دورية أكاديمية

Baseline [ 18 F]GTP1 tau PET imaging is associated with subsequent cognitive decline in Alzheimer's disease.

التفاصيل البيبلوغرافية
العنوان: Baseline [ 18 F]GTP1 tau PET imaging is associated with subsequent cognitive decline in Alzheimer's disease.
المؤلفون: Teng E; Early Clinical Development, Genentech, Inc., South San Francisco, CA, USA. teng.edmond@gene.com., Manser PT; Clinical Biostatistics, Genentech, Inc., South San Francisco, CA, USA., Sanabria Bohorquez S; Clinical Imaging Group, Genentech, Inc., South San Francisco, CA, USA., Wildsmith KR; Biomarker Development, Genentech, Inc., South San Francisco, CA, USA., Pickthorn K; Early Clinical Development, Genentech, Inc., South San Francisco, CA, USA., Baker SL; Clinical Imaging Group, Genentech, Inc., South San Francisco, CA, USA.; Molecular Biophysics and Integrated Bioimaging, Lawrence Berkeley National Laboratory, Berkeley, CA, USA., Ward M; Early Clinical Development, Genentech, Inc., South San Francisco, CA, USA.; Current Address: Alector, Inc., South San Francisco, CA, USA., Kerchner GA; Early Clinical Development, Genentech, Inc., South San Francisco, CA, USA.; Current Address: F. Hoffmann-La Roche AG, Basel, Switzerland., Weimer RM; Biomedical Imaging, Genentech, Inc., South San Francisco, CA, USA.
المصدر: Alzheimer's research & therapy [Alzheimers Res Ther] 2021 Dec 01; Vol. 13 (1), pp. 196. Date of Electronic Publication: 2021 Dec 01.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: BioMed Central Ltd Country of Publication: England NLM ID: 101511643 Publication Model: Electronic Cited Medium: Internet ISSN: 1758-9193 (Electronic) NLM ISO Abbreviation: Alzheimers Res Ther Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : BioMed Central Ltd.
مواضيع طبية MeSH: Alzheimer Disease*/diagnostic imaging , Alzheimer Disease*/psychology , Cognitive Dysfunction*/diagnostic imaging , Cognitive Dysfunction*/psychology, Amyloid beta-Peptides ; Humans ; Positron-Emission Tomography/methods ; tau Proteins
مستخلص: Background: The role and implementation of tau PET imaging for predicting subsequent cognitive decline in Alzheimer's disease (AD) remains uncertain. This study was designed to evaluate the relationship between baseline [ 18 F]GTP1 tau PET and subsequent longitudinal change across multiple cognitive measures over 18 months.
Methods: Our analyses incorporated data from 67 participants, including cognitively normal controls (n = 10) and β-amyloid (Aβ)-positive individuals ([ 18 F] florbetapir Aβ PET) with prodromal (n = 26), mild (n = 16), or moderate (n = 15) AD. Baseline measurements included cortical volume (MRI), tau burden ([ 18 F]GTP1 tau PET), and cognitive assessments [Mini-Mental State Examination (MMSE), Clinical Dementia Rating (CDR), 13-item version of the Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog13), and Repeatable Battery for the Assessment of Neuropsychological Status (RBANS)]. Cognitive assessments were repeated at 6-month intervals over an 18-month period. Associations between baseline [ 18 F]GTP1 tau PET indices and longitudinal cognitive performance were assessed via univariate (Spearman correlations) and multivariate (linear mixed effects models) approaches. The utility of potential prognostic tau PET cut points was assessed with ROC curves.
Results: Univariate analyses indicated that greater baseline [ 18 F]GTP1 tau PET signal was associated with faster rates of subsequent decline on the MMSE, CDR, and ADAS-Cog13 across regions of interest (ROIs). In multivariate analyses adjusted for baseline age, cognitive performance, cortical volume, and Aβ PET SUVR, the prognostic performance of [ 18 F]GTP1 SUVR was most robust in the whole cortical gray ROI. When AD participants were dichotomized into low versus high tau subgroups based on baseline [ 18 F]GTP1 PET standardized uptake value ratios (SUVR) in the temporal (cutoff = 1.325) or whole cortical gray (cutoff = 1.245) ROIs, high tau subgroups demonstrated significantly more decline on the MMSE, CDR, and ADAS-Cog13.
Conclusions: Our results suggest that [ 18 F]GTP1 tau PET represents a prognostic biomarker in AD and are consistent with data from other tau PET tracers. Tau PET imaging may have utility for identifying AD patients at risk for more rapid cognitive decline and for stratification and/or enrichment of participant selection in AD clinical trials. Trial registration ClinicalTrials.gov NCT02640092 . Registered on December 28, 2015.
(© 2021. The Author(s).)
