FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2940947821> ?p ?o ?g. }

• W2940947821 endingPage "10" @default.
• W2940947821 startingPage "6" @default.
• W2940947821 abstract "The underlining mechanism in neural mitochondrial dysfunction and consequences neurotoxicity, and cognitive behavior after methylphenidate (MPH) prolonged uses is unclear and proposing of therapeutic approaches for treatment of these types of neurotoxicity is one of the main goals of scientist in this manner. MPH-induced mitochondrial dysfunction in neural cells caused induction of oxidative stress, apoptosis, inflammation and cognition impairment, which leads to neurotoxicity, was reported previously but role of key neural cells proteins and involved signaling pathway in this manner remained indeterminate. Tau protein aggregation is a biomarker for mitochondrial dysfunction, neurodegenerative event and cognition impairment. Tau aggregation occur by stimulation effects of Glycogen synthase kinase-3(GSK3β) and phosphatidylinositol 3-kinase (PI3K) which activates protein kinase B(Akt) and causes inhibition of phosphorylation(activation) of GSK3β, thus Akt activation can cause inhibition of tau aggregation (hyper-phosphorylation). Management of mentioned MPH-induced mitochondrial dysfunction and consequences of neurotoxicity, and cognitive behavior through a new generation neuroprotective combination, based on modulation of disturbed in Akt function and inhibition of GSK3β and tau hyper-phosphorylation can be a prefect therapeutic interventions. Therefore, finding, introduction and development of new neuroprotective properties and explanation of their effects with potential capacity for modulation of tau hyper-phosphorylation via PI3/Akt/GSK signaling pathway is necessitated. During recent years, using new neuroprotective compounds with therapeutic probability for treatment of psychostimulant-induced mitochondrial dysfunction, neurotoxicity and cognitive malicious effects have been amazingly increased. Many previous studies have reported the neuroprotective roles of minocycline (a broad-spectrum and long-acting antibiotic) in multiple neurodegenerative events and diseases in animal model. But the role of neuroprotective effects of this agent against MPH induced mitochondrial dysfunction, neurotoxicity and cognitive malicious and also role of tau hyper-phosphorylation by modulation of PI3/Akt/GSK signaling pathway in this manner remain unknown. Thus we suggested and theorized that by using minocycline in MPH addicted subject, it would provide neuroprotection against MPH-induced mitochondrial dysfunction, neurotoxicity and cognitive malicious. Also we hypothesized that minocycline, via modulation of PI3/Akt/GSK and inhibition of tau hyper-phosphorylation, can inhibit MPH-induced mitochondrial dysfunction, neurotoxicity and cognitive malicious. In this article, we tried to discuss our hypothesis regarding the possible role of minocycline, as a powerful neuroprotective agent, and also role of tau hyper-phosphorylation related to PI3/Akt/GSK signaling pathway in treatment of MPH-induced mitochondrial dysfunction, neurotoxicity and cognitive disturbance." @default.
• W2940947821 created "2019-05-03" @default.
• W2940947821 creator A5003582324 @default.
• W2940947821 creator A5017513860 @default.
• W2940947821 creator A5037530197 @default.
• W2940947821 creator A5040350787 @default.
• W2940947821 creator A5057747959 @default.
• W2940947821 creator A5064875737 @default.
• W2940947821 creator A5071334852 @default.
• W2940947821 creator A5073096181 @default.
• W2940947821 creator A5079160850 @default.
• W2940947821 date "2019-07-01" @default.
• W2940947821 modified "2023-09-29" @default.
• W2940947821 title "A hypothetic role of minocycline as a neuroprotective agent against methylphenidate-induced neuronal mitochondrial dysfunction and tau protein hyper-phosphorylation: Possible role of PI3/Akt/GSK3β signaling pathway" @default.
• W2940947821 cites W1514649841 @default.
• W2940947821 cites W1600934558 @default.
• W2940947821 cites W1811346881 @default.
• W2940947821 cites W1968553823 @default.
• W2940947821 cites W1971221903 @default.
• W2940947821 cites W1976301160 @default.
• W2940947821 cites W1995992264 @default.
