Palmitoylated Prolactin-releasing Peptide Reduced A beta Plaques and Microgliosis in the Cerebellum: APP/PS1 Mice Study

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F21%3A10434788" target="_blank" >RIV/00216208:11110/21:10434788 - isvavai.cz</a>

Výsledek na webu

<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=W.2_wKhxfa" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=W.2_wKhxfa</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.2174/1567205018666210922110652" target="_blank" >10.2174/1567205018666210922110652</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Palmitoylated Prolactin-releasing Peptide Reduced A beta Plaques and Microgliosis in the Cerebellum: APP/PS1 Mice Study

Popis výsledku v původním jazyce

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&apos;s Disease (AD)-like amyloid-beta (A beta) pathology, reducing the A beta plaque load, microgliosis and astrocytosis in the hippocampus and cortex. Objective: 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. Methods: 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. Results: 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. Conclusion: These results suggest palm(11)-PrRP31 is a promising agent for the treatment of neurodegenerative disorders.

Název v anglickém jazyce

Palmitoylated Prolactin-releasing Peptide Reduced A beta Plaques and Microgliosis in the Cerebellum: APP/PS1 Mice Study

Popis výsledku anglicky

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&apos;s Disease (AD)-like amyloid-beta (A beta) pathology, reducing the A beta plaque load, microgliosis and astrocytosis in the hippocampus and cortex. Objective: 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. Methods: 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. Results: 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. Conclusion: These results suggest palm(11)-PrRP31 is a promising agent for the treatment of neurodegenerative disorders.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30103 - Neurosciences (including psychophysiology)

Projekt

—

Návaznosti

V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

Rok uplatnění

2021

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Current Alzheimer Research

ISSN

1567-2050

e-ISSN

—

Svazek periodika

18

Číslo periodika v rámci svazku

8

Stát vydavatele periodika

NL - Nizozemsko

Počet stran výsledku

16

Strana od-do

607-622

Kód UT WoS článku

000723717100001

EID výsledku v databázi Scopus

2-s2.0-85125720272