Serum tau protein elevation in migraine: a cross-sectional case-control study.
CSF
Headache
Migraine
Tau protein
Trigeminal Nerve
Journal
The journal of headache and pain
ISSN: 1129-2377
Titre abrégé: J Headache Pain
Pays: England
ID NLM: 100940562
Informations de publication
Date de publication:
19 Sep 2023
19 Sep 2023
Historique:
received:
17
07
2023
accepted:
01
09
2023
medline:
21
9
2023
pubmed:
20
9
2023
entrez:
19
9
2023
Statut:
epublish
Résumé
Migraine is a disorder associated with neuropeptide release, pain and inflammation. Tau protein has recently been linked to inflammatory diseases and can be influenced by neuropeptides such as CGRP, a key neurotransmitter in migraine. Here, we report serum concentrations of total-tau protein in migraine patients and healthy controls. In this cross-sectional study, interictal blood samples from n = 92 patients with episodic migraine (EM), n = 93 patients with chronic migraine (CM), and n = 42 healthy matched controls (HC) were studied. We assessed serum total-tau protein (t-tau) and for comparison neurofilament light chain protein (NfL), glial fibrillary acidic protein (GFAP), and ubiquitin carboxy-terminal hydrolase L (UCH-L1) concentrations using the Neurology 4-plex kit, on a single molecule array HD-X Analyzer (Quanterix Corp Lexington, MA). Matched serum/cerebrospinal fluid (CSF) samples were used for post-hoc evaluations of a central nervous system (CNS) source of relevant findings. We applied non-parametric tests to compare groups and assess correlations. Serum t-tau concentrations were elevated in EM [0.320 (0.204 to 0.466) pg/mL] and CM [0.304 (0.158 to 0.406) pg/mL] patients compared to HC [0.200 (0.114 to 0.288) pg/mL] (p = 0.002 vs. EM; p = 0.025 vs. CM). EM with aura [0.291 (0.184 to 0.486 pg/mL); p = 0.013] and EM without aura [0.332 (0.234 to 0.449) pg/mL; p = 0.008] patients had higher t-tau levels than HC but did not differ between each other. Subgroup analysis of CM with/without preventive treatment revealed elevated t-tau levels compared to HC only in the non-prevention group [0.322 (0.181 to 0.463) pg/mL; p = 0.009]. T-tau was elevated in serum (p = 0.028) but not in cerebrospinal fluid (p = 0.760). In contrast to t-tau, all proteins associated with cell damage (NfL, GFAP, and UCH-L1), did not differ between groups. Migraine is associated with t-tau elevation in serum but not in the CSF. Our clinical study identifies t-tau as a new target for migraine research.
Sections du résumé
BACKGROUND
BACKGROUND
Migraine is a disorder associated with neuropeptide release, pain and inflammation. Tau protein has recently been linked to inflammatory diseases and can be influenced by neuropeptides such as CGRP, a key neurotransmitter in migraine. Here, we report serum concentrations of total-tau protein in migraine patients and healthy controls.
METHODS
METHODS
In this cross-sectional study, interictal blood samples from n = 92 patients with episodic migraine (EM), n = 93 patients with chronic migraine (CM), and n = 42 healthy matched controls (HC) were studied. We assessed serum total-tau protein (t-tau) and for comparison neurofilament light chain protein (NfL), glial fibrillary acidic protein (GFAP), and ubiquitin carboxy-terminal hydrolase L (UCH-L1) concentrations using the Neurology 4-plex kit, on a single molecule array HD-X Analyzer (Quanterix Corp Lexington, MA). Matched serum/cerebrospinal fluid (CSF) samples were used for post-hoc evaluations of a central nervous system (CNS) source of relevant findings. We applied non-parametric tests to compare groups and assess correlations.
RESULTS
RESULTS
Serum t-tau concentrations were elevated in EM [0.320 (0.204 to 0.466) pg/mL] and CM [0.304 (0.158 to 0.406) pg/mL] patients compared to HC [0.200 (0.114 to 0.288) pg/mL] (p = 0.002 vs. EM; p = 0.025 vs. CM). EM with aura [0.291 (0.184 to 0.486 pg/mL); p = 0.013] and EM without aura [0.332 (0.234 to 0.449) pg/mL; p = 0.008] patients had higher t-tau levels than HC but did not differ between each other. Subgroup analysis of CM with/without preventive treatment revealed elevated t-tau levels compared to HC only in the non-prevention group [0.322 (0.181 to 0.463) pg/mL; p = 0.009]. T-tau was elevated in serum (p = 0.028) but not in cerebrospinal fluid (p = 0.760). In contrast to t-tau, all proteins associated with cell damage (NfL, GFAP, and UCH-L1), did not differ between groups.
DISCUSSION
CONCLUSIONS
Migraine is associated with t-tau elevation in serum but not in the CSF. Our clinical study identifies t-tau as a new target for migraine research.
Identifiants
pubmed: 37726712
doi: 10.1186/s10194-023-01663-5
pii: 10.1186/s10194-023-01663-5
pmc: PMC10507851
doi:
Substances chimiques
tau Proteins
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
130Subventions
Organisme : Novartis
ID : 125184
Informations de copyright
© 2023. Springer-Verlag Italia S.r.l., part of Springer Nature.
Références
Cephalalgia. 2018 Jan;38(1):1-211
pubmed: 29368949
Biomedicines. 2021 Dec 30;10(1):
pubmed: 35052756
Nat Rev Neurol. 2019 Aug;15(8):483-490
pubmed: 31263254
Nature. 2017 Sep 28;549(7673):523-527
pubmed: 28959956
Pain. 2011 Jan;152(1):140-149
pubmed: 21036476
Neurobiol Dis. 2006 Jul;23(1):87-96
pubmed: 16624562
Brain Res Bull. 2003 Aug 15;61(3):261-4
pubmed: 12909296
Exp Neurol. 2014 Nov;261:486-93
pubmed: 25079367
Neurosci Lett. 2008 Oct 3;443(2):67-71
pubmed: 18672021
Ann Neurol. 2020 Jun;87(6):939-949
pubmed: 32239542
Pharmaceuticals (Basel). 2010 Jun 17;3(6):1966-1987
pubmed: 27713337
Biomed J. 2018 Feb;41(1):21-33
pubmed: 29673549
Sci Rep. 2021 Apr 23;11(1):8861
pubmed: 33893374
J Neurosci Rural Pract. 2014 Apr;5(2):128-34
pubmed: 24966549
Ann Neurol. 1990 Aug;28(2):183-7
pubmed: 1699472
Headache. 2015 Jul-Aug;55 Suppl 4:221-35
pubmed: 26178694
Int J Mol Sci. 2021 Aug 19;22(16):
pubmed: 34445635
Headache. 2022 Jul;62(7):780-791
pubmed: 35676889
Lancet. 2017 Sep 16;390(10100):1211-1259
pubmed: 28919117
Proc Natl Acad Sci U S A. 2001 Apr 10;98(8):4687-92
pubmed: 11287655
Sci Transl Med. 2021 May 26;13(595):
pubmed: 34039738
Handb Exp Pharmacol. 2019;255:121-130
pubmed: 30725283
Brain. 2009 Jan;132(Pt 1):16-25
pubmed: 19052139
Mol Biol Rep. 2020 Sep;47(9):7125-7138
pubmed: 32951099
Neurology. 2006 Oct 24;67(8):1470-2
pubmed: 17060576
Elife. 2021 Apr 15;10:
pubmed: 33856345
Neuroreport. 1997 Jul 7;8(9-10):2237-40
pubmed: 9243618
Lancet Neurol. 2019 Aug;18(8):795-804
pubmed: 31160203
Neuropharmacology. 2020 May 15;168:108017
pubmed: 32113968
N Engl J Med. 2020 Nov 5;383(19):1866-1876
pubmed: 33211930
J Autoimmun. 2019 Jul;101:56-69
pubmed: 31010726
J Neurol Neurosurg Psychiatry. 2019 Aug;90(8):870-881
pubmed: 30967444
Ann Neurol. 1986 Sep;20(3):282-8
pubmed: 3767313
Neuroreport. 2002 Mar 25;13(4):507-9
pubmed: 11930171
Neurol Sci. 2013 May;34(5):655-61
pubmed: 22526766
Eur J Neurol. 2022 Sep;29(9):2810-2822
pubmed: 35638376
Neurochem Int. 2007 Jul-Sep;51(2-4):105-11
pubmed: 17586089
Proc Natl Acad Sci U S A. 2012 Nov 13;109(46):18985-90
pubmed: 23112192
Int J Alzheimers Dis. 2012;2012:731526
pubmed: 22690349
Biomed Pharmacother. 2010 Jul;64(6):430-6
pubmed: 20537498
Neurobiol Dis. 2023 May;180:106072
pubmed: 36907522