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Lithium and autophagy.
ACS Chem Neurosci. 2014 Jun 18; 5(6):434-42.AC

Abstract

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 α-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-3β (GSK3β) in other diseases. Lithium's autophagy-enhancing property may contribute to the therapeutic benefit of patients with neuropsychiatric disorders.

Authors+Show Affiliations

†Department of Diagnosis, Prevention and Treatment of Dementia, ‡Department of Neurology, and §Department of Pharmacy, Juntendo University School of Medicine, Tokyo 113-8421, Japan.†Department of Diagnosis, Prevention and Treatment of Dementia, ‡Department of Neurology, and §Department of Pharmacy, Juntendo University School of Medicine, Tokyo 113-8421, Japan.†Department of Diagnosis, Prevention and Treatment of Dementia, ‡Department of Neurology, and §Department of Pharmacy, Juntendo University School of Medicine, Tokyo 113-8421, Japan.†Department of Diagnosis, Prevention and Treatment of Dementia, ‡Department of Neurology, and §Department of Pharmacy, Juntendo University School of Medicine, Tokyo 113-8421, Japan.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

24738557

Citation

Motoi, Yumiko, et al. "Lithium and Autophagy." ACS Chemical Neuroscience, vol. 5, no. 6, 2014, pp. 434-42.
Motoi Y, Shimada K, Ishiguro K, et al. Lithium and autophagy. ACS Chem Neurosci. 2014;5(6):434-42.
Motoi, Y., Shimada, K., Ishiguro, K., & Hattori, N. (2014). Lithium and autophagy. ACS Chemical Neuroscience, 5(6), 434-42. https://doi.org/10.1021/cn500056q
Motoi Y, et al. Lithium and Autophagy. ACS Chem Neurosci. 2014 Jun 18;5(6):434-42. PubMed PMID: 24738557.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lithium and autophagy. AU - Motoi,Yumiko, AU - Shimada,Kohei, AU - Ishiguro,Koichi, AU - Hattori,Nobutaka, Y1 - 2014/04/30/ PY - 2014/4/18/entrez PY - 2014/4/18/pubmed PY - 2015/10/9/medline KW - GSK3β, IMPase KW - Huntingtin KW - Lithium KW - autophagy KW - prion protein KW - tau KW - α-synuclein SP - 434 EP - 42 JF - ACS chemical neuroscience JO - ACS Chem Neurosci VL - 5 IS - 6 N2 - 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 α-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-3β (GSK3β) in other diseases. Lithium's autophagy-enhancing property may contribute to the therapeutic benefit of patients with neuropsychiatric disorders. SN - 1948-7193 UR - https://www.unboundmedicine.com/medline/citation/24738557/Lithium_and_autophagy_ L2 - https://dx.doi.org/10.1021/cn500056q DB - PRIME DP - Unbound Medicine ER -