Suppr超能文献

阿尔茨海默病谱系中神经退行性变成像生物标志物从临床正常到痴呆的演变。

Evolution of neurodegeneration-imaging biomarkers from clinically normal to dementia in the Alzheimer disease spectrum.

作者信息

Knopman David S, Jack Clifford R, Lundt Emily S, Weigand Stephen D, Vemuri Prashanthi, Lowe Val J, Kantarci Kejal, Gunter Jeffrey L, Senjem Matthew L, Mielke Michelle M, Machulda Mary M, Roberts Rosebud O, Boeve Bradley F, Jones David T, Petersen Ronald C

机构信息

Department of Neurology, Mayo Clinic and Foundation, Rochester, MN, USA; Mayo Clinic Alzheimer's Disease Research Center, Mayo Clinic and Foundation, Rochester, MN, USA.

Mayo Clinic Alzheimer's Disease Research Center, Mayo Clinic and Foundation, Rochester, MN, USA; Department of Radiology, Mayo Clinic and Foundation, Rochester, MN, USA.

出版信息

Neurobiol Aging. 2016 Oct;46:32-42. doi: 10.1016/j.neurobiolaging.2016.06.003. Epub 2016 Jun 16.

Abstract

The availability of antemortem biomarkers for Alzheimer's disease (AD) enables monitoring the evolution of neurodegenerative processes in real time. Pittsburgh compound B (PIB) positron emission tomography (PET) was used to select participants in the Mayo Clinic Study of Aging and the Mayo Alzheimer's Disease Research Center with elevated β-amyloid, designated as "A+," and hippocampal volume and (18)fluorodeoxyglucose (FDG) positron emission tomography were used to characterize participants as having evidence of neurodegeneration ("N+") at the baseline evaluation. There were 145 clinically normal (CN) A+ individuals, 62 persons with mild cognitive impairment (MCI) who were A+ and 20 with A+ AD dementia. Over a period of 1-6 years, MCI A+N+ individuals showed declines in medial temporal, lateral temporal, lateral parietal, and to a lesser extent, medial parietal regions for both FDG standardized uptake value ratio and gray matter volume that exceeded declines seen in the CN A+N+ group. The AD dementia group showed declines in the same regions on FDG standardized uptake value ratio and gray matter volume with rates that exceeded that in MCI A+N+. Expansion of regional involvement and faster rate of neurodegeneration characterizes progression in the AD pathway.

摘要

阿尔茨海默病(AD)生前生物标志物的可用性使得实时监测神经退行性变过程的进展成为可能。匹兹堡化合物B(PIB)正电子发射断层扫描(PET)被用于在梅奥诊所衰老研究和梅奥阿尔茨海默病研究中心中挑选β-淀粉样蛋白水平升高的参与者,这些参与者被指定为“A+”,同时利用海马体积和(18)氟脱氧葡萄糖(FDG)正电子发射断层扫描在基线评估时将参与者表征为有神经退行性变证据(“N+”)。有145名临床正常(CN)的A+个体、62名轻度认知障碍(MCI)的A+个体以及20名A+的AD痴呆患者。在1至6年的时间里,MCI A+N+个体在FDG标准化摄取值比率和灰质体积方面,在内侧颞叶、外侧颞叶、外侧顶叶以及程度较轻的内侧顶叶区域出现的下降超过了CN A+N+组。AD痴呆组在相同区域的FDG标准化摄取值比率和灰质体积下降速率超过了MCI A+N+组。区域受累范围的扩大和更快的神经退行性变速率是AD病程进展的特征。

