ArticlePloS one2013
Long-term treatment of thalidomide ameliorates amyloid-like pathology through inhibition of β-secretase in a mouse model of Alzheimer's disease.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Anticancer drugs repurposed for Alzheimer's disease: a systematic review.Alzheimer's research & therapy · 2021Pooled it
- Small Molecule Therapeutics Targeting Amyloid-β in Alzheimer's Disease: Mechanisms, Clinical Progress, and Future Strategies.Experimental neurobiology · 2026Review
- APP-C31 pathology as a target in neurodegenerative diseases.Journal of biomedical science · 2026Review
- Targeting Microglia in Alzheimer's Disease: Pathogenesis and Potential Therapeutic Strategies.Biomolecules · 2024Review
- Inflammation, Autoimmunity and Neurodegenerative Diseases, Therapeutics and Beyond.Current neuropharmacology · 2024Article
- Cancer drugs with high repositioning potential for Alzheimer's disease.Expert opinion on emerging drugs · 2023Review
- Neuroinflammation in neurological disorders: pharmacotherapeutic targets from bench to bedside.Metabolic brain disease · 2021Review
- Neuroinflammation in Alzheimer's Disease.Biomedicines · 2021Review
- Repurposing Immunomodulatory Imide Drugs (IMiDs) in Neuropsychiatric and Neurodegenerative Disorders.Frontiers in neuroscience · 2021Review
- TNF Production and Release from Microglia via Extracellular Vesicles: Impact on Brain Functions.Cells · 2020Review
- Marine Natural Products, Multitarget Therapy and Repurposed Agents in Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Repositioning of Immunomodulators: A Ray of Hope for Alzheimer's Disease?Frontiers in neuroscience · 2020Review
- Bispecific Antibody Fragment Targeting APP and Inducing α-Site Cleavage Restores Neuronal Health in an Alzheimer's Mouse Model.Molecular neurobiology · 2019Article
- Neuroinflammation as a Factor of Neurodegenerative Disease: Thalidomide Analogs as Treatments.Frontiers in cell and developmental biology · 2019Review
- Systemic Injection of Thalidomide Prevent and Attenuate Neuropathic Pain and Alleviate Neuroinflammatory Response in the Spinal Dorsal Horn.Journal of pain research · 2019Article
- Preventing synaptic deficits in Alzheimer's disease by inhibiting tumor necrosis factor alpha signaling.IBRO reports · 2018Review
- A New Venue of TNF Targeting.International journal of molecular sciences · 2018Review
- COEXPEDIA: exploring biomedical hypotheses via co-expressions associated with medical subject headings (MeSH).Nucleic acids research · 2017Article
- Alzheimer's Disease: The Role of Microglia in Brain Homeostasis and Proteopathy.Frontiers in neuroscience · 2017Review
- Inhibition of Inflammation Mediated Through the Tumor Necrosis Factor α Biochemical Pathway Can Lead to Favorable Outcomes in Alzheimer Disease.Journal of central nervous system disease · 2017Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
Abstract
Thalidomide is a tumor necrosis factor alpha (TNFα) inhibitor which has been found to have abilities against tumor growth, angiogenesis and inflammation. Recently, it has been applied in clinic for the treatment of multiple myeloma as well as some inflammatory diseases. However, whether thalidomide has any therapeutic effects on neurodegenerative disorders, i.e. Alzheimer's disease (AD) is not clear. AD is characterized by excessive amount of amyloid β peptides (Aβ), which results in a significant release of inflammatory factors, including TNFα in the brain. Studies have shown that inhibition of TNFα reduces amyloid-associated pathology, prevents neuron loss and improves cognition. Our recent report showed that genetic inhibition of TNFα/TNF receptor signal transduction down-regulates β amyloid cleavage enzyme 1 (BACE1) activity, reduces Aβ generation and improves learning and memory deficits. However, the mechanism of thalidomide involving in the mitigation of AD neuropathological features remains unclear. Here, we chronically administrated thalidomide on human APPswedish mutation transgenic (APP23) mice from 9 months old (an onset of Aβ deposits and early stage of AD-like changes) to 12 months old. We found that, in addition of dramatic decrease in the activation of both astrocytes and microglia, thalidomide significantly reduces Aβ load and plaque formation. Furthermore, we found a significant decrease in BACE1 level and activity with long-term thalidomide application. Interestingly, these findings cannot be observed in the brains of 12-month-old APP23 mice with short-term treatment of thalidomide (3 days). These results suggest that chronic thalidomide administration is an alternative approach for AD prevention and therapeutics.
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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.