References: Brain. 2019 Jan 1;143(1):320-335. (PMID: 31886494)
JAMA Neurol. 2019 Aug 1;76(8):915-924. (PMID: 31157827)
Lancet Neurol. 2013 Feb;12(2):207-16. (PMID: 23332364)
Neuron. 2016 Mar 2;89(5):971-982. (PMID: 26938442)
JAMA. 2014 Oct 1;312(13):1342-3. (PMID: 25268441)
J Clin Exp Neuropsychol. 1998 Jun;20(3):310-9. (PMID: 9845158)
Ann Neurol. 2016 Jan;79(1):110-9. (PMID: 26505746)
J Nucl Med. 2019 Jan;60(1):107-114. (PMID: 29880509)
Int Psychogeriatr. 1997;9 Suppl 1:173-6; discussion 177-8. (PMID: 9447441)
Mol Psychiatry. 2019 Aug;24(8):1112-1134. (PMID: 30635637)
Alzheimers Dement. 2018 Apr;14(4):535-562. (PMID: 29653606)
J Psychiatr Res. 1975 Nov;12(3):189-98. (PMID: 1202204)
Hum Brain Mapp. 2003 Aug;19(4):224-47. (PMID: 12874777)
J Nucl Med. 2020 Jun;61(6):911-919. (PMID: 31712323)
J Nucl Med. 2012 Mar;53(3):378-84. (PMID: 22331215)
JAMA Neurol. 2015 Oct;72(10):1183-90. (PMID: 26280102)
Brain. 2019 Jun 1;142(6):1723-1735. (PMID: 31009046)
Neurology. 2016 Jul 26;87(4):375-83. (PMID: 27358341)
Alzheimer Dis Assoc Disord. 1997;11 Suppl 2:S13-21. (PMID: 9236948)
Alzheimers Dement. 2011 May;7(3):270-9. (PMID: 21514249)
Ann Neurol. 2019 Feb;85(2):181-193. (PMID: 30549303)
Brain. 2020 May 1;143(5):1588-1602. (PMID: 32380523)
Neurobiol Aging. 2019 Sep;81:138-145. (PMID: 31280117)
Eur J Nucl Med Mol Imaging. 2019 Sep;46(10):2077-2089. (PMID: 31254035)
Appl Neuropsychol Adult. 2019 May-Jun;26(3):268-274. (PMID: 29319337)
Brain. 2019 Oct 1;142(10):3230-3242. (PMID: 31501889)
J Alzheimers Dis. 2021 Nov 18;:. (PMID: 34806603)
Neurobiol Aging. 1995 May-Jun;16(3):271-8; discussion 278-84. (PMID: 7566337)
N Engl J Med. 2010 Jan 28;362(4):329-44. (PMID: 20107219)
Clin Neuropsychol. 2015;29(7):905-23. (PMID: 26548428)
Neuropsychiatr Dis Treat. 2014 May 24;10:929-52. (PMID: 24926196)
NeuroRx. 2004 Apr;1(2):182-8. (PMID: 15717018)
Eur J Nucl Med Mol Imaging. 2020 Aug;47(9):2155-2164. (PMID: 31915896)
J Neurol Neurosurg Psychiatry. 2012 Feb;83(2):171-3. (PMID: 22019547)
Dement Geriatr Cogn Disord. 1999 Nov-Dec;10(6):534-40. (PMID: 10559571)
Brain. 2020 Feb 1;143(2):650-660. (PMID: 31834365)
Neurology. 2018 Aug 28;91(9):e859-e866. (PMID: 30068637)
JAMA Neurol. 2021 Aug 1;78(8):961-971. (PMID: 34180956)
JAMA. 2019 Jun 18;321(23):2316-2325. (PMID: 31211344)
Alzheimers Dement. 2017 Mar;13(3):205-216. (PMID: 27697430)
BMC Neurosci. 2010 Sep 16;11:118. (PMID: 20846444)
Eur J Nucl Med Mol Imaging. 2021 Jul;48(7):2295-2305. (PMID: 34041562)
Alzheimers Dement. 2011 May;7(3):263-9. (PMID: 21514250)
Ann Intern Med. 2008 Mar 4;148(5):370-8. (PMID: 18316755)
فهرسة مساهمة: Keywords: Alzheimer’s disease; Cognition; PET; Prognosis; Tau
سلسلة جزيئية: ClinicalTrials.gov NCT02640092
المشرفين على المادة: 0 (Amyloid beta-Peptides)
0 (tau Proteins)
تواريخ الأحداث: Date Created: 20211202 Date Completed: 20220309 Latest Revision: 20220309
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC8638526
DOI: 10.1186/s13195-021-00937-x
PMID: 34852837
قاعدة البيانات: MEDLINE
الوصف
تدمد:1758-9193
DOI:10.1186/s13195-021-00937-x