ArticleCell reports2024
Machine learning reveals prominent spontaneous behavioral changes and treatment efficacy in humanized and transgenic Alzheimer's disease models.
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Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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9citing papers in PubMed, 1 pooled it
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Does advancement in marker-less pose-estimation mean more quality research? A systematic review.Frontiers in behavioral neuroscience · 2025Pooled it
- Considerations for the selection and phenotyping of mouse models for the study of Alzheimer's disease.STAR protocols · 2026Review
- Therapeutic targeting of fibrin-microglia interactions ameliorates Alzheimer's disease-related hyperexcitability and brain network dysfunction.bioRxiv : the preprint server for biology · 2026Article
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- Sleep-Wake Transitions Are Impaired in thebioRxiv : the preprint server for biology · 2025Article
- Development of a humanized anti-fibrin monoclonal antibody for the treatment of neuroinflammatory and retinal diseases.Journal of neuroinflammation · 2025Article
- APOE4-Aβ synergy drives brain network dysfunction and neuronal lysosomal-ER proteostasis dysregulation a preclinical Alzheimer's disease model.bioRxiv : the preprint server for biology · 2025Article
- Article
- AI-driven transformation of precision medicine: a comprehensive narrative review of key application areas, emerging paradigms, and future directions.Frontiers in public health · 2025Review
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Authors and funding
25 authors.
Stephanie R MillerGladstone Institute of Neurological Disease, San Francisco, CA 94158, USA; Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94158, USA. Electronic address: stephanie.miller@gladstone.ucsf.edu.
Kevin LuxemGerman Center for Neurodegenerative Diseases (DZNE), 39118 Bonn and Magdeburg, Germany; Department of Cellular Neuroscience, Leibniz Institute for Neurobiology, 39118 Magdeburg, Germany; Center for Behavioral Brain Sciences (CBBS), 39106 Magdeburg, Germany.
Kelli LauderdaleGladstone Institute of Neurological Disease, San Francisco, CA 94158, USA; Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94158, USA.
Pranav NambiarGladstone Institute of Neurological Disease, San Francisco, CA 94158, USA.
Patrick S HonmaGladstone Institute of Neurological Disease, San Francisco, CA 94158, USA; Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94158, USA.
Katie K LyGladstone Institute of Neurological Disease, San Francisco, CA 94158, USA; Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94158, USA.
Shreya BangeraGladstone Institute of Neurological Disease, San Francisco, CA 94158, USA; Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94158, USA.
Mary BullockCenter for Neurodegeneration and Experimental Therapeutics, Alzheimer's Disease Center, Department of Neurology, University of Alabama at Birmingham, Birmingham, AL 35233, USA.
Jia ShinGladstone Institute of Neurological Disease, San Francisco, CA 94158, USA; Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94158, USA.
Nick KalissGladstone Institute of Neurological Disease, San Francisco, CA 94158, USA.
Yuechen QiuGladstone Institute of Neurological Disease, San Francisco, CA 94158, USA.
Catherine CaiGladstone Institute of Neurological Disease, San Francisco, CA 94158, USA.
Kevin ShenGladstone Institute of Neurological Disease, San Francisco, CA 94158, USA.
K Dakota MallenGladstone Institute of Neurological Disease, San Francisco, CA 94158, USA.
Zhaoqi YanGladstone Institute of Neurological Disease, San Francisco, CA 94158, USA; Center for Neurovascular Brain Immunology at Gladstone and UCSF, San Francisco, CA 94158, USA.
Andrew S MendiolaGladstone Institute of Neurological Disease, San Francisco, CA 94158, USA; Center for Neurovascular Brain Immunology at Gladstone and UCSF, San Francisco, CA 94158, USA.
Takashi SaitoDepartment of Neurocognitive Science, Nagoya City University Graduate School of Medical Sciences, Nagoya 467-8601, Japan.
Takaomi C SaidoLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Wako-shi 351-0198, Japan.
Alexander R PicoGladstone Institute of Data Science and Biotechnology, San Francisco, CA 94158, USA.
Reuben ThomasGladstone Institute of Data Science and Biotechnology, San Francisco, CA 94158, USA.
Erik D RobersonCenter for Neurodegeneration and Experimental Therapeutics, Alzheimer's Disease Center, Department of Neurology, University of Alabama at Birmingham, Birmingham, AL 35233, USA.
Katerina AkassoglouGladstone Institute of Neurological Disease, San Francisco, CA 94158, USA; Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94158, USA; Center for Neurovascular Brain Immunology at Gladstone and UCSF, San Francisco, CA 94158, USA.
Pavol BauerGerman Center for Neurodegenerative Diseases (DZNE), 39118 Bonn and Magdeburg, Germany; Department of Cellular Neuroscience, Leibniz Institute for Neurobiology, 39118 Magdeburg, Germany; Center for Behavioral Brain Sciences (CBBS), 39106 Magdeburg, Germany.
