Abstract
Fibrinogen has emerged as a promising therapeutic target against Alzheimer's disease because of its dual role in altered vascular function and amyloid-β aggregation. Here we provide evidence regarding cognitive improvement and reduction of brain parenchyma amyloid-β deposition in AβPP/PS1 mice after treatment for one month with the fibrinogen-blocking peptide Fibγ377-395. No alteration in glial response or other neuroinflammatory markers was observed in the cortex of treated animals. Considering these results and the fact that Fibγ377-395 does not affect coagulation function, this peptide could be considered as a promising and safe candidate for chronic treatment of Alzheimer's disease.
Keywords:
Alzheimer’s disease; AβPP/PS1 mice; amyloid; fibrinogen; inflammation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amyloid / drug effects*
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Amyloid / metabolism
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Amyloid beta-Protein Precursor / genetics
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Amyloid beta-Protein Precursor / metabolism
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Animals
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Cerebral Cortex / drug effects*
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Cerebral Cortex / pathology
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Cerebral Cortex / physiopathology
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Cognition / drug effects*
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Cognition / physiology
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Exploratory Behavior / drug effects
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Exploratory Behavior / physiology
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Fibrinogen / metabolism
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Fibrinogen / pharmacology*
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Male
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Mice, Transgenic
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Neuroglia / drug effects
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Neuroglia / metabolism
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Neuroglia / pathology
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Neuroimmunomodulation / drug effects*
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Neuroimmunomodulation / physiology
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Neuroprotective Agents / pharmacology
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Nootropic Agents / pharmacology*
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Peptide Fragments / pharmacology*
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Presenilin-1 / genetics
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Presenilin-1 / metabolism
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RNA, Messenger / metabolism
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Random Allocation
Substances
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APP protein, human
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Amyloid
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Amyloid beta-Protein Precursor
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Neuroprotective Agents
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Nootropic Agents
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PSEN1 protein, human
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Peptide Fragments
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Presenilin-1
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RNA, Messenger
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fibrinogen gamma (377-395)
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Fibrinogen