Abdolkarim Talebi Taheri
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Abdolkarim Talebi Taheri has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Azam Alinaghipour
Islamic Azad University
1 shared publication - Ehsan Dadgostar
Halal Research Center of IRI, FDA, Tehran, Iran
1 shared publication - Fatemeh Nabavizadeh
Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Islamic Republic of Iran
1 shared publication - Hamed Mirzaei
Research Center for Biochemistry and Nutrition in Metabolic Diseases, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, Iran
1 shared publication - Hamidreza Zare
University of Szeged, Szeged, Hungary
1 shared publication - Michael Aschner
Department of Molecular Pharmacology, Albert Einstein College of Medicine
1 shared publication
Latest Publications
- Open Access
- 10 March 2024
- Published by Springer Nature in Cellular and Molecular Neurobiology
- Vol. 44 (1) , 1-16
The Potential of Targeting Autophagy-Related Non-coding RNAs in the Treatment of Alzheimer’s and Parkinson’s Diseases
Clearance of accumulated protein aggregates is one of the functions of autophagy. Recently, a clearer understanding of non-coding RNAs (ncRNAs) functions documented that ncRNAs have important roles in several biological processes associated with the development and progression of neurodegenerative disorders. Subtypes of ncRNA, including microRNA (miRNA), long noncoding RNA (lncRNA), and circular RNA (circRNA), are commonly dysregulated in neurodegenerative disorders such as Alzheimer and Parkinson diseases. Dysregulation of these non-coding RNAs has been associated with inhibition or stimulation of autophagy. Decreased miR-124 led to decreased/increased autophagy in experimental model of Alzheimer and Parkinson diseases. Increased BACE1-AS showed enhanced autophagy in Alzheimer disease by targeting miR-214-3p, Beclin-1, LC3-I/LC3-II, p62, and ATG5. A significant increase in NEAT1led to stimulated autophagy in experimental model of PD by targeting PINK1, LC3-I, LC3-II, p62 and miR-374c-5p. In addition, increased BDNF-AS and SNHG1 decreased autophagy in MPTP-induced PD by targeting miR-125b-5p and miR-221/222, respectively. The upregulation of circNF1-419 and circSAMD4A resulted in an increased autophagy by regulating Dynamin-1 and miR-29c 3p, respectively. A detailed discussion of miRNAs, circRNAs, and lncRNAs in relation to their autophagy-related signaling pathways is presented in this study. Graphical Abstract Autophagy-related non-coding RNAs in neurodegenerative diseases.
- 10 March 2024
- Published by Springer Nature in Cellular and Molecular Neurobiology
- Vol. 44 (1) , 1-16
Open AccessThe Potential of Targeting Autophagy-Related Non-coding RNAs in the Treatment of Alzheimer’s and Parkinson’s Diseases
Clearance of accumulated protein aggregates is one of the functions of autophagy. Recently, a clearer understanding of non-coding RNAs (ncRNAs) functions documented that ncRNAs have important roles in several biological processes associated with the development and progression of neurodegenerative disorders. Subtypes of ncRNA, including microRNA (miRNA), long noncoding RNA (lncRNA), and circular RNA (circRNA), are commonly dysregulated in neurodegenerative disorders such as Alzheimer and Parkinson diseases. Dysregulation of these non-coding RNAs has been associated with inhibition or stimulation of autophagy. Decreased miR-124 led to decreased/increased autophagy in experimental model of Alzheimer and Parkinson diseases. Increased BACE1-AS showed enhanced autophagy in Alzheimer disease by targeting miR-214-3p, Beclin-1, LC3-I/LC3-II, p62, and ATG5. A significant increase in NEAT1led to stimulated autophagy in experimental model of PD by targeting PINK1, LC3-I, LC3-II, p62 and miR-374c-5p. In addition, increased BDNF-AS and SNHG1 decreased autophagy in MPTP-induced PD by targeting miR-125b-5p and miR-221/222, respectively. The upregulation of circNF1-419 and circSAMD4A resulted in an increased autophagy by regulating Dynamin-1 and miR-29c 3p, respectively. A detailed discussion of miRNAs, circRNAs, and lncRNAs in relation to their autophagy-related signaling pathways is presented in this study. Graphical Abstract Autophagy-related non-coding RNAs in neurodegenerative diseases.