ArticleMolecular neurobiology2015
Pan-PPAR modulation effectively protects APP/PS1 mice from amyloid deposition and cognitive deficits.
Article in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Effect of antidiabetic drugs in Alzheimer´s disease: a systematic review of preclinical and clinical studies.Molecular neurodegeneration · 2025Pooled it
- Phlorizin Ameliorates Amyloid-β Toxicity and Enhances Fatty Acid β-Oxidation inInternational journal of molecular sciences · 2025Article
- Peony Seed Oil Inhibited Neuroinflammation by PPAR/RXR Signaling Pathway in D-Gal Induced Mice.Food science & nutrition · 2025Article
- Associations between triglyceride-glucose indices and delirium risk in critically ill patients with acute kidney injury: a retrospective study.Frontiers in endocrinology · 2025Article
- Targeting Microglia in Alzheimer's Disease: Pathogenesis and Potential Therapeutic Strategies.Biomolecules · 2024Review
- PPARs (Peroxisome Proliferator-activated Receptors) and Their Agonists in Alzheimer's Disease.Medicinal chemistry (Shariqah (United Arab Emirates)) · 2024Review
- Oleoylethanolamide facilitates PPARα and TFEB signaling and attenuates Aβ pathology in a mouse model of Alzheimer's disease.Molecular neurodegeneration · 2023Article
- PPARs and Their Neuroprotective Effects in Parkinson's Disease: A Novel Therapeutic Approach in α-Synucleinopathy?International journal of molecular sciences · 2023Review
- Oleoylethanolamide facilitates PPARa and TFEB signaling and attenuates Ab pathology in a mouse model of Alzheimer's disease.Research square · 2023Article
- Increasing brain glucose metabolism by ligustrazine piperazine ameliorates cognitive deficits through PPARγ-dependent enhancement of mitophagy in APP/PS1 mice.Alzheimer's research & therapy · 2022Article
- Bezafibrate Exerts Neuroprotective Effects in a Rat Model of Sporadic Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Renal Denervation Attenuates Neuroinflammation in the Brain by Regulating Gut-Brain Axis in Rats With Myocardial Infarction.Frontiers in cardiovascular medicine · 2021Article
- The Synaptic Vesicle Protein 2A Interacts With Key Pathogenic Factors in Alzheimer's Disease: Implications for Treatment.Frontiers in cell and developmental biology · 2021Article
- Intestinal Barrier Dysfunction Exacerbates Neuroinflammation via the TLR4 Pathway in Mice With Heart Failure.Frontiers in physiology · 2021Article
- The roles of PPARγ and its agonists in autoimmune diseases: A comprehensive review.Journal of autoimmunity · 2020Review
- The Novel Role of PPAR Alpha in the Brain: Promising Target in Therapy of Alzheimer's Disease and Other Neurodegenerative Disorders.Neurochemical research · 2020Review
- Paricalcitol accelerates BACE1 lysosomal degradation and inhibits calpain-1 dependent neuronal loss in APP/PS1 transgenic mice.EBioMedicine · 2019Article
- Current Progress on Peroxisome Proliferator-activated Receptor Gamma Agonist as an Emerging Therapeutic Approach for the Treatment of Alzheimer's Disease: An Update.Current neuropharmacology · 2019Review
- Divergent Mechanisms for PPARγ Agonism in Ameliorating Aging-Related Versus Cranial Irradiation-Induced Context Discrimination Deficits.Frontiers in aging neuroscience · 2019Article
- Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a neurodegenerative condition that leads to neuronal death and memory dysfunction. In the past, specific peroxisome proliferator-activated receptor (PPAR)γ-agonists, such as pioglitazone, have been tested with limited success to improve AD pathology. Here, we investigated the therapeutic efficacy of GFT1803, a novel potent PPAR agonist that activates all the three PPAR isoforms (α/δ/γ) in the APP/PS1 mouse model in comparison to the selective PPARγ-agonist pioglitazone. Both compounds showed similar brain/plasma partitioning ratios, although whole body and brain exposure to GFT1803 was significantly lower as compared to pioglitazone, at doses used in this study. Oral treatment of APP/PS1 mice with GFT1803 decreased microglial activation, amyloid β (Aβ) plaque area, Aβ levels in sodium dodecyl sulfate- and formic acid-soluble fractions in a concentration-dependent manner. With a single exception of Aβ38 and Aβ40 levels, measured by ELISA, these effects were not observed in mice treated with pioglitazone. Both ligands decreased glial fibrillary acidic protein (GFAP) expression to similar extent and did not affect ApoE expression. Finally, GFT1803 increased insulin-degrading enzyme expression. Analysis of spatial memory formation in the Morris water maze demonstrated that both compounds were able to partially revert the phenotype of APP/PS1 mice in comparison to wild-type mice with GFT1803 being most effective. As compared to pioglitazone, GFT1803 (pan-PPAR agonist) produced both quantitatively superior and qualitatively different therapeutic effects with respect to amyloid plaque burden, insoluble Aβ content, and neuroinflammation at significantly lower whole body and brain exposure rates.
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Registered trials
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.