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Tytuł pozycji:

Histamine H3 Inverse Agonist BF 2649 or Antagonist with Partial H4 Agonist Activity Clobenpropit Reduces Amyloid Beta Peptide-Induced Brain Pathology in Alzheimer's Disease.

Tytuł :
Histamine H3 Inverse Agonist BF 2649 or Antagonist with Partial H4 Agonist Activity Clobenpropit Reduces Amyloid Beta Peptide-Induced Brain Pathology in Alzheimer's Disease.
Autorzy :
Patnaik R; School of Biomedical Engineering, Department of Biomaterials, Indian Institute of Technology, Banaras Hindu University, Varanasi, India.; Department of Surgical Sciences, Anesthesiology and Intensive Care Medicine, Uppsala University Hospital, Uppsala University, SE-75185, Uppsala, Sweden.
Sharma A; Department of Surgical Sciences, Anesthesiology and Intensive Care Medicine, Uppsala University Hospital, Uppsala University, SE-75185, Uppsala, Sweden.; International Experimental Central Nervous System Injury and Repair (IECNSIR), University Hospital, Uppsala University, Frödingsgatan 12, Bldg. 28, SE-75421, Uppsala, Sweden.; LaNCE, Department of Neuroscience, University of the Basque Country (UPV/EHU), Leioa, Bizkaia, Spain.
Skaper SD; Department of Pharmaceutical and Pharmacological Sciences, University of Padua, Largo 'E. Meneghetti' 2, 35131, Padua, Italy.
Muresanu DF; 'RoNeuro' Institute for Neurological Research and Diagnostic, 37 Mircea Eliade Street, 400364, Cluj-Napoca, Romania.; Department of Clinical Neurosciences, University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Lafuente JV; LaNCE, Department of Neuroscience, University of the Basque Country (UPV/EHU), Leioa, Bizkaia, Spain.; Nanoneurosurgery Group, BioCruces Health Research Institute, 48903, Barakaldo, Bizkaia, Spain.; Faculty of Health Science, Universidad Autónoma de Chile, Santiago de Chile, Chile.
Castellani RJ; University of Maryland, Department of Pathology, Baltimore, MD, USA.
Nozari A; Anesthesiology, Massachusetts General Hospital, Harvard University, Boston, MA, USA.
Sharma HS; Department of Surgical Sciences, Anesthesiology and Intensive Care Medicine, Uppsala University Hospital, Uppsala University, SE-75185, Uppsala, Sweden. .; International Experimental Central Nervous System Injury and Repair (IECNSIR), University Hospital, Uppsala University, Frödingsgatan 12, Bldg. 28, SE-75421, Uppsala, Sweden. .; LaNCE, Department of Neuroscience, University of the Basque Country (UPV/EHU), Leioa, Bizkaia, Spain. .
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Źródło :
Molecular neurobiology [Mol Neurobiol] 2018 Jan; Vol. 55 (1), pp. 312-321.
Typ publikacji :
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
Język :
English
Imprint Name(s) :
Original Publication: Clifton, NJ : Humana Press, c1987-
MeSH Terms :
Alzheimer Disease/*pathology
Amyloid beta-Peptides/*toxicity
Brain/*pathology
Histamine Agonists/*therapeutic use
Histamine H3 Antagonists/*therapeutic use
Imidazoles/*therapeutic use
Receptors, Histamine H4/*agonists
Thiourea/*analogs & derivatives
Alzheimer Disease/chemically induced ; Alzheimer Disease/drug therapy ; Animals ; Brain/drug effects ; Drug Inverse Agonism ; Drug Partial Agonism ; Histamine Agonists/pharmacology ; Histamine H3 Antagonists/pharmacology ; Imidazoles/pharmacology ; Male ; Rats ; Rats, Sprague-Dawley ; Thiourea/pharmacology ; Thiourea/therapeutic use
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Grant Information :
R01 AG028679 United States AG NIA NIH HHS
Contributed Indexing :
Keywords: Alzheimer’s disease (AD)*; Amyloid beta peptide (AβP)*; BF2649*; Blood-brain barrier*; Brain pathology*; Clobenpropit*; H3 receptor inverse agonist*; H3 receptors antagonist with partial H4 agonist*; Histamine*
Substance Nomenclature :
0 (Amyloid beta-Peptides)
0 (Histamine Agonists)
0 (Histamine H3 Antagonists)
0 (Hrh4 protein, rat)
0 (Imidazoles)
0 (Receptors, Histamine H4)
GYV9AM2QAG (Thiourea)
RKU631JF4H (clobenpropit)
Entry Date(s) :
Date Created: 20170902 Date Completed: 20190312 Latest Revision: 20190312
Update Code :
20210301
DOI :
10.1007/s12035-017-0743-8
PMID :
28861757
Czasopismo naukowe
Alzheimer's disease (AD) is one of the leading causes for disability and death affecting millions of people worldwide. Thus, novel therapeutic strategies are needed to reduce brain pathology associated with AD. In view of increasing awareness regarding involvement of histaminergic pathways in AD, we explored the role of one H3 receptor inverse agonist BF 2649 and one selective H3 receptor antagonist with partial H4 agonist activity in amyloid beta peptide (AβP) infusion-induced brain pathology in a rat model. AD-like pathology was produced by administering AβP (1-40) intracerebroventricular (i.c.v.) in the left lateral ventricle (250 ng/10 μl, once daily) for 4 weeks. Control rats received saline. In separate group of rats, either BF 2649 (1 mg/kg, i.p.) or clobenpropit (1 mg/kg, i.p.) was administered once daily for 1 week after 3 weeks of AβP administration. After 30 days, blood-brain barrier (BBB) breakdown, edema formation, neuronal, glial injuries, and AβP deposits were examined in the brain. A significant reduction in AβP deposits along with marked reduction in neuronal or glial reactions was seen in the drug-treated group. The BBB breakdown to Evans blue albumin and radioiodine in the cortex, hippocampus, hypothalamus, and cerebellum was also significantly reduced in these drug-treated groups. Clobenpropit showed superior effects than the BF2649 in reducing brain pathology in AD. Taken together, our observations are the first to show that blockade of H3 and stimulation of H4 receptors are beneficial for the treatment of AD pathology, not reported earlier.

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