The role of transforming growth factor β1 /Smad pathway in Alzheimer’s disease inflammation pathology
Author:
Funder
the National natural science foundation of China
Publisher
Springer Science and Business Media LLC
Subject
Genetics,Molecular Biology,General Medicine
Link
https://link.springer.com/content/pdf/10.1007/s11033-022-07951-8.pdf
Reference88 articles.
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2. Torrisi SA, Geraci F, Tropea MR, Grasso M, Caruso G, Fidilio A et al (2019) Fluoxetine and Vortioxetine Reverse Depressive-Like Phenotype and Memory Deficits Induced by Aβ1–42 Oligomers in Mice: A Key Role of Transforming Growth Factor-β1. Front Pharmacol 21:693. https://doi.org/10.3389/fphar.2019.00693
3. Caraci F, Spampinato SF, Morgese MG, Tascedda F, Salluzzo MG, Giambirtone MC et al (2018) Neurobiological links between depression and AD: The role of TGF-β1 signaling as a new pharmacological target. Pharmacol Res 130:374–384. https://doi.org/10.1016/j.phrs.2018.02.007
4. Hasegawa H, Liu L, Tooyama I, Murayama S, Nishimura M (2014) The FAM3 superfamily member ILEI ameliorates Alzheimer’s disease-like pathology by destabilizing the penultimate amyloid-β precursor. Nat Commun 5:3917. https://doi.org/10.1038/ncomms4917
5. Karch CM, Goate AM (2015) Alzheimer’s Disease Risk Genes and Mechanisms of Disease Pathogenesis. Biol Psychiatry 77:43–51. https://doi.org/10.1016/j.biopsych.2014.05.006
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