Abstract | RATIONALE: RESULTS: Intracerebroventricular injection of oligomeric amyloid-β [25-35] peptide in three-month-old wildtype mice induced learning deficits, oxidative stress, synaptic marker alterations, activation of glycogen synthase kinase-3β, inhibition of protein kinase B (AKT), and apoptotic pathways as compared to scrambled peptide-treated wildtype mice. Scrambled peptide-treated Tc1 mice presented high levels of toxicity markers as compared to wildtype mice. Amyloid-β [25-35] peptide injection in Tc1 mice induced significant learning deficits and enhanced glycogen synthase kinase-3β activity in the cortex and expression of apoptotic markers in the hippocampus and cortex. Interestingly, several markers, including oxidative stress, synaptic markers, glycogen synthase kinase-3β activity in the hippocampus and AKT activity in the hippocampus and cortex, were unaffected by amyloid-β [25-35] peptide injection in Tc1 mice. CONCLUSIONS:
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Authors | Gaëlle Naert, Valentine Ferré, Emeline Keller, Amy Slender, Dorota Gibbins, Elizabeth Mc Fisher, Victor Lj Tybulewicz, Tangui Maurice |
Journal | Journal of psychopharmacology (Oxford, England)
(J Psychopharmacol)
Vol. 32
Issue 2
Pg. 174-190
(02 2018)
ISSN: 1461-7285 [Electronic] United States |
PMID | 29215943
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Amyloid beta-Peptides
- Biomarkers
- Peptide Fragments
- amyloid beta-protein (25-35)
- Glycogen Synthase Kinase 3 beta
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Topics |
- Alzheimer Disease
(genetics, physiopathology)
- Amyloid beta-Peptides
(administration & dosage, toxicity)
- Animals
- Biomarkers
(metabolism)
- Cerebral Cortex
(pathology)
- Disease Models, Animal
- Down Syndrome
(complications, genetics, physiopathology)
- Female
- Glycogen Synthase Kinase 3 beta
(metabolism)
- Hippocampus
(metabolism)
- Injections, Intraventricular
- Male
- Memory Disorders
(physiopathology)
- Mice
- Mice, Inbred C57BL
- Oxidative Stress
- Peptide Fragments
(administration & dosage, toxicity)
- Severity of Illness Index
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