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024 7 _ |a 10.1002/alz70856_104796
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024 7 _ |a 1552-5279
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037 _ _ |a DZNE-2026-00041
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Bathe, Tim
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111 2 _ |a Alzheimer’s Association International Conference
|g AAIC 25
|c Toronto
|d 2025-07-27 - 2025-07-31
|w Canada
245 _ _ |a Multi‐tracer PET monitoring of an immunomodulatory therapy in 4R tauopathy: Evaluating a novel drug's impact on glial function and protein pathology
260 _ _ |c 2025
336 7 _ |a Abstract
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336 7 _ |a Conference Paper
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520 _ _ |a The prevalence of neurodegenerative diseases (ND), including Alzheimer's disease (AD) and non-AD tauopathies, is projected to rise significantly by 2050 due to an aging global population. Chronic neuroinflammation, driven by glial activation in response to protein pathologies, is a major contributor to disease progression. Targeting glial dysfunction through immunomodulatory therapies offers a promising approach to mitigate the effects of tauopathies and other ND.PS19 mice receive chronic treatment with GV1001 over 5 months. Serial neuroimaging techniques, including PET scans targeting tau protein, microglial activation, and astrocytic responses, are employed to assess treatment effects in vivo (Figure 1). Postmortem validation is performed using immunohistochemistry and biochemical methods, comparing treated mice to placebo and non-transgenic controls.The research scope is to monitor the efficacy of GV1001 in a transgenic tau mouse model (PS19) with an early-intervention biomarker study using molecular biology and neuroimaging techniques including TSPO (microglia) PET, deprenyl (astroglia) PET, tau PET (perfusion and retention) and CSF markers of inflammation (e.g. sTREM2) and neurodegeneration (NfL). Preliminary findings, expected to be presented at the conference, will provide insights into the drug's ability to modulate glial activity, restore homeostasis, and reduce tau pathology.This study highlights the potential of monitoring immunomodulatory strategies to address the complex interplay between chronic neuroinflammation and protein aggregation in ND. If successful, these findings could inform the development of novel therapeutic approaches for AD and related disorders, bridging the gap between preclinical research and clinical application.
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650 _ 7 |a Biomarkers
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650 _ 7 |a tau Proteins
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650 _ 2 |a Animals
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650 _ 2 |a Biomarkers: cerebrospinal fluid
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650 _ 2 |a Biomarkers: metabolism
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Mice, Transgenic
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650 _ 2 |a Disease Models, Animal
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650 _ 2 |a Alzheimer Disease: drug therapy
|2 MeSH
650 _ 2 |a Positron-Emission Tomography
|2 MeSH
650 _ 2 |a tau Proteins: metabolism
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Brain: metabolism
|2 MeSH
650 _ 2 |a Brain: pathology
|2 MeSH
650 _ 2 |a Brain: diagnostic imaging
|2 MeSH
650 _ 2 |a Brain: drug effects
|2 MeSH
650 _ 2 |a Tauopathies: drug therapy
|2 MeSH
650 _ 2 |a Microglia: metabolism
|2 MeSH
700 1 _ |a Salomasova, Svetlana
|b 1
700 1 _ |a Lalia, Manvir
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700 1 _ |a Kunze, Lea
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700 1 _ |a Palumbo, Giovanna
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700 1 _ |a Oos, Rosel
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700 1 _ |a Joseph, Emanuel
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700 1 _ |a Brendel, Matthias
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773 _ _ |a 10.1002/alz70856_104796
|g Vol. 21, no. S2, p. e104796
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|t Alzheimer's and dementia
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