EOPD than GU-EOPD.Meanwhile,the DAT binding was associ-ated with the severity of motor dysfunction in patients with GU-EOPD only.Patients with PRKN-EOPD showed increased glucose metabolism in the contralateral medial frontal gyrus(supplementary motor area(SMA)),contralateral substantia nigra,contralateral thalamus,and contralateral cerebellum.Notably,glucose metabolic activity in the contralateral medial frontal gyrus was inversely associated with regional DAT binding in the bilateral putamen.Patients with PRKN-EOPD showed enhanced metabolic connectivity within the bilateral putamen,ipsilateral paracentral and precentral lobules,and the ipsilateral SMA.Collectively,compared to GU-EOPD,PRKN-EOPD is characterized by symmetrical,more severe dopaminergic dysfunction and relative increased glucose metabolism.Meanwhile,SMA with elevated glucose metabolism and enhanced connectivity may act as compensatory mechanisms in PRKN-EOPD.
