Photobiomodulation by low-power laser irradiation attenuates Aβ-induced cell apoptosis through the Akt/GSK3β/β-catenin pathway

Liang, Jiangang; Liu, Lei; Xing, Da

doi:10.1016/j.freeradbiomed.2012.08.003

Cited by 94 publications

(96 citation statements)

References 49 publications

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“…Extracellular accumulation of amyloid β (Aβ) peptide aggregates, which results in the formation of senile plaques, indicates one of the neuropathological markers of AD [39]. In recent years, accumulating evidence has suggested that transcranial LLLT suppresses Aβ-induced hippocampal neurodegeneration Increased the nuclear translocation of -catenin and enhanced its T cell factor/ lymphocyte enhancer factor-dependent transcriptional activity [17,18] hippocampus were significantly down-regulated in Ahi1 KO mice, which reveals depressive-like behaviors [4]. Transcranial LLLT attenuated depressive-like behaviors in Ahi1 KO mice, which could be involved in the enhancement of serotonin and dopamine levels in the brain [4].…”

Section: The Mechanisms Of Lllt In Depression Lllt Might Increase Thementioning

confidence: 99%

“…Moreover, LLLT increased the nuclear translocation of β-catenin and enhanced its T cell factor/lymphocyte enhancer factor-dependent transcriptional activity via the Akt/GSK3β pathway to promote cell survival upon treatment with Aβ 25-35 [19]. LLLT has a prosurvival effect on Aβ-induced apoptosis and may be an effective therapeutic strategy in treating AD by targeting GSK3b [17]. In addition, another study on EGCG has also found that irradiation with moderate levels of 670-nm light and EGCG supplementation complementarily reduces Aβ aggregation in human neuroblastoma SH-EP cells [18].…”

Section: Lllt Regulates/modulates Multiple Intracellular Down-stream mentioning

confidence: 99%

“…As a noninvasive treatment, accumulating evidence has shown that transcranial LLLT is a beneficial treatment for depression [4,5] and AD [10][11][12][13][14][15][16][17] in rodent models. In addition, transcranial LLLT has been carried out on depression and chronic TBI patients in preclinical trials [6][7][8]26,27].…”

Section: Conclusion and Perspectivementioning

confidence: 99%

“…Recently, researchers have shifted the focus of research to the application of LLLT on brain disorders [1][2][3]. During the past decade, LLLT has been widely used to study neurological and psychological diseases [3] such as depressionlike behaviors [4][5][6][7][8], Alzheimer's disease (AD) [9][10][11][12][13][14][15][16][17][18][19][20], Parkinson's disease [21], stroke [22,23] and traumatic brain injury (TBI