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Phosphodiesterase inhibitors say NO to Alzheimer's disease.
Food Chem Toxicol 2019; 134:110822FC

Abstract

Phosphodiesterases (PDEs) consisted of 11 subtypes (PDE1 to PDE11) and over 40 isoforms that regulate levels of cyclic guanosine monophosphate (cGMP) and cyclic adenosine monophosphate (cAMP), the second messengers in cell functions. PDE inhibitors (PDEIs) have been attractive therapeutic targets due to their involvement in diverse medical conditions, e.g. cardiovascular diseases, autoimmune diseases, Alzheimer's disease (AD), etc. Among them; AD with a complex pathology is a progressive neurodegenerative disorder which affect mostly senile people in the world and only symptomatic treatment particularly using cholinesterase inhibitors in clinic is available at the moment for AD. Consequently, novel treatment strategies towards AD are still searched extensively. Since PDEs are broadly expressed in the brain, PDEIs are considered to modulate neurodegenerative conditions through regulating cAMP and cGMP in the brain. In this sense, several synthetic or natural molecules inhibiting various PDE subtypes such as rolipram and roflumilast (PDE4 inhibitors), vinpocetine (PDE1 inhibitor), cilostazol and milrinone (PDE3 inhibitors), sildenafil and tadalafil (PDE5 inhibitors), etc have been reported showing encouraging results for the treatment of AD. In this review, PDE superfamily will be scrutinized from the view point of structural features, isoforms, functions and pharmacology particularly attributed to PDEs as target for AD therapy.

Authors+Show Affiliations

Applied Biotechnology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran. Electronic address: Nabavi208@gmail.com.Department of Pharmacology and Pharmacodynamics, Medical University of Lublin, Chodźki 4a St, 20-093, Lublin, Poland. Electronic address: Sylwia.Talarek@umlub.bl.Department of Pharmacology and Pharmacodynamics, Medical University of Lublin, Chodźki 4a St, 20-093, Lublin, Poland. Electronic address: a.listos@umlub.pl.Applied Biotechnology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran. Electronic address: Nabavisf@gmail.com.Department of Biotechnology, Alagappa University, Karaikudi, 630003, Tamil Nadu, India. Electronic address: devikasi@yahoo.com.Departamento de Química (DQ), Instituto de Ciências Exatas e da Terra (ICET), Universidade Federal de Mato Grosso (UFMT), Cuiabá, Brazil. Electronic address: marcos.oliveira@uniuv.edu.br.Department of Pharmacognosy, School of Pharmaceutical Sciences, Lovely Professional University, Phagwara, 144411, Punjab, India. Electronic address: dtewari3@gmail.com.Department of Physiology, Faculty of Pharmacy, University of Seville, Seville, Spain. Electronic address: sarguelles1@us.es.Razi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran. Electronic address: mehrzadi.s@iums.ac.ir.Razi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran.Geriatric Unit and Gerontology-Geriatrics Research Laboratory, Department of Medical Sciences, IRCCS "Casa Sollievo della Sofferenza", Viale Cappuccini 1, 71013, San Giovanni Rotondo, FG, Italy. Electronic address: donofrio@operapadrepio.it.Department of Pharmacognosy, Faculty of Pharmacy, Gazi University, 06330, Ankara, Turkey. Electronic address: iorhan@gazi.edu.tr.Research Group on Community Nutrition and Oxidative Stress, University of Balearic Islands, CIBEROBN (Physiopathology of Obesity and Nutrition), E-07122, Palma de Mallorca, Balearic Islands, Spain. Electronic address: tosugo@hotmail.com.Aab Cardiovascular Research Institute, University of Rochester, Rochester, NY, 14623, USA. Electronic address: suowen.xu@gmail.com.Medicinal Plants Research Center, Institute of Medicinal Plants, ACECR, Karaj, Iran; Toxicology and Diseases Group, The Institute of Pharmaceutical Sciences (TIPS), Tehran University of Medical Sciences, Tehran, Iran.Pharmaceutical Sciences Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran. Electronic address: mh.farzaei@gmail.com.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

