Skip to main content
U.S. flag

An official website of the United States government

Neuroprotection by hypothalamic peptide proline-rich peptide-1 in Aβ25–35 model of Alzheimer’s disease

Bibliographic

Year of Publication:
2008
Contact PI Name:
John S. Sarkissian
Contact PI Affiliation:
Buniatyan Institute of Biochemistry, National Academy of Sciences of the Republic of Armenia, Yerevan, Armenia
Co-Authors:
Armen A. Galoyan, Vergineh A. Chavushyan, Irina B. Meliksetyan, Zaruhi E. Avagyan, Mikhail V. Poghosyan, Hasmik G. Vahradyan, Hovhannes H. Mkrtchian, Davit O. Abrahamyan
Primary Reference (PubMED ID):
Funding Source:
Not Reported
Study Goal and Principal Findings:

Background: This work sought to determine the effects of hypothalamic proline-rich peptide (PRP)-1 in a rat model of Alzheimer's disease.

Methods: Complex histochemical, electrophysiologic, and behavioral analyses were performed on intact or diseased Wistar rats (n = 28). Pathologic conditions were induced by bilateral intracerebroventricular injection of amyloid peptide Abeta25-35. The diseased rats received systemic administration of PRP-1 or placebo control.

Results: Abeta25-35 caused cellular neurodegeneration with marked glial reaction in the hippocampal complex and almost full destruction of the dentate fascia, which was not observed in conditions of PRP-1 administration after Abeta25-35 injection. Hippocampal neurons of intact animals responded to high-frequency (tetanic) stimulation of entorhinal cortex of ipsilateral cerebral hemisphere by tetanic and posttetanic potentiation of a different intensity and duration, which was accompanied by posttetanic depression. Abeta25-35 led to significant changes in the level and pattern of hippocampal neuronal activity, indicating the absence of both tetanic and posttetanic activity. Poststimulus activity manifestations rarely occurred and rapidly decreased after repeated trials. This indicated the focal character of lesion. Regular administration of PRP-1 for 4 weeks resulted in optimal restoration of electrophysiologic parameters. PRP-1 maintained the initial learning level achieved in a behavioral study in a Morris water maze.

Conclusions: Systemic administration of PRP-1 possesses neuroprotective effects and can prevent the neurodegeneration in hippocampus induced by Abeta25-35. This suggests that PRP-1 could be a potential therapeutic agent for specific neurodegenerative diseases.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Biologic - Peptide
Therapeutic Agent:
Proline-rich Peptide 1 (PRP-1)
Therapeutic Target:
Multi Target

Animal Model

Model Information:
Species:
Rat
Model Type:
beta Amyloid Peptide Injection
Strain/Genetic Background:
Not Applicable

Experimental Design

Is the following information reported in the study?:
Power/Sample Size Calculation
Randomized into Groups
Blinded for Treatment
Blinded for Outcome Measures
Pharmacokinetic Measures
Pharmacodynamic Measures
Toxicology Measures
ADME Measures
Biomarkers
Dose
Formulation
Route of Delivery
Duration of Treatment
Frequency of Administration
Age of Animal at the Beginning of Treatment
Age of Animal at the End of Treatment
Sex as a Biological Variable
Study Balanced for Sex as a Biological Variable
Number of Premature Deaths
Number of Excluded Animals
Statistical Plan
Genetic Background
Inclusion/Exclusion Criteria Included
Conflict of Interest
Experiment Notes

Age of Animal: In studies using rats, typically the rat weight is reported rather than age. A male Wistar rat weighing 300-350g is between 8-10 weeks old. A female Wistar rat weighing 300-350g is between 12-14 weeks old.
Balancing for Sex: Behavioral experiments were balanced for sex. It is unclear if electrophysiology and immunochemical experiments were balanced for sex.

Outcomes

Outcome Measured
Outcome Parameters
Behavioral
Morris Water Maze
Histopathology
Activated Microglia
Neuronal Loss
Immunochemistry
Activated Microglia
Neuronal Loss
Microscopy
Neuronal Cell Number
Neuronal Morphology
Neuronal Loss
Electrophysiology
Action Potentials
Inter-Spike Interval
In Vivo Extracellular Single Unit Recording
Post-Tetanic Depression (PTD)
Post-Tetanic Potentiation (PTP)
Toxicology
General Health
Motor Function
Food Intake
Water Consumption