ReviewJournal of neural transmission (Vienna, Austria : 1996)2023
Repurposing drugs against Alzheimer's disease: can the anti-multiple sclerosis drug fingolimod (FTY720) effectively tackle inflammation processes in AD?
Review in Journal of neural transmission (Vienna, Austria : 1996), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Uncovering the Causal Link Between Obesity-Associated Genes and Multiple Sclerosis: A Systematic Literature Review.Brain and behavior · 2025Pooled it
- Potential Role of Sphingosine-1-Phosphate and Its Receptors in the Reparative Processes of the Adult Brain.International journal of molecular sciences · 2026Review
- The meningeal lymphatic vessel-peripheral immune axis: a novel therapeutic target in neurodegenerative diseases.Journal of neuroinflammation · 2026Review
- Unlocking Novel Therapeutic Potential of Angiotensin II Receptor Blockers.International journal of molecular sciences · 2025Review
- Fingolimod ameliorates amyloid deposition and neurodegeneration in APP/PS1 mouse model of Alzheimer's disease.The journal of prevention of Alzheimer's disease · 2025Article
- Beyond Transgenic Mice: Emerging Models and Translational Strategies in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Deep learning and generative artificial intelligence in aging research and healthy longevity medicine.Aging · 2025Review
- From Lab to Clinic: Success Stories of Repurposed Drugs in Treating Major Diseases.Advances in pharmacological and pharmaceutical sciences · 2025Review
- Sphingosine 1-phosphate receptor 1 modulators exert neuroprotective effects in central nervous system disorders.Frontiers in pharmacology · 2025Review
- Novel Compounds as S1P5 Modulators for Treating Neurodegenerative Diseases.ACS medicinal chemistry letters · 2024Article
- In-vivo neuronal dysfunction by Aβ and tau overlaps with brain-wide inflammatory mechanisms in Alzheimer's disease.Frontiers in aging neuroscience · 2024Article
- Carboxylic Acid-Containing Indanyl Compounds as S1P5 Modulators for Treating Neurodegenerative Diseases.ACS medicinal chemistry letters · 2023Article
- Molecular and neuroimmune pharmacology of S1P receptor modulators and other disease-modifying therapies for multiple sclerosis.Pharmacology & therapeutics · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Therapeutic approaches providing effective medication for Alzheimer's disease (AD) patients after disease onset are urgently needed. Previous studies in AD mouse models and in humans suggested that physical exercise or changed lifestyle can delay AD-related synaptic and memory dysfunctions when treatment started in juvenile animals or in elderly humans before onset of disease symptoms. However, a pharmacological treatment that can reverse memory deficits in AD patients was thus far not identified. Importantly, AD disease-related dysfunctions have increasingly been associated with neuro-inflammatory mechanisms and searching for anti-inflammatory medication to treat AD seems promising. Like for other diseases, repurposing of FDA-approved drugs for treatment of AD is an ideally suited strategy to reduce the time to bring such medication into clinical practice. Of note, the sphingosine-1-phosphate analogue fingolimod (FTY720) was FDA-approved in 2010 for treatment of multiple sclerosis patients. It binds to the five different isoforms of Sphingosine-1-phosphate receptors (S1PRs) that are widely distributed across human organs. Interestingly, recent studies in five different mouse models of AD suggest that FTY720 treatment, even when starting after onset of AD symptoms, can reverse synaptic deficits and memory dysfunction in these AD mouse models. Furthermore, a very recent multi-omics study identified mutations in the sphingosine/ceramide pathway as a risk factor for sporadic AD, suggesting S1PRs as promising drug target in AD patients. Therefore, progressing with FDA-approved S1PR modulators into human clinical trials might pave the way for these potential disease modifying anti-AD drugs.
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