31536753

Citation

Nabavi, Seyed Mohammad, et al. "Phosphodiesterase Inhibitors Say NO to Alzheimer's Disease." Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association, vol. 134, 2019, p. 110822.
Nabavi SM, Talarek S, Listos J, et al. Phosphodiesterase inhibitors say NO to Alzheimer's disease. Food Chem Toxicol. 2019;134:110822.
Nabavi, S. M., Talarek, S., Listos, J., Nabavi, S. F., Devi, K. P., Roberto de Oliveira, M., ... Farzaei, M. H. (2019). Phosphodiesterase inhibitors say NO to Alzheimer's disease. Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association, 134, p. 110822. doi:10.1016/j.fct.2019.110822.
Nabavi SM, et al. Phosphodiesterase Inhibitors Say NO to Alzheimer's Disease. Food Chem Toxicol. 2019;134:110822. PubMed PMID: 31536753.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Phosphodiesterase inhibitors say NO to Alzheimer's disease. AU - Nabavi,Seyed Mohammad, AU - Talarek,Sylwia, AU - Listos,Joanna, AU - Nabavi,Seyed Fazel, AU - Devi,Kasi Pandima, AU - Roberto de Oliveira,Marcos, AU - Tewari,Devesh, AU - Argüelles,Sandro, AU - Mehrzadi,Saeed, AU - Hosseinzadeh,Azam, AU - D'onofrio,Grazia, AU - Orhan,Ilkay Erdogan, AU - Sureda,Antoni, AU - Xu,Suowen, AU - Momtaz,Saeedeh, AU - Farzaei,Mohammad Hosein, Y1 - 2019/09/16/ PY - 2019/04/27/received PY - 2019/09/13/revised PY - 2019/09/14/accepted PY - 2019/9/20/pubmed PY - 2019/9/20/medline PY - 2019/9/20/entrez KW - Alzheimer's disease KW - Isoform KW - Phosphodiesterase KW - Subtype KW - cAMP KW - cGMP SP - 110822 EP - 110822 JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association JO - Food Chem. Toxicol. VL - 134 N2 - Phosphodiesterases (PDEs) consisted of 11 subtypes (PDE1 to PDE11) and over 40 isoforms that regulate levels of cyclic guanosine monophosphate (cGMP) and cyclic adenosine monophosphate (cAMP), the second messengers in cell functions. PDE inhibitors (PDEIs) have been attractive therapeutic targets due to their involvement in diverse medical conditions, e.g. cardiovascular diseases, autoimmune diseases, Alzheimer's disease (AD), etc. Among them; AD with a complex pathology is a progressive neurodegenerative disorder which affect mostly senile people in the world and only symptomatic treatment particularly using cholinesterase inhibitors in clinic is available at the moment for AD. Consequently, novel treatment strategies towards AD are still searched extensively. Since PDEs are broadly expressed in the brain, PDEIs are considered to modulate neurodegenerative conditions through regulating cAMP and cGMP in the brain. In this sense, several synthetic or natural molecules inhibiting various PDE subtypes such as rolipram and roflumilast (PDE4 inhibitors), vinpocetine (PDE1 inhibitor), cilostazol and milrinone (PDE3 inhibitors), sildenafil and tadalafil (PDE5 inhibitors), etc have been reported showing encouraging results for the treatment of AD. In this review, PDE superfamily will be scrutinized from the view point of structural features, isoforms, functions and pharmacology particularly attributed to PDEs as target for AD therapy. SN - 1873-6351 UR - https://www.unboundmedicine.com/medline/citation/31536753/Phosphodiesterase_inhibitors_say_NO_to_Alzheimer's_disease L2 - https://linkinghub.elsevier.com/retrieve/pii/S0278-6915(19)30612-X DB - PRIME DP - Unbound Medicine ER -