Abstract | BACKGROUND: OBJECTIVE: In this study, we focused on the neuroprotective and anti-inflammatory effects of palm11-PrRP31 and its possible impact on synaptogenesis in the cerebellum of APP/PS1 mice, because others have suggested that cerebellar Aβ plaques contribute to cognitive deficits in AD. METHODS: APP/PS1 mice were treated subcutaneously with palm11-PrRP31 for 2 months, then immunoblotting and immunohistochemistry were used to quantify pathological markers connected to AD, compared to control mice. RESULTS: In the cerebella of 8 months old APP/PS1 mice, we found widespread Aβ plaques surrounded by activated microglia detected by ionized calcium-binding adapter molecule (Iba1), but no increase in astrocytic marker Glial Fibrillary Acidic Protein (GFAP) compared to controls. Interestingly, no difference in both presynaptic markers syntaxin1A and postsynaptic marker spinophilin was registered between APP/PS1 and control mice. Palm11-PrRP31 treatment significantly reduced the Aβ plaque load and microgliosis in the cerebellum. Furthermore, palm11-PrRP31 increased synaptogenesis and attenuated neuroinflammation and apoptosis in the hippocampus of APP/PS1 mice. CONCLUSION:
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Authors | Anna Mengr, Lucie Hrubá, Aneta Exnerová, Martina Holubová, Andrea Popelová, Blanka Železná, Jaroslav Kuneš, Lenka Maletínská |
Journal | Current Alzheimer research
(Curr Alzheimer Res)
Vol. 18
Issue 8
Pg. 607-622
( 2021)
ISSN: 1875-5828 [Electronic] United Arab Emirates |
PMID | 34551697
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright© Bentham Science Publishers; For any queries, please email at [email protected]. |
Chemical References |
- Amyloid beta-Peptides
- Amyloid beta-Protein Precursor
- Presenilin-1
- Prolactin-Releasing Hormone
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Topics |
- Alzheimer Disease
(metabolism)
- Amyloid beta-Peptides
(metabolism)
- Amyloid beta-Protein Precursor
(genetics, metabolism)
- Animals
- Cerebellum
- Diabetes Mellitus, Type 2
- Disease Models, Animal
- Humans
- Mice
- Mice, Transgenic
- Plaque, Amyloid
(pathology)
- Presenilin-1
(genetics, metabolism)
- Prolactin-Releasing Hormone
(metabolism, pharmacology)
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