Serum DBI and biomarkers of neuroinflammation in Alzheimer's disease and delirium.

Alzheimer’s disease Cytokines Delirium Diazepam binding inhibitor Monocytes Serum

Journal

Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
ISSN: 1590-3478
Titre abrégé: Neurol Sci
Pays: Italy
ID NLM: 100959175

Informations de publication

Date de publication:
Mar 2021
Historique:
received: 06 05 2020
accepted: 16 07 2020
pubmed: 25 7 2020
medline: 15 5 2021
entrez: 25 7 2020
Statut: ppublish

Résumé

Alzheimer's disease (AD) patients often express significant behavioral symptoms: for this reason, accessible related biomarkers could be very useful. Neuroinflammation is a key pathogenic process in both AD and delirium (DEL), a clinical condition with behavioral symptoms resembling those of AD. A total of n = 30 AD patients were recruited together with n = 30 DEL patients and n = 15 healthy controls (CTRL). Serum diazepam binding inhibitor (DBI), IL-17, IL-6, and TNF-α were assessed by ELISA. DBI serum levels were increased in AD patients with respect to CTRL (+ 81%), while DEL values were 70% higher than AD. IL-17 was increased in DEL with respect to CTRL (+ 146%), while AD showed dispersed values and failed to reach significant differences. On the other hand, IL-6 showed a more robust increase in DEL with respect to the other two groups (+ 185% and + 205% vs. CTRL and AD, respectively), and TNF-α failed to show any change. DBI may be a very promising candidate for AD, perhaps marking psychomotor DEL-like symptoms, in view of developing future helping tool for practicing physicians. Furthermore, DBI rise in DEL offers novel cues for a better comprehension of the pathogenesis of this potentially fatal condition.

Sections du résumé

BACKGROUND BACKGROUND
Alzheimer's disease (AD) patients often express significant behavioral symptoms: for this reason, accessible related biomarkers could be very useful. Neuroinflammation is a key pathogenic process in both AD and delirium (DEL), a clinical condition with behavioral symptoms resembling those of AD.
METHODS METHODS
A total of n = 30 AD patients were recruited together with n = 30 DEL patients and n = 15 healthy controls (CTRL). Serum diazepam binding inhibitor (DBI), IL-17, IL-6, and TNF-α were assessed by ELISA.
RESULTS RESULTS
DBI serum levels were increased in AD patients with respect to CTRL (+ 81%), while DEL values were 70% higher than AD. IL-17 was increased in DEL with respect to CTRL (+ 146%), while AD showed dispersed values and failed to reach significant differences. On the other hand, IL-6 showed a more robust increase in DEL with respect to the other two groups (+ 185% and + 205% vs. CTRL and AD, respectively), and TNF-α failed to show any change.
CONCLUSIONS CONCLUSIONS
DBI may be a very promising candidate for AD, perhaps marking psychomotor DEL-like symptoms, in view of developing future helping tool for practicing physicians. Furthermore, DBI rise in DEL offers novel cues for a better comprehension of the pathogenesis of this potentially fatal condition.

Identifiants

pubmed: 32705487
doi: 10.1007/s10072-020-04608-x
pii: 10.1007/s10072-020-04608-x
pmc: PMC7870594
doi:

Substances chimiques

Biomarkers 0
Diazepam Binding Inhibitor 0
Tumor Necrosis Factor-alpha 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1003-1007

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Auteurs

Elisa Conti (E)

School of Medicine and Surgery and Milan Center for Neuroscience (NeuroMI), University of Milano-Bicocca, Room 2043, Building U8, via Cadore 48, 20900, Monza, MB, Italy.

Simona Andreoni (S)

School of Medicine and Surgery and Milan Center for Neuroscience (NeuroMI), University of Milano-Bicocca, Room 2043, Building U8, via Cadore 48, 20900, Monza, MB, Italy.

Davide Tomaselli (D)

School of Medicine and Surgery and Milan Center for Neuroscience (NeuroMI), University of Milano-Bicocca, Room 2043, Building U8, via Cadore 48, 20900, Monza, MB, Italy.

Benedetta Storti (B)

School of Medicine and Surgery and Milan Center for Neuroscience (NeuroMI), University of Milano-Bicocca, Room 2043, Building U8, via Cadore 48, 20900, Monza, MB, Italy.
Neurology Unit, "San Gerardo" Hospital, Monza, Italy.

Francesco Brovelli (F)

School of Medicine and Surgery and Milan Center for Neuroscience (NeuroMI), University of Milano-Bicocca, Room 2043, Building U8, via Cadore 48, 20900, Monza, MB, Italy.
Neurology Unit, "San Gerardo" Hospital, Monza, Italy.

Roberto Acampora (R)

School of Medicine and Surgery and Milan Center for Neuroscience (NeuroMI), University of Milano-Bicocca, Room 2043, Building U8, via Cadore 48, 20900, Monza, MB, Italy.
Neurology Unit, "San Gerardo" Hospital, Monza, Italy.

Fulvio Da Re (F)

School of Medicine and Surgery and Milan Center for Neuroscience (NeuroMI), University of Milano-Bicocca, Room 2043, Building U8, via Cadore 48, 20900, Monza, MB, Italy.
Neurology Unit, "San Gerardo" Hospital, Monza, Italy.

Ildebrando Appollonio (I)

School of Medicine and Surgery and Milan Center for Neuroscience (NeuroMI), University of Milano-Bicocca, Room 2043, Building U8, via Cadore 48, 20900, Monza, MB, Italy.
Neurology Unit, "San Gerardo" Hospital, Monza, Italy.

Carlo Ferrarese (C)

School of Medicine and Surgery and Milan Center for Neuroscience (NeuroMI), University of Milano-Bicocca, Room 2043, Building U8, via Cadore 48, 20900, Monza, MB, Italy.
Neurology Unit, "San Gerardo" Hospital, Monza, Italy.

Lucio Tremolizzo (L)

School of Medicine and Surgery and Milan Center for Neuroscience (NeuroMI), University of Milano-Bicocca, Room 2043, Building U8, via Cadore 48, 20900, Monza, MB, Italy. lucio.tremolizzo@unimib.it.
Neurology Unit, "San Gerardo" Hospital, Monza, Italy. lucio.tremolizzo@unimib.it.

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