{"id":36374,"date":"2025-05-19T08:10:14","date_gmt":"2025-05-19T08:10:14","guid":{"rendered":"https:\/\/www.etap-lab.com\/?p=15392"},"modified":"2026-08-28T12:28:42","modified_gmt":"2026-08-28T10:28:42","slug":"poster-neuroinflammation-models-of-neurodegenerative-diseases","status":"publish","type":"ressource","link":"https:\/\/www.etap-lab.com\/en\/ressource\/poster-neuroinflammation-models-of-neurodegenerative-diseases\/","title":{"rendered":"POSTER: &#8220;NEUROINFLAMMATION MODELS OF NEURODEGENERATIVE DISEASES&#8221;"},"content":{"rendered":"<p><strong>Dr Ahmad Allouche<\/strong>, Head of\u00a0<em>in vitro<\/em> biology, presented the team\u2019s research* during at <strong>Venusberg Neuroinflammation Meeting\u00a02025<\/strong> in Luxembourg in his poster \u201c<strong>NEUROINFLAMMATION MODELS OF NEURODEGENERATIVE DISEASES<\/strong>\u201c.<\/p>\n<p>Learn more about our cutting-edge platform for target identification &amp; drug discovery in the poster!<\/p>\n\n\n<div class=\"wp-block-buttons is-layout-flex wp-block-buttons-is-layout-flex\">\n<div class=\"wp-block-button is-style-primary\"><a class=\"wp-block-button__link wp-element-button\" href=\"mailto:marketing@etap-lab.com?subject=Poster%20Request%20-%20ETAP-LAB%20-[muInterest]%20&amp;body=Hello%2C%20%0ACan%20you%20send%20me%20the%20poster%20dealing%20with%20[myInterest]%20\/%20[title]%20.%20Thank%20you.%20\">EASY POSTER REQUEST<\/a><\/div>\n<\/div>\n\n\n\n<p class=\"wp-block-paragraph\"><strong>Authors<\/strong>: <em>*Ahmad ALLOUCHE, Valentin TALLANDIER, L\u00e9ane DIER, Sonia KRIDI, Julie COLIN, Nicolas VIOLLE.<\/em><\/p>\n\n\n\n<p class=\"wp-block-paragraph\"><strong>Affiliation<\/strong>: <em>1 ETAP-LAB, 54500, Vand\u0153uvre-l\u00e8s-Nancy, France<\/em><\/p>\n\n\n\n<p class=\"wp-block-paragraph\"><strong>Abstract<\/strong>: <\/p>\n\n\n\n<p class=\"wp-block-paragraph\">Neuroinflammation plays a pivotal role in the pathogenesis of neurodegenerative diseases (NDDs), such as Alzheimer\u2019s disease (AD), Parkinson\u2019s disease (PD) and amyotrophic lateral sclerosis (ALS). While inflammation is essential for brain defense, chronic neuroinflammation can lead to neuronal damage and accelerate disease progression. Understanding the relationship between neuroinflammation and disease development is crucial for developing effective therapeutic strategies.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">In this study, we investigated age-related changes in glial cell reactivity following neuroinflammatory stimulation. Using young and aged wild-type mice, we analyzed the response of astrocytes and microglia after a single intracerebral injection of either vehicle or amyloid-beta oligomers (A\u03b2O), a major toxic species implicated in AD. To further investigate the underlying mechanisms of neuroinflammation and bridge the gap between animal models and human systems, we assessed A\u03b2O-induced astrocyte activation in human induced pluripotent stem cell (hiPSC)-derived astrocytes using high-throughput imaging. This approach overcomes the limitations of traditional animal models and provides a more physiologically relevant representation of human neuroinflammatory responses.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\">Our results showed that while the overall astrocyte population remains stable with aging, the proportion of reactive astrocytes increases significantly across multiple brain regions. Moreover, a significant expansion of microglial population was observed in aged mice, suggesting a progressive neuroinflammatory response. A\u03b2O administration exacerbates astrocyte reactivity and microglial activation in both young and aged mice, highlighting the pro-inflammatory effects of this neurotoxin. While these findings in the murine model provide valuable insights into the neuroinflammatory processes underlying AD, we extend our investigation to human-derived astrocytes to further explore the cellular response mechanisms to A\u03b2O. In hiPSC-derived astrocytes, A\u03b2O exposure triggered reactivation <em>via<\/em> the nuclear factor kappa B (NF-\u03baB) pathway, providing a more precise understanding of the disease mechanism in human cells. Interestingly, treatment with Etanercept, a TNF-\u03b1 inhibitor, attenuates astrocyte reactivation in a dose-dependent manner.<\/p>\n\n\n\n<p class=\"wp-block-paragraph\"><strong>These findings highlight the impact of aging and A\u03b2O exposure on glial cell function and suggest potential therapeutic strategies targeting NF-\u03baB pathway, a key inflammatory pathway, to mitigate astrocyte reactivation and its downstream effects in neurodegenerative diseases.<\/strong><\/p>\n","protected":false},"excerpt":{"rendered":"<p>Discover POSTER: &#8220;NEUROINFLAMMATION MODELS OF NEURODEGENERATIVE DISEASES&#8221;: Dr Ahmad Allouche , Head of in vitro biology, presented the team\u2019s research* during at Venusberg\u2026<\/p>\n","protected":false},"featured_media":0,"template":"","meta":{"_acf_changed":false},"categorie-de-ressource":[236],"marque-de-ressource":[240],"class_list":["post-36374","ressource","type-ressource","status-publish","hentry","categorie-de-ressource-posters","marque-de-ressource-brainxplore"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v28.4 - 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