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10.1021/cn500056q http://scihub22266oqcxt.onion/10.1021/cn500056q C4063500!4063500 !24738557     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\24738557 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       ACS+Chem+Neurosci 2014 ; 5 (6 ): 434-42 Nephropedia Template TP {{tp|p=24738557 |t=2014. Lithium and autophagy |pdf=|usr=}}{{24738557 }} gab.com Text Lithium and autophagy JO: ACS Chem Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=24738557 #FOAvip Lithium, a drug used to treat bipolar disorders, has a variety of neuroprotective mechanisms, including autophagy regulation, in various neuropsychiatric conditions. In neurodegenerative diseases, lithium enhances degradation of aggregate-prone proteins, including mutated huntingtin, phosphorylated tau, and ?-synuclein, and causes damaged mitochondria to degrade, while in a mouse model of cerebral ischemia and Alzheimer's disease autophagy downregulation by lithium is observed. The signaling pathway of lithium as an autophagy enhancer might be associated with the mammalian target of rapamycin (mTOR)-independent pathway, which is involved in myo-inositol-1,4,5-trisphosphate (IP3) in Huntington's disease and Parkinson's disease. However, the mTOR-dependent pathway might be involved in inhibiting glycogen synthase kinase-3? (GSK3?) in other diseases. Lithium's autophagy-enhancing property may contribute to the therapeutic benefit of patients with neuropsychiatric disorders. Twit Text FOAVip Lithium and autophagy ????ACS Chem Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=24738557 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24738557 #FOAvip English Wikipedia <ref>{{Cite pmid|24738557 }}</ref> Lithium and autophagy #MMPMID24738557 Motoi Y ; Shimada K ; Ishiguro K ; Hattori N ACS Chem Neurosci 2014[Jun]; 5 (6 ): 434-42 PMID24738557 show ga Lithium, a drug used to treat bipolar disorders, has a variety of neuroprotective mechanisms, including autophagy regulation, in various neuropsychiatric conditions. In neurodegenerative diseases, lithium enhances degradation of aggregate-prone proteins, including mutated huntingtin, phosphorylated tau, and ?-synuclein, and causes damaged mitochondria to degrade, while in a mouse model of cerebral ischemia and Alzheimer's disease autophagy downregulation by lithium is observed. The signaling pathway of lithium as an autophagy enhancer might be associated with the mammalian target of rapamycin (mTOR)-independent pathway, which is involved in myo-inositol-1,4,5-trisphosphate (IP3) in Huntington's disease and Parkinson's disease. However, the mTOR-dependent pathway might be involved in inhibiting glycogen synthase kinase-3? (GSK3?) in other diseases. Lithium's autophagy-enhancing property may contribute to the therapeutic benefit of patients with neuropsychiatric disorders. |Animals [MESH] |Autophagy/*drug effects [MESH] |Humans [MESH] |Lithium Compounds/*pharmacology [MESH] |Nervous System Diseases/drug therapy/physiopathology [MESH]Lithium and autophagy (epmc).pdf DeepDyve Pubget Overpricing