Association Between Cerebrospinal Fluid Biomarkers and Age-related Brain Changes in Patients with Normal Pressure Hydrocephalus.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
04 06 2020
Historique:
received: 31 03 2020
accepted: 16 05 2020
entrez: 6 6 2020
pubmed: 6 6 2020
medline: 20 1 2021
Statut: epublish

Résumé

Our study aimed to: 1)investigate the diagnostic utility of CSF Aβ42, t-tau, and p-tau to differentiate normal-pressure-hydrocephalus(NPH) from Alzheimer's-disease(AD) and normal-controls; and 2)investigate if age and ventricular size affect the levels of CSF biomarkers in NPH patients. We recruited 131 participants: (a)Suspected-NPH: 72 with ventriculomegaly and clinical symptoms of NPH. These participants were then divided into two groups of 1)Probable-NPH (N = 38) and 2)Unlikely-NPH (N = 34) based on whether participants experienced gait improvement after removal of a large amount of CSF; (b)AD group: 30 participants with CSF biomarkers and cognitive symptoms consistent with AD; (c)Control-group: 29 participants who were cognitively and functionally normal. Lower levels of CSF Aβ42 and p-tau were observed in the probable-NPH compared to the normal controls(444.22 ± 163.3 vs. 1213.75 ± 556.5; and 26.05 ± 9.2 vs. 46.16 ± 13.3 pg/mL; respectively). Lower levels of CSF p-tau and t-tau were found in the probable-NPH compared to the AD(26.05 ± 9.2 vs. 114.95 ± 28.2; and 193.29 ± 92.3 vs. 822.65 ± 311.5 pg/mL; respectively) but the CSF-Aβ42 was low in both the probable-NPH and AD. CSF-Aβ42 correlated with age and Evans-index only in the probable-NPH(r = 0.460, p = 0.004; and r = -0.530, p = 0.001; respectively). Our study supports the hypothesis that age-related atrophy results in better Aβ42 clearance in the CSF because of the increase in the interstitial space.

Identifiants

pubmed: 32499567
doi: 10.1038/s41598-020-66154-y
pii: 10.1038/s41598-020-66154-y
pmc: PMC7272629
doi:

Substances chimiques

Amyloid beta-Peptides 0
Biomarkers 0
Peptide Fragments 0
amyloid beta-protein (1-42) 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

9106

Références

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Auteurs

Foad Taghdiri (F)

Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto, 60 Leonard avenue, Toronto, ON, M5T 2S8, Canada.
Department of medicine, Division of Neurology, University of Toronto, Toronto, ON, Canada.

Melisa Gumus (M)

Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto, 60 Leonard avenue, Toronto, ON, M5T 2S8, Canada.

Musleh Algarni (M)

Edmond J. Safra Program in Parkinson's Disease, Morton and Gloria Shulman Movement Disorders Clinic, Toronto Western Hospital, UHN, Toronto, Ontario, Canada. Division of Neurology, University of Toronto, Toronto, Ontario, Canada.

Alfonso Fasano (A)

Department of medicine, Division of Neurology, University of Toronto, Toronto, ON, Canada.
Edmond J. Safra Program in Parkinson's Disease, Morton and Gloria Shulman Movement Disorders Clinic, Toronto Western Hospital, UHN, Toronto, Ontario, Canada. Division of Neurology, University of Toronto, Toronto, Ontario, Canada.
Krembil Brain Institute, Toronto, Ontario, Canada.

David Tang-Wai (D)

Department of medicine, Division of Neurology, University of Toronto, Toronto, ON, Canada.

Maria Carmela Tartaglia (MC)

Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto, 60 Leonard avenue, Toronto, ON, M5T 2S8, Canada. carmela.tartaglia@uhn.ca.
Department of medicine, Division of Neurology, University of Toronto, Toronto, ON, Canada. carmela.tartaglia@uhn.ca.

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