Palmitoylated Prolactin-releasing Peptide Reduced Aβ Plaques and Microgliosis in the Cerebellum: APP/PS1 Mice Study
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F21%3A00551939" target="_blank" >RIV/67985823:_____/21:00551939 - isvavai.cz</a>
Alternative codes found
RIV/61388963:_____/21:00549436
Result on the web
<a href="https://dx.doi.org/10.2174/1567205018666210922110652" target="_blank" >https://dx.doi.org/10.2174/1567205018666210922110652</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.2174/1567205018666210922110652" target="_blank" >10.2174/1567205018666210922110652</a>
Alternative languages
Result language
angličtina
Original language name
Palmitoylated Prolactin-releasing Peptide Reduced Aβ Plaques and Microgliosis in the Cerebellum: APP/PS1 Mice Study
Original language description
Background: Prolactin-releasing peptide (PrRP) is a potential drug for the treatment of obesity and associated Type 2 Diabetes Mellitus (T2DM) due to its strong anorexigenic and antidiabetic properties. In our recent study, the lipidized PrRP analog palm(II)-PrRP31 was proven to exert beneficial effects in APP/PS1 mice, a model of Alzheimer's Disease (AD)-like amyloid-beta (A beta) pathology, reducing the A beta plaque load, microgliosis and astrocytosis in the hippocampus and cortex.nObjective: In this study, we focused on the neuroprotective and anti-inflammatory effects of palm(11)-PrRP31 and its possible impact on synaptogenesis in the cerebellum of APP/PS1 mice, be cause others have suggested that cerebellar A beta plaques contribute to cognitive deficits in AD.nMethods: APP/PS1 mice were treated subcutaneously with palm(11)-PrRP31 for 2 months, then immunoblotting and immunohistochemistry were used to quantify pathological markers connected to AD, compared to control mice.nResults: In the cerebella of 8 months old APP/PS1 mice, we found widespread A beta 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. Palm(11)-PrRP31 treatment significantly reduced the A beta plaque load and microgliosis in the cerebellum. Furthermore, palm(11)-PrRP31 increased synaptogenesis and attenuated neuroinflammation and apoptosis in the hippocampus of APP/PS1 mice.nConclusion: These results suggest palm(11)-PrRP31 is a promising agent for the treatment of neurodegenerative disorders.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30105 - Physiology (including cytology)
Result continuities
Project
<a href="/en/project/GA20-00546S" target="_blank" >GA20-00546S: Obesity, diabetes and neurodegeneration crosstalk: New therapeutic potential of prolactin-releasing peptide analogs</a><br>
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Others
Publication year
2021
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Current Alzheimer Research
ISSN
1567-2050
e-ISSN
1875-5828
Volume of the periodical
18
Issue of the periodical within the volume
8
Country of publishing house
NL - THE KINGDOM OF THE NETHERLANDS
Number of pages
16
Pages from-to
607-622
UT code for WoS article
000723717100001
EID of the result in the Scopus database
2-s2.0-85125720272