Neuroprotective effects of anorexigenic peptidic analogs in APP/PS1 model: Impact of a high-fat diet on Aβ pathology and neuroinflammation

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388963%3A_____%2F25%3A00645834" target="_blank" >RIV/61388963:_____/25:00645834 - isvavai.cz</a>

Výsledek na webu

<a href="https://hdl.handle.net/11104/0375619" target="_blank" >https://hdl.handle.net/11104/0375619</a>

DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Neuroprotective effects of anorexigenic peptidic analogs in APP/PS1 model: Impact of a high-fat diet on Aβ pathology and neuroinflammation

Popis výsledku v původním jazyce

Alzheimer’s disease (AD) shares several pathological features with type 2 diabetes, including impaired insulin signaling, insulin resistance, and altered lipid metabolism, and is therefore often referred to as “type 3 diabetes.” Mid-life obesity has also been identified as an important risk factor for the development of AD. This study follows our previous findings showing that a high-fat diet aggravates amyloid-β pathology, neuroinflammation, and Tau pathology in APP/PS1 mice. The aim of the present work was to evaluate how these pathological changes are affected by a three-month treatment with a prolactin-releasing peptide analog, palm¹¹-PrRP31, and the glucagon-like peptide-1 receptor agonist liraglutide. The study focuses on assessing the potential neuroprotective effects of anorexigenic peptidic analogs in a mouse model of diet-induced metabolic impairment and Alzheimer’s disease.

Název v anglickém jazyce

Neuroprotective effects of anorexigenic peptidic analogs in APP/PS1 model: Impact of a high-fat diet on Aβ pathology and neuroinflammation

Popis výsledku anglicky

Alzheimer’s disease (AD) shares several pathological features with type 2 diabetes, including impaired insulin signaling, insulin resistance, and altered lipid metabolism, and is therefore often referred to as “type 3 diabetes.” Mid-life obesity has also been identified as an important risk factor for the development of AD. This study follows our previous findings showing that a high-fat diet aggravates amyloid-β pathology, neuroinflammation, and Tau pathology in APP/PS1 mice. The aim of the present work was to evaluate how these pathological changes are affected by a three-month treatment with a prolactin-releasing peptide analog, palm¹¹-PrRP31, and the glucagon-like peptide-1 receptor agonist liraglutide. The study focuses on assessing the potential neuroprotective effects of anorexigenic peptidic analogs in a mouse model of diet-induced metabolic impairment and Alzheimer’s disease.

Druh

O - Ostatní výsledky

CEP obor

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OECD FORD obor

10608 - Biochemistry and molecular biology

Projekt

<a href="/cs/project/TN02000109" target="_blank" >TN02000109: Personalizovaná medicína: Translačním výzkumem k biomedicínským aplikacím</a><br>

Návaznosti

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

Rok uplatnění

2025

Kód důvěrnosti údajů

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