Are Linear Measurements of the Nucleus Basalis of Meynert Suitable as a Diagnostic Biomarker in Mild Cognitive Impairment and Alzheimer Disease?
Aged
Aged, 80 and over
Alzheimer Disease
/ diagnostic imaging
Amyloid beta-Peptides
/ cerebrospinal fluid
Basal Nucleus of Meynert
/ diagnostic imaging
Cognitive Dysfunction
/ diagnostic imaging
Disease Progression
Female
Humans
Magnetic Resonance Imaging
Male
Middle Aged
Neuroimaging
Neuropsychological Tests
Radionuclide Imaging
Reproducibility of Results
Sensitivity and Specificity
tau Proteins
/ cerebrospinal fluid
Journal
AJNR. American journal of neuroradiology
ISSN: 1936-959X
Titre abrégé: AJNR Am J Neuroradiol
Pays: United States
ID NLM: 8003708
Informations de publication
Date de publication:
12 2019
12 2019
Historique:
received:
30
05
2019
accepted:
03
09
2019
pubmed:
16
11
2019
medline:
1
7
2020
entrez:
16
11
2019
Statut:
ppublish
Résumé
Cell loss within the nucleus basalis of Meynert is an early event in Alzheimer disease. The thickness of the nucleus basalis of Meynert (NBM) can be measured on structural MR imaging. We investigated NBM thickness in relation to cognitive state and biochemical markers. Mean bilateral nucleus basalis of Meynert thickness was measured on coronal T1-weighted MR imaging scans from the Alzheimer's Disease Neuroimaging Initiative dataset. Three hundred and fifteen scans (80 controls, 79 cases of early mild cognitive impairment, 77 cases of late mild cognitive impairment and 79 cases of Alzheimer disease) were assessed. Alzheimer's Disease Assessment Scale-Cognitive scores, CSF tau, and amyloid quantification were extracted. Group differences in NBM thickness, their correlates and measurement reliability were assessed. Mean NBM thickness ± SD progressively declined from 2.9 ± 0.3, 2.5 ± 0.3, and 2.3 ± 0.3 to 1.8 ± 0.4 mm in healthy controls, patients with early mild cognitive impairment, late mild cognitive impairment and Alzheimer disease respectively ( There is progressive NBM thinning across the aging-dementia spectrum, which correlates with cognitive decline and CSF markers of amyloid-β pathology. We show high diagnostic accuracy but limited reliability, representing an area for future improvement. NBM thickness is a promising, readily available MR imaging biomarker of Alzheimer disease warranting diagnostic-accuracy testing in clinical practice.
Sections du résumé
BACKGROUND AND PURPOSE
Cell loss within the nucleus basalis of Meynert is an early event in Alzheimer disease. The thickness of the nucleus basalis of Meynert (NBM) can be measured on structural MR imaging. We investigated NBM thickness in relation to cognitive state and biochemical markers.
MATERIALS AND METHODS
Mean bilateral nucleus basalis of Meynert thickness was measured on coronal T1-weighted MR imaging scans from the Alzheimer's Disease Neuroimaging Initiative dataset. Three hundred and fifteen scans (80 controls, 79 cases of early mild cognitive impairment, 77 cases of late mild cognitive impairment and 79 cases of Alzheimer disease) were assessed. Alzheimer's Disease Assessment Scale-Cognitive scores, CSF tau, and amyloid quantification were extracted. Group differences in NBM thickness, their correlates and measurement reliability were assessed.
RESULTS
Mean NBM thickness ± SD progressively declined from 2.9 ± 0.3, 2.5 ± 0.3, and 2.3 ± 0.3 to 1.8 ± 0.4 mm in healthy controls, patients with early mild cognitive impairment, late mild cognitive impairment and Alzheimer disease respectively (
CONCLUSIONS
There is progressive NBM thinning across the aging-dementia spectrum, which correlates with cognitive decline and CSF markers of amyloid-β pathology. We show high diagnostic accuracy but limited reliability, representing an area for future improvement. NBM thickness is a promising, readily available MR imaging biomarker of Alzheimer disease warranting diagnostic-accuracy testing in clinical practice.
Identifiants
pubmed: 31727757
pii: ajnr.A6313
doi: 10.3174/ajnr.A6313
pmc: PMC6975347
doi:
Substances chimiques
Amyloid beta-Peptides
0
tau Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2039-2044Informations de copyright
© 2019 by American Journal of Neuroradiology.
Références
Cancer. 1950 Jan;3(1):32-5
pubmed: 15405679
Am J Ment Defic. 1981 Sep;86(2):127-37
pubmed: 7315877
Biol Psychiatry. 2012 May 1;71(9):805-13
pubmed: 21816388
J Neurosci. 1994 Jul;14(7):4507-19
pubmed: 8027790
Alzheimers Dement. 2014 Oct;10(5 Suppl):S344-53
pubmed: 24418052
Magn Reson Imaging. 2019 Sep;61:296-299
pubmed: 31202788
Lancet Neurol. 2014 Jun;13(6):614-29
pubmed: 24849862
Acta Neuropathol. 2006 Oct;112(4):389-404
pubmed: 16906426
Physiol Rev. 2001 Apr;81(2):741-66
pubmed: 11274343
AJNR Am J Neuroradiol. 1998 Apr;19(4):659-71
pubmed: 9576651
Acta Neuropathol. 2015 Apr;129(4):527-40
pubmed: 25633602
Neuroimage. 2006 Jul 1;31(3):1116-28
pubmed: 16545965
Brain. 2007 Oct;130(Pt 10):e82
pubmed: 17615094
Behav Neurol. 2012;25(2):61-72
pubmed: 22530263
Acta Neuropathol. 2000 Sep;100(3):259-69
pubmed: 10965795
Neurology. 2008 Dec 9;71(24):1986-92
pubmed: 19064880
Nucl Med Commun. 2008 Jun;29(6):568-73
pubmed: 18458605
Pharmacopsychiatry. 1994 Jan;27(1):11-5
pubmed: 8159776
Radiology. 2018 Dec;289(3):775-785
pubmed: 30204076
J Comp Neurol. 2013 Dec 15;521(18):4124-44
pubmed: 23852922
Brain. 2016 Apr;139(Pt 4):1226-36
pubmed: 26936941
Neurobiol Aging. 2011 Oct;32(10):1756-64
pubmed: 20005600
AJNR Am J Neuroradiol. 2002 Jan;23(1):27-32
pubmed: 11827872
Neurosci Lett. 2002 Feb 8;319(1):33-6
pubmed: 11814647
Cereb Cortex. 2016 Jun;26(6):2411-2426
pubmed: 25840425
Brain. 2005 Nov;128(Pt 11):2626-44
pubmed: 16014654