相似文献

1
Evolution of neurodegeneration-imaging biomarkers from clinically normal to dementia in the Alzheimer disease spectrum.
Neurobiol Aging. 2016 Oct;46:32-42. doi: 10.1016/j.neurobiolaging.2016.06.003. Epub 2016 Jun 16.
2
Role of β-Amyloidosis and Neurodegeneration in Subsequent Imaging Changes in Mild Cognitive Impairment.
JAMA Neurol. 2015 Dec;72(12):1475-83. doi: 10.1001/jamaneurol.2015.2323.
6
18F-fluorodeoxyglucose positron emission tomography, aging, and apolipoprotein E genotype in cognitively normal persons.
Neurobiol Aging. 2014 Sep;35(9):2096-106. doi: 10.1016/j.neurobiolaging.2014.03.006. Epub 2014 Mar 11.
7
Association of short-term cognitive decline and MCI-to-AD dementia conversion with CSF, MRI, amyloid- and F-FDG-PET imaging.
Neuroimage Clin. 2019;22:101771. doi: 10.1016/j.nicl.2019.101771. Epub 2019 Mar 13.

引用本文的文献

1
Alzheimer's disease: insights into pathology, molecular mechanisms, and therapy.
Protein Cell. 2025 Feb 1;16(2):83-120. doi: 10.1093/procel/pwae026.
2
Brain morphometry in older adults with and without dementia using extremely rapid structural scans.
Neuroimage. 2023 Aug 1;276:120173. doi: 10.1016/j.neuroimage.2023.120173. Epub 2023 May 16.
5
Dietary Regulation of Gut-Brain Axis in Alzheimer's Disease: Importance of Microbiota Metabolites.
Front Neurosci. 2021 Nov 19;15:736814. doi: 10.3389/fnins.2021.736814. eCollection 2021.
7
Pathological drivers of neurodegeneration in suspected non-Alzheimer's disease pathophysiology.
Alzheimers Res Ther. 2021 May 14;13(1):100. doi: 10.1186/s13195-021-00835-2.
8
Alzheimer disease.
Nat Rev Dis Primers. 2021 May 13;7(1):33. doi: 10.1038/s41572-021-00269-y.
10
Imaging Translocator Protein as a Biomarker of Neuroinflammation in Dementia.
Adv Pharmacol. 2018;82:163-185. doi: 10.1016/bs.apha.2017.08.004. Epub 2017 Nov 10.

本文引用的文献

1
Tau and Aβ imaging, CSF measures, and cognition in Alzheimer's disease.
Sci Transl Med. 2016 May 11;8(338):338ra66. doi: 10.1126/scitranslmed.aaf2362.
2
PET Imaging of Tau Deposition in the Aging Human Brain.
Neuron. 2016 Mar 2;89(5):971-982. doi: 10.1016/j.neuron.2016.01.028.
4
Tau positron emission tomographic imaging in aging and early Alzheimer disease.
Ann Neurol. 2016 Jan;79(1):110-9. doi: 10.1002/ana.24546. Epub 2015 Dec 15.
5
Mapping 3-year changes in gray matter and metabolism in Aβ-positive nondemented subjects.
Neurobiol Aging. 2015 Nov;36(11):2913-2924. doi: 10.1016/j.neurobiolaging.2015.08.007. Epub 2015 Aug 18.
6
Role of β-Amyloidosis and Neurodegeneration in Subsequent Imaging Changes in Mild Cognitive Impairment.
JAMA Neurol. 2015 Dec;72(12):1475-83. doi: 10.1001/jamaneurol.2015.2323.
7
Different definitions of neurodegeneration produce similar amyloid/neurodegeneration biomarker group findings.
Brain. 2015 Dec;138(Pt 12):3747-59. doi: 10.1093/brain/awv283. Epub 2015 Sep 30.
8
Amyloid accelerates tau propagation and toxicity in a model of early Alzheimer's disease.
Acta Neuropathol Commun. 2015 Mar 24;3:14. doi: 10.1186/s40478-015-0199-x.
10
Accelerated vs. unaccelerated serial MRI based TBM-SyN measurements for clinical trials in Alzheimer's disease.
Neuroimage. 2015 Jun;113:61-9. doi: 10.1016/j.neuroimage.2015.03.026. Epub 2015 Mar 20.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验