• W2940947821 cites W1997258141 @default.
• W2940947821 cites W2004108294 @default.
• W2940947821 cites W2010752387 @default.
• W2940947821 cites W2013061587 @default.
• W2940947821 cites W2018493386 @default.
• W2940947821 cites W2021047287 @default.
• W2940947821 cites W2023316908 @default.
• W2940947821 cites W2038112013 @default.
• W2940947821 cites W2043741522 @default.
• W2940947821 cites W2044156764 @default.
• W2940947821 cites W2045509178 @default.
• W2940947821 cites W2045558460 @default.
• W2940947821 cites W2049263381 @default.
• W2940947821 cites W2049817176 @default.
• W2940947821 cites W2059397560 @default.
• W2940947821 cites W2062612291 @default.
• W2940947821 cites W2065034252 @default.
• W2940947821 cites W2075164296 @default.
• W2940947821 cites W2079040308 @default.
• W2940947821 cites W2082004863 @default.
• W2940947821 cites W2082198190 @default.
• W2940947821 cites W2083946532 @default.
• W2940947821 cites W2086729582 @default.
• W2940947821 cites W2089620979 @default.
• W2940947821 cites W2093536482 @default.
• W2940947821 cites W2094119231 @default.
• W2940947821 cites W2112685706 @default.
• W2940947821 cites W2116936712 @default.
• W2940947821 cites W2120494170 @default.
• W2940947821 cites W2121402226 @default.
• W2940947821 cites W2133132296 @default.
• W2940947821 cites W2137140827 @default.
• W2940947821 cites W2139518712 @default.
• W2940947821 cites W2143176748 @default.
• W2940947821 cites W2145636236 @default.
• W2940947821 cites W2148274266 @default.
• W2940947821 cites W2149085698 @default.
• W2940947821 cites W2155880922 @default.
• W2940947821 cites W2159126784 @default.
• W2940947821 cites W2166555967 @default.
• W2940947821 cites W2191245370 @default.
• W2940947821 cites W2279499263 @default.
• W2940947821 cites W2525986321 @default.
• W2940947821 cites W2569212199 @default.
• W2940947821 cites W2576031861 @default.
• W2940947821 cites W2619323433 @default.
• W2940947821 cites W2776048200 @default.
• W2940947821 doi "https://doi.org/10.1016/j.mehy.2019.04.017" @default.
• W2940947821 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31203911" @default.
• W2940947821 hasPublicationYear "2019" @default.
• W2940947821 type Work @default.
• W2940947821 sameAs 2940947821 @default.
• W2940947821 citedByCount "9" @default.
• W2940947821 countsByYear W29409478212021 @default.
• W2940947821 countsByYear W29409478212022 @default.
• W2940947821 countsByYear W29409478212023 @default.
• W2940947821 crossrefType "journal-article" @default.
• W2940947821 hasAuthorship W2940947821A5003582324 @default.
• W2940947821 hasAuthorship W2940947821A5017513860 @default.
• W2940947821 hasAuthorship W2940947821A5037530197 @default.
• W2940947821 hasAuthorship W2940947821A5040350787 @default.
• W2940947821 hasAuthorship W2940947821A5057747959 @default.
• W2940947821 hasAuthorship W2940947821A5064875737 @default.
• W2940947821 hasAuthorship W2940947821A5071334852 @default.
• W2940947821 hasAuthorship W2940947821A5073096181 @default.
• W2940947821 hasAuthorship W2940947821A5079160850 @default.
• W2940947821 hasConcept C11960822 @default.
• W2940947821 hasConcept C126322002 @default.
• W2940947821 hasConcept C169760540 @default.
• W2940947821 hasConcept C182996813 @default.
• W2940947821 hasConcept C25498285 @default.
• W2940947821 hasConcept C2778670691 @default.
• W2940947821 hasConcept C2779134260 @default.
• W2940947821 hasConcept C2779491297 @default.
• W2940947821 hasConcept C29730261 @default.
• W2940947821 hasConcept C502032728 @default.
• W2940947821 hasConcept C62478195 @default.

• next