ArticleAlzheimer's research & therapy2019
Late-stage Anle138b treatment ameliorates tau pathology and metabolic decline in a mouse model of human Alzheimer's disease tau.
Article in Alzheimer's research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Trial
- Anle138b ameliorates pathological phenotypes in mouse and cellular models of Huntington's disease.EMBO molecular medicine · 2026Article
- Anle138b binds predominantly to the central cavity in lipidic Aβ₄₀ fibrils and modulates fibril formation.Nature communications · 2025Article
- Targeting Protein Misfolding and Aggregation as a Therapeutic Perspective in Neurodegenerative Disorders.International journal of molecular sciences · 2024Review
- Review
- Inhibition of miR-4763-3p expression activates the PI3K/mTOR/Bcl2 autophagy signaling pathway to ameliorate cognitive decline.International journal of biological sciences · 2024Article
- Inhibition of Protein Aggregation and Endoplasmic Reticulum Stress as a Targeted Therapy for α-Synucleinopathy.Pharmaceutics · 2023Review
- Mechanism of action deconvolution of the small-molecule pathological tau aggregation inhibitor Anle138b.Alzheimer's research & therapy · 2023Article
- Article
- Disease modification in Parkinsonism: obstacles and ways forward.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Potent Tau Aggregation Inhibitor D-Peptides Selected against Tau-Repeat 2 Using Mirror Image Phage Display.Chembiochem : a European journal of chemical biology · 2021Article
- Feasibility of short imaging protocols for [European journal of nuclear medicine and molecular imaging · 2021Article
- Brain metabolism in tau and amyloid mouse models of Alzheimer's disease: An MRI study.NMR in biomedicine · 2021Article
- Alpha-Synuclein PET Tracer Development-An Overview about Current Efforts.Pharmaceuticals (Basel, Switzerland) · 2021Review
- The informed road map to prevention of Alzheimer Disease: A call to arms.Molecular neurodegeneration · 2021Review
- Amyloid Oligomers: A Joint Experimental/Computational Perspective on Alzheimer's Disease, Parkinson's Disease, Type II Diabetes, and Amyotrophic Lateral Sclerosis.Chemical reviews · 2021Review
- Positron Emission Tomography in Animal Models of Tauopathies.Frontiers in aging neuroscience · 2021Review
- Pharmacological Modulators of Tau Aggregation and Spreading.Brain sciences · 2020Review
- Soluble endogenous oligomeric α-synuclein species in neurodegenerative diseases: Expression, spreading, and cross-talk.Journal of Parkinson's disease · 2020Review
- Constant Levels of Tau Phosphorylation in the Brain of htau Mice.Frontiers in molecular neuroscience · 2020Article
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Authors and funding
21 authors at 7 institutions in 3 countries.
Funding
Abstract
backgroundAugmenting the brain clearance of toxic oligomers with small molecule modulators constitutes a promising therapeutic concept against tau deposition. However, there has been no test of this concept in animal models of Alzheimer's disease (AD) with initiation at a late disease stage. Thus, we aimed to investigate the effects of interventional late-stage Anle138b treatment, which previously indicated great potential to inhibit oligomer accumulation by binding of pathological aggregates, on the metabolic decline in transgenic mice with established tauopathy in a longitudinal
methodsTwelve transgenic mice expressing all six human tau isoforms (hTau) and ten controls were imaged by FDG-PET at baseline (14.5 months), followed by randomization into Anle138b treatment and vehicle groups for 3 months. FDG-PET was repeated after treatment for 3 months, and brains were analyzed by tau immunohistochemistry. Longitudinal changes of glucose metabolism were compared between study groups, and the end point tau load was correlated with individual FDG-PET findings.
resultsTau pathology was significantly ameliorated by late-stage Anle138b treatment when compared to vehicle (frontal cortex - 53%, p < 0.001; hippocampus - 59%, p < 0.005). FDG-PET revealed a reversal of metabolic decline during Anle138b treatment, whereas the vehicle group showed ongoing deterioration. End point glucose metabolism in the brain of hTau mice had a strong correlation with tau deposition measured by immunohistochemistry (R = 0.92, p < 0.001).
conclusionLate-stage oligomer modulation effectively ameliorated tau pathology in hTau mice and rescued metabolic function. Molecular imaging by FDG-PET can serve for monitoring effects of Anle138b treatment.
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