Stefan RemyGerman Center for Neurodegenerative Diseases (DZNE), 39118 Bonn and Magdeburg, Germany; Department of Cellular Neuroscience, Leibniz Institute for Neurobiology, 39118 Magdeburg, Germany; Center for Behavioral Brain Sciences (CBBS), 39106 Magdeburg, Germany; German Center for Mental Health (DZPG), 39118 Magdeburg, Germany.
Jorge J PalopGladstone Institute of Neurological Disease, San Francisco, CA 94158, USA; Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94158, USA. Electronic address: jorge.palop@gladstone.ucsf.edu.
Funding
UCSD Shiley-Marcos Alzheimer's Disease Research Center P30P30AG062429 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DOUGLAS R GALASKO · 2019 to 2026
$34.9MProject 4: Cross-species Dissection of Cellular Response to APOE Genotype and AD Pathology Using Single-cell Multi-omicsP01AG073082 · NIA · J. DAVID GLADSTONE INSTITUTES · PI MUCKE, LENNART · 2021 to 2025
$23.4MUC San Diego FIRST ProgramU54CA272220 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MARIA ELENA MARTINEZ, Joann Trejo · 2022 to 2026
$21.2MNeurovascular Interactions: Mechanisms, imaging, therapeutic potentialR35NS097976 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI AKASSOGLOU, KATERINA · 2016 to 2023
$11.1MMOLECULAR AND CELLULAR IMMUNOLOGYT32AI007334 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CYSTER, JASON G · 1988 to 2023
$11.0MMultidimensional mapping of vulnerable cell types in humanized Alzheimer's disease mouse modelsR01AG082147 · NIA · STANFORD UNIVERSITY · PI Inma Cobos, Jorge J Palop · 2023 to 2026
$9.3MFibrinogen and vascular cognitive impairment: mechanisms, imaging, therapeuticsRF1AG064926 · NIA · J. DAVID GLADSTONE INSTITUTES · PI AKASSOGLOU, KATERINA, ELLISMAN, MARK H · 2019 to 2019
$4.5MCircadian changes in network excitability and Alzheimer disease pathogenesisR01AG061785 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GAMBLE, KAREN L, ROBERSON, ERIK D · 2021 to 2025
$3.9MOptogenetic dissection of cellular and circuit mechanisms of network dysfunction and amyloid deposition in mouse models of Alzheimer's disease in vivoRF1AG062234 · NIA · J. DAVID GLADSTONE INSTITUTES · PI PALOP, JORGE J · 2018 to 2021
$3.8MDeciphering molecular pathways of inhibitory interneuron dysfunction in Alzheimer's diseaseR01AG062629 · NIA · J. DAVID GLADSTONE INSTITUTES · PI PALOP, JORGE J · 2019 to 2023
$3.6MBIN1, Interneuron Activity, and Network Dysfunction in Alzheimer DiseaseRF1AG059405 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ROBERSON, ERIK D · 2018 to 2018
$2.6MRestoring Brain Functions in Alzheimer Models with Interneuron TransplantsR01AG047313 · NIA · J. DAVID GLADSTONE INSTITUTES · PI PALOP, JORGE J · 2014 to 2018
$1.9MNCI NIH HHS U54 CA272220NIAID NIH HHS T32 AI007334NIA NIH HHS K01 AG083732NIA NIH HHS P01 AG073082NIA NIH HHS P30 AG062429NIA NIH HHS R01 AG047313NIA NIH HHS R01 AG061785NIA NIH HHS R01 AG062629NIA NIH HHS R01 AG082147NIA NIH HHS RF1 AG059405NIA NIH HHS RF1 AG062234NIA NIH HHS RF1 AG064926NINDS NIH HHS K99 NS126707NINDS NIH HHS R00 NS126707NINDS NIH HHS R35 NS097976
Abstract
Computer-vision and machine-learning (ML) approaches are being developed to provide scalable, unbiased, and sensitive methods to assess mouse behavior. Here, we used the ML-based variational animal motion embedding (VAME) segmentation platform to assess spontaneous behavior in humanized App knockin and transgenic APP models of Alzheimer's disease (AD) and to test the role of AD-related neuroinflammation in these behavioral manifestations. We found marked alterations in spontaneous behavior in App
Indexed as
Alzheimer DiseaseBehavior, AnimalDisease Models, AnimalMachine LearningMice, TransgenicAmyloid beta-Protein PrecursorAnimalsFemaleHumansMaleMiceMice, Inbred C57BLTreatment OutcomeAmyloid beta-Protein PrecursoramyloidApp-KIbehavioral segmentationcognitionCP: NeuroscienceDeepLabCutKeypoint-MoSeqnaturalistic behavioropen fieldpose estimationpreclinical
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.