Lithium: A Novel Therapeutic Drug for Traumatic Brain Injury

Shim, Seong S.

doi:10.4172/2161-0460.1000327

Cited by 3 publications

(5 citation statements)

References 27 publications

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“…With the low cost and high efficacy toward BD treatment, the application of lithium was expanded to other diseases in recent years. For example, lithium has also been found to display neuroprotective properties that can attenuate the effects of traumatic brain injury (TBI) . Despite its advantages in treating BD and TBI, lithium treatment is complicated by its extremely narrow therapeutic window of 0.6–1.2 mM and bimodal response from patients .…”

Section: Introductionmentioning

confidence: 99%

“…For example, lithium has also been found to display neuroprotective properties that can attenuate the effects of traumatic brain injury (TBI). 6 Despite its advantages in treating BD and TBI, lithium treatment is complicated by its extremely narrow therapeutic window of 0.6−1.2 mM and bimodal response from patients. 7 For example, lithium toxicity, a concentration only slightly above the therapeutic window has severe side effects including tremors, renal failure, hypothyroidism, and cognitive impairment.…”

Section: ■ Introductionmentioning

confidence: 99%

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DNAzyme-Based Lithium-Selective Imaging Reveals Higher Lithium Accumulation in Bipolar Disorder Patient-Derived Neurons

et al. 2021

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Lithium has been a drug for bipolar disorders (BD) for over 70 years; however, its usage has been limited by its narrow therapeutic window (between 0.6 and 1.2 mM). Understanding the cellular distribution of lithium ions (Li + ) in patient cells will offer deep insight into this limitation, but selective imaging of Li + in living cells under biomedically relevant concentration ranges has not been achieved. Herein, we report in vitro selection and development of a Li + -specific DNAzyme fluorescent sensor with >100-fold selectivity over other biorelevant metal ions. This sensor allows comparative Li + visualization in HeLa cells, human neuronal progenitor cells (NPCs), and neurons derived from BD patients and healthy controls. Strikingly, we detected enhanced accumulation of Li + in cells derived from BD patients compared with healthy controls in differentiated neurons but not NPCs. These results establish the DNAzyme-based sensor as a novel platform for biomedical research into BD and related areas using lithium drugs.

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Section: Introductionmentioning

confidence: 99%

Section: ■ Introductionmentioning

confidence: 99%

DNAzyme-Based Lithium-Selective Imaging Reveals Higher Lithium Accumulation in Bipolar Disorder Patient-Derived Neurons

et al. 2021

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“…The mutation sites cover the whole protein and could also be in the introns affecting the RNA splicing [67]. Some much more common mutations have been selected in generating transgenic models for studying tauopathies [70]. To date, 28 tauopathy mouse models have been reported according to Alzhforum.org and many of which are overexpressing models [67].…”

Section: Tauopathy Animal Modelsmentioning

confidence: 99%

“…if not in combined with other tauopathy-related protein expression [67, 70,75,77]. The most commonly adopted tau mutations in transgenic animal models are P301L, P301S, R406W, and V337 M [59,77].…”

Section: Tauopathy Animal Modelsmentioning

confidence: 99%

“…All these mutants were found in FTD patients, and their expression showed reduced binding affinity to the microtubule. Importantly, all of them could efficiently induce tau filaments formations in mouse models, although the composition of the filaments may be different for different tau mutations [66,70]. Among them, three mouse models stand out in terms of their wide usage in basic research, as well as in the pre-clinical tests of drug development.…”

Section: Tauopathy Animal Modelsmentioning

confidence: 99%

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Tauopathy

Ran¹,

Sang²,

Chang³

2019

Cognitive Disorders

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Tauopathy is a category of neurodegenerative diseases that are caused or associated with pathological tau protein. Some of the diseases are relatively common, which include Alzheimer's disease (AD) and various Parkinsonism (PD). Tau protein is a type of microtubule-associated protein (MAP), encoded by the gene MAPT (microtubule-associated protein tau). Normally, tau binds to microtubule, supporting the assembling and structure of cytoskeletons. However, in tauopathy, normal tau protein undergoes abnormal posttranslational modifications and detaches from microtubule; furthermore, they may aggregate forming paired helical filaments (PHF) or straight filaments (SF). Abundant PHF could be observed under microscope as fibrillary tangles. In this chapter, we will introduce the pathogenesis process of tauopathy with regard to the posttranslational modifications of the protein, the animal models, and the developing treatments against tauopathy from a clinical prospective.

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