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Palmitoylated Prolactin-releasing Peptide Reduced A beta 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%2F00216208%3A11110%2F21%3A10434788" target="_blank" >RIV/00216208:11110/21:10434788 - isvavai.cz</a>

  • Result on the web

    <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>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Palmitoylated Prolactin-releasing Peptide Reduced A beta 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&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.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30103 - Neurosciences (including psychophysiology)

Result continuities

  • Project

  • Continuities

    V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

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

  • 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