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Tytuł pozycji:

Involvement of the Chemokine Prokineticin-2 (PROK2) in Alzheimer's Disease: From Animal Models to the Human Pathology.

Tytuł :
Involvement of the Chemokine Prokineticin-2 (PROK2) in Alzheimer's Disease: From Animal Models to the Human Pathology.
Autorzy :
Lattanzi R; Department of Physiology and Pharmacology 'Vittorio Erspamer', Sapienza University of Rome, P.za A. Moro 5, 00185 Rome, Italy.
Maftei D; Department of Physiology and Pharmacology 'Vittorio Erspamer', Sapienza University of Rome, P.za A. Moro 5, 00185 Rome, Italy.
Petrella C; Institute of Biochemistry and Cell Biology, IBBC, CNR, Viale del Policlinico, 155, 00161 Rome, Italy.
Pieri M; Department of Experimental Medicine and Surgery, University of Rome Tor Vergata, 00133 Rome, Italy.
Sancesario G; Neuroimmunology Unit, IRCCS Santa Lucia Foundation, v. Ardeatina 354, 00179 Rome, Italy.
Schirinzi T; Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, Italy.
Bernardini S; Department of Experimental Medicine and Surgery, University of Rome Tor Vergata, 00133 Rome, Italy.
Barbato C; Institute of Biochemistry and Cell Biology, IBBC, CNR, Viale del Policlinico, 155, 00161 Rome, Italy.
Ralli M; Department of Sense Organs, University Sapienza of Rome, Viale del Policlinico 155, 00161 Rome, Italy.
Greco A; Department of Sense Organs, University Sapienza of Rome, Viale del Policlinico 155, 00161 Rome, Italy.
Possenti R; Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, Italy.
Sancesario G; Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, Italy.
Severini C; Institute of Biochemistry and Cell Biology, IBBC, CNR, Viale del Policlinico, 155, 00161 Rome, Italy.
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Źródło :
Cells [Cells] 2019 Nov 13; Vol. 8 (11). Date of Electronic Publication: 2019 Nov 13.
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
Język :
English
Imprint Name(s) :
Original Publication: Basel, Switzerland : MDPI
MeSH Terms :
Disease Susceptibility*
Alzheimer Disease/*etiology
Alzheimer Disease/*metabolism
Gastrointestinal Hormones/*genetics
Gastrointestinal Hormones/*metabolism
Neuropeptides/*genetics
Neuropeptides/*metabolism
Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Animals ; Biomarkers ; Brain/metabolism ; Brain/pathology ; Disease Models, Animal ; Gastrointestinal Hormones/blood ; Gene Expression Regulation ; Humans ; Mice ; Mice, Transgenic ; Neuropeptides/blood ; Protein Aggregates ; Protein Aggregation, Pathological/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Rats
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Contributed Indexing :
Keywords: Alzheimer’s disease*; blood biomarkers*; chemokines*; neuroinflammation*; prokineticins*
Substance Nomenclature :
0 (Amyloid beta-Peptides)
0 (Biomarkers)
0 (Gastrointestinal Hormones)
0 (Neuropeptides)
0 (PROK2 protein, human)
0 (Protein Aggregates)
0 (RNA, Messenger)
Entry Date(s) :
Date Created: 20191127 Date Completed: 20200707 Latest Revision: 20200707
Update Code :
20210210
PubMed Central ID :
PMC6912774
DOI :
10.3390/cells8111430
PMID :
31766244
Czasopismo naukowe
Among mediators of inflammation, chemokines play a pivotal role in the neuroinflammatory process related to Alzheimer's disease (AD). The chemokine Bv8/prokineticin 2 (PROK2) is a critical player in inflammatory and neuroinflammatory diseases and has been demonstrated to be involved in Aβ toxicity. The aim of the present study was to extend the research to rats chronically intracerebroventricularly (i.c.v.) injected with Aβ, to an AD transgenic mouse model, and subsequently to AD patients, mainly with the aim of detecting a potential biomarker. Real-time PCR and immunofluorescence analysis were used to evaluate Prokineticin-2 (PROK2) mRNA and the corresponding protein levels in both animal and human AD brain extracts, and the ELISA test was used to measure the amount of PROK2 in the serum of AD patients. We demonstrated a significant upregulation of PROK2 levels in brain tissues of Aβ 1-42 i.c.v. injected rats, transgenic AD mice (Tg2576), and in the hippocampus of AD patients. Additionally, through a pilot study, an approximate twofold increase of PROK2 levels has been proved in the serum of AD patients, compared to the control subjects, identifying a potential blood-based biomarker of the disease.
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