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

Identifikátory výsledku

  • Kód výsledku v 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>

  • Nalezeny alternativní kódy

    RIV/61388963:_____/21:00549436

  • Výsledek na webu

    <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>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

    Palmitoylated Prolactin-releasing Peptide Reduced Aβ 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'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.

  • Název v anglickém jazyce

    Palmitoylated Prolactin-releasing Peptide Reduced Aβ 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'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.

Klasifikace

  • Druh

    J<sub>imp</sub> - Článek v periodiku v databázi Web of Science

  • CEP obor

  • OECD FORD obor

    30105 - Physiology (including cytology)

Návaznosti výsledku

  • Projekt

    <a href="/cs/project/GA20-00546S" target="_blank" >GA20-00546S: Souvislost obezity, diabetu a neurodegenerace: nový terapeutický potenciál analogů peptidu uvolňujícího prolaktin</a><br>

  • Návaznosti

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Ostatní

  • Rok uplatnění

    2021

  • Kód důvěrnosti údajů

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

Údaje specifické pro druh výsledku

  • Název periodika

    Current Alzheimer Research

  • ISSN

    1567-2050

  • e-ISSN

    1875-5828

  • 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