Longitudinal anatomic, functional, and molecular characterization of Pick disease phenotypes.
Aged
Amyloid beta-Peptides
/ metabolism
Aphasia, Primary Progressive
/ diagnostic imaging
Atrophy
/ pathology
Cerebral Cortex
/ diagnostic imaging
Cross-Sectional Studies
Female
Gray Matter
/ diagnostic imaging
Humans
Longitudinal Studies
Magnetic Resonance Imaging
Male
Middle Aged
Phenotype
Pick Disease of the Brain
/ diagnostic imaging
Positron-Emission Tomography
Primary Progressive Nonfluent Aphasia
/ diagnostic imaging
White Matter
/ diagnostic imaging
Journal
Neurology
ISSN: 1526-632X
Titre abrégé: Neurology
Pays: United States
ID NLM: 0401060
Informations de publication
Date de publication:
15 12 2020
15 12 2020
Historique:
received:
17
04
2020
accepted:
30
07
2020
pubmed:
30
9
2020
medline:
26
1
2021
entrez:
29
9
2020
Statut:
ppublish
Résumé
To characterize longitudinal MRI and PET abnormalities in autopsy-confirmed Pick disease (PiD) and determine how patterns of neurodegeneration differ with respect to clinical syndrome. Seventeen patients with PiD were identified who had antemortem MRI (8 with behavioral variant frontotemporal dementia [bvFTD-PiD], 6 with nonfluent/agrammatic primary progressive aphasia [naPPA-PiD], 1 with semantic primary progressive aphasia, 1 with unclassified primary progressive aphasia, and 1 with corticobasal syndrome). Thirteen patients had serial MRI for a total of 56 MRIs, 7 had [ The bvFTD-PiD and naPPA-PiD groups showed different foci of volume loss and hypometabolism early in the disease, with bvFTD-PiD involving bilateral prefrontal and anterior temporal cortices and naPPA-PiD involving left inferior frontal gyrus, insula, and orbitofrontal cortex. However, patterns merged over time, with progressive spread into prefrontal and anterior temporal lobe in naPPA-PiD, and eventual involvement of posterior temporal lobe, motor cortex, and parietal lobe in both groups. Rates of frontotemporal atrophy were faster in bvFTD-PiD than naPPA-PiD. One patient was β-amyloid-positive on PET with low Alzheimer neuropathologic changes at autopsy. Flortaucipir PET showed elevated uptake in frontotemporal white matter. Patterns of atrophy and hypometabolism differ in PiD according to presenting syndrome, although patterns of neurodegeneration appear to converge over time.
Identifiants
pubmed: 32989107
pii: WNL.0000000000010948
doi: 10.1212/WNL.0000000000010948
pmc: PMC7836669
doi:
Substances chimiques
Amyloid beta-Peptides
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
e3190-e3202Subventions
Organisme : NIDCD NIH HHS
ID : R01 DC014942
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG011378
Pays : United States
Organisme : NIDCD NIH HHS
ID : R01 DC012519
Pays : United States
Organisme : NIDCD NIH HHS
ID : R01 DC010367
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG062677
Pays : United States
Organisme : NINDS NIH HHS
ID : R21 NS094684
Pays : United States
Organisme : NIA NIH HHS
ID : U01 AG006786
Pays : United States
Informations de copyright
© 2020 American Academy of Neurology.
Références
Neurology. 2011 Jan 18;76(3):253-9
pubmed: 21242493
Acta Neuropathol. 1991;82(4):239-59
pubmed: 1759558
Brain. 2019 Aug 1;142(8):2466-2482
pubmed: 31199471
Alzheimers Dement. 2019 Feb;15(2):205-216
pubmed: 30347188
Brain. 2011 Sep;134(Pt 9):2565-81
pubmed: 21908872
Acta Neuropathol Commun. 2016 Jun 13;4(1):58
pubmed: 27296779
Ann Neurol. 2015 Nov;78(5):787-800
pubmed: 26344059
Neurology. 2020 Jan 21;94(3):e282-e291
pubmed: 31862783
J Mol Neurosci. 2011 Nov;45(3):594-608
pubmed: 21881831
Neurology. 2019 Feb 12;92(7):e710-e722
pubmed: 30635491
Arch Neurol. 2010 May;67(5):596-605
pubmed: 20457960
Neurology. 2002 Jun 25;58(12):1791-800
pubmed: 12084879
Alzheimers Dement. 2019 Jul;15(7):927-939
pubmed: 31175025
Neurology. 1991 Apr;41(4):479-86
pubmed: 2011243
Neurology. 2001 Jun;56(11 Suppl 4):S16-20
pubmed: 11402145
Brain. 2011 Sep;134(Pt 9):2456-77
pubmed: 21810890
Ann Neurol. 2004 Sep;56(3):399-406
pubmed: 15349867
Brain. 2019 Oct 1;142(10):3230-3242
pubmed: 31501889
Neurol Clin Pract. 2021 Feb;11(1):e11-e14
pubmed: 33968481
Arch Neurol. 2005 Sep;62(9):1402-8
pubmed: 16157747
Ann Neurol. 2016 Feb;79(2):272-87
pubmed: 26583316
Brain. 2005 Sep;128(Pt 9):1996-2005
pubmed: 16033782
Neurology. 2013 Jan 29;80(5):496-503
pubmed: 23359374
Ann Neurol. 2020 Nov;88(5):1009-1022
pubmed: 32869362
Acta Neuropathol. 2011 Aug;122(2):137-53
pubmed: 21614463
Neurology. 2011 Mar 15;76(11):1006-14
pubmed: 21325651
Ann Neurol. 2017 Mar;81(3):430-443
pubmed: 28133816
Brain. 2006 Jun;129(Pt 6):1385-98
pubmed: 16613895
J Nucl Med. 1995 Jul;36(7):1238-48
pubmed: 7790950
J Mol Neurosci. 2011 Nov;45(3):372-8
pubmed: 21556732
Neurology. 2014 May 6;82(18):1605-12
pubmed: 24706010
Neurology. 2006 Jan 10;66(1):41-8
pubmed: 16401843
Alzheimers Dement. 2016 Nov;12(11):1116-1124
pubmed: 26892233
Brain Lang. 2013 Jun;125(3):245-52
pubmed: 23542727
Ann Neurol. 2018 Mar;83(3):599-611
pubmed: 29451323
Neuroimage. 2005 Jul 1;26(3):839-51
pubmed: 15955494
Ann Neurol. 2004 Mar;55(3):335-46
pubmed: 14991811
Acta Neuropathol. 2012 Jan;123(1):1-11
pubmed: 22101365
Brain. 2015 May;138(Pt 5):1370-81
pubmed: 25805643
Acta Neuropathol. 2007 Jul;114(1):31-8
pubmed: 17569065