ArticleMolecular neurobiology2022
Fingolimod Rescues Memory and Improves Pathological Hallmarks in the 3xTg-AD Model of Alzheimer's Disease.
Article in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 44 citations in OpenAlex.
- TogoPhosTAC as a delivery-ready platform for targeted protein dephosphorylation.Nature communications · 2026Article
- The Role of Sphingosine-1-Phosphate Signaling in Cerebral Ischemia/Reperfusion Injury and Alzheimer's Disease Pathology.International journal of molecular sciences · 2026Review
- Dual Mechanisms of Cognitive Function and Pathological Improvements by the Selective S1PR1/5 Modulator Siponimod in 3xTg-AD Mice.Molecular neurobiology · 2025Article
- Drug repurposing for Alzheimer's disease: a Delphi consensus and stakeholder consultation.Alzheimer's research & therapy · 2025Review
- Regulation of presynaptic homeostatic plasticity by glial signalling in Alzheimer's disease.The Journal of physiology · 2025Review
- CD8 T cell dynamics and immune cell trafficking in ZIKV infection: implications for neuroinflammation and therapy.Virology journal · 2025Review
- Adaptive immune changes associate with clinical progression of Alzheimer's disease.Molecular neurodegeneration · 2024Article
- Blocking Microglial Proliferation by CSF-1R Inhibitor Does Not Alter the Neuroprotective Effects of Adoptive Regulatory T Cells in 3xTg Alzheimer's Disease Mice.Current issues in molecular biology · 2024Article
- The Effect of FTY720 on Sphingolipid Imbalance and Cognitive Decline in Aged EFAD Mice.Journal of Alzheimer's disease reports · 2024Article
- Glial Sphingosine-Mediated Epigenetic Regulation Stabilizes Synaptic Function inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Repurposing drugs against Alzheimer's disease: can the anti-multiple sclerosis drug fingolimod (FTY720) effectively tackle inflammation processes in AD?Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
- Does modulation of tau hyperphosphorylation represent a reasonable therapeutic strategy for Alzheimer's disease? From preclinical studies to the clinical trials.Molecular psychiatry · 2023Review
- Molecular and neuroimmune pharmacology of S1P receptor modulators and other disease-modifying therapies for multiple sclerosis.Pharmacology & therapeutics · 2023Review
- Review
- Prenatal alcohol exposure causes persistent microglial activation and age- and sex- specific effects on cognition and metabolic outcomes in an Alzheimer's Disease mouse model.The American journal of drug and alcohol abuse · 2023Article
- Fingolimod mitigates memory loss in a mouse model of Gulf War Illness amid decreasing the activation of microglia, protein kinase R, and NFκB.Neurotoxicology · 2023Article
- Review
- Time- and Sex-Dependent Effects of Fingolimod Treatment in a Mouse Model of Alzheimer's Disease.Biomolecules · 2023Article
- Enhanced and complementary benefits of a nalfurafine and fingolimod combination to treat immune-driven demyelination.Clinical & translational immunology · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Therapeutic strategies for Alzheimer's disease (AD) have largely focused on the regulation of amyloid pathology while those targeting tau pathology, and inflammatory mechanisms are less explored. In this regard, drugs with multimodal and concurrent targeting of Aβ, tau, and inflammatory processes may offer advantages. Here, we investigate one such candidate drug in the triple transgenic 3xTg-AD mouse model of AD, namely the disease-modifying oral neuroimmunomodulatory therapeutic used in patients with multiple sclerosis, called fingolimod. In this study, administration of fingolimod was initiated after behavioral symptoms are known to emerge, at 6 months of age. Treatment continued to 12 months when behavioral tests were performed and thereafter histological and biochemical analysis was conducted on postmortem tissue. The results demonstrate that fingolimod reverses deficits in spatial working memory at 8 and 12 months of age as measured by novel object location and Morris water maze tests. Inflammation in the brain is alleviated as demonstrated by reduced Iba1-positive and CD3-positive cell number, less ramified microglial morphology, and improved cytokine profile. Finally, treatment with fingolimod was shown to reduce phosphorylated tau and APP levels in the hippocampus and cortex. These results highlight the potential of fingolimod as a multimodal therapeutic for the treatment of AD.
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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.