Evaluation of aquaporins in the cerebrospinal fluid in patients with idiopathic normal pressure hydrocephalus.
Aged
Aged, 80 and over
Alzheimer Disease
/ cerebrospinal fluid
Amyloid beta-Peptides
/ genetics
Aquaporin 1
/ cerebrospinal fluid
Aquaporin 4
/ cerebrospinal fluid
Biomarkers
/ cerebrospinal fluid
Diagnosis, Differential
Female
Humans
Hydrocephalus, Normal Pressure
/ cerebrospinal fluid
Male
Middle Aged
Peptide Fragments
/ cerebrospinal fluid
tau Proteins
/ genetics
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2021
2021
Historique:
received:
11
06
2021
accepted:
21
09
2021
entrez:
1
10
2021
pubmed:
2
10
2021
medline:
27
11
2021
Statut:
epublish
Résumé
Brain aquaporin 1 (AQP1) and AQP4 are involved in cerebrospinal fluid (CSF) homeostasis and might participate in the origin of hydrocephalus. Studies have shown alterations of perivascular AQP4 expression in idiopathic normal pressure hydrocephalus (iNPH) and Alzheimer's disease (AD). Due to the overlapping of clinical signs between iNPH and certain neurological conditions, mainly AD, specific biomarkers might improve the diagnostic accuracy for iNPH. The goal of the present study was to analyze and quantify the presence of AQP1 and AQP4 in the CSF of patients with iNPH and AD to determine whether these proteins can be used as biomarkers of iNPH. We examined AQP1 and AQP4 protein levels in the CSF of 179 participants (88 women) classified into 5 groups: possible iNPH (81 participants), hydrocephalus associated with other neurological disorders (13 participants), AD (41 participants), non-AD dementia (32 participants) and healthy controls (12 participants). We recorded each participant's demographic and clinical variables and indicated, when available in the clinical history, the record of cardiovascular and respiratory complications. An ELISA showed virtually no AQP content in the CSF. Information on the vascular risk factors (available for 61 patients) confirmed some type of vascular risk factor in 86% of the patients with possible iNPH and 58% of the patients with AD. In conclusion, the ELISA analysis showed insufficient sensitivity to detect the presence of AQP1 and AQP4 in CSF, ruling out the possible use of these proteins as biomarkers for diagnosing iNPH.
Identifiants
pubmed: 34597351
doi: 10.1371/journal.pone.0258165
pii: PONE-D-21-19251
pmc: PMC8486078
doi:
Substances chimiques
AQP1 protein, human
0
AQP4 protein, human
0
Amyloid beta-Peptides
0
Aquaporin 4
0
Biomarkers
0
Peptide Fragments
0
tau Proteins
0
Aquaporin 1
146410-94-8
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0258165Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
Références
J Neurol Neurosurg Psychiatry. 2019 Oct;90(10):1117-1123
pubmed: 31167811
BMC Neurol. 2014 Jul 01;14:139
pubmed: 24980919
Cells. 2019 Feb 24;8(2):
pubmed: 30813473
Neuropathol Appl Neurobiol. 2018 Aug;44(5):474-490
pubmed: 28627088
PLoS One. 2019 May 29;14(5):e0217705
pubmed: 31141553
Gerontology. 2019;65(2):106-119
pubmed: 29996134
Curr Neurol Neurosci Rep. 2019 May 29;19(7):39
pubmed: 31144048
Childs Nerv Syst. 2011 Jan;27(1):27-33
pubmed: 20625739
Brain. 2017 Oct 1;140(10):2691-2705
pubmed: 28969373
Clin Neurol Neurosurg. 2016 Jul;146:76-81
pubmed: 27155076
Neurosurgery. 2005 Sep;57(3 Suppl):S17-28; discussion ii-v
pubmed: 16160426
Neurobiol Dis. 2016 Sep;93:215-25
pubmed: 27234656
Clin Interv Aging. 2021 Jan 15;16:139-153
pubmed: 33488070
Int J Mol Sci. 2016 Jul 23;17(8):
pubmed: 27455255
Biochim Biophys Acta Mol Basis Dis. 2018 Oct;1864(10):3515-3526
pubmed: 30293570
Neurology. 2010 Jul 20;75(3):208-16
pubmed: 20644148
Int J Mol Sci. 2019 Nov 19;20(22):
pubmed: 31752329
J Neurol Neurosurg Psychiatry. 2013 May;84(5):562-8
pubmed: 23250963
Neuroscientist. 2017 Oct;23(5):454-465
pubmed: 28466758
Fluids Barriers CNS. 2014 Aug 19;11:19
pubmed: 25180074
Trends Mol Med. 2020 Mar;26(3):285-295
pubmed: 31959516
Glia. 2019 Jan;67(1):91-100
pubmed: 30306658
Neurol Med Chir (Tokyo). 2012;52(11):775-809
pubmed: 23183074
J Neural Transm (Vienna). 2018 Apr;125(4):673-679
pubmed: 29353355
PLoS One. 2012;7(5):e37435
pubmed: 22624030
J Neuropathol Exp Neurol. 2019 Jul 1;78(7):641-647
pubmed: 31039249
Med Hypotheses. 2009 Nov;73(5):718-24
pubmed: 19640656
Lancet Neurol. 2014 Jun;13(6):614-29
pubmed: 24849862
Cerebrospinal Fluid Res. 2010 Oct 31;7:18
pubmed: 21040519
J Alzheimers Dis. 2019;69(3):663-669
pubmed: 31156164
J Alzheimers Dis. 2015;45(1):109-15
pubmed: 25428256
Ann Neurol. 2020 Oct;88(4):703-711
pubmed: 32662116
Neurology. 2017 Feb 7;88(6):577-585
pubmed: 28062721
J Clin Neurosci. 2019 Mar;61:10-13
pubmed: 30409528
J Med Case Rep. 2019 Jan 30;13(1):27
pubmed: 30696485
Acta Neurol Scand. 2012 Oct;126(4):229-37
pubmed: 22587624
Continuum (Minneap Minn). 2016 Apr;22(2 Dementia):579-99
pubmed: 27042909
Neurosci Lett. 2011 Oct 17;504(1):23-7
pubmed: 21896312
Neurosurg Rev. 2020 Dec;43(6):1451-1464
pubmed: 31705404
JAMA Neurol. 2017 Jan 1;74(1):91-99
pubmed: 27893874
Neurosurgery. 2005 Sep;57(3 Suppl):S4-16; discussion ii-v
pubmed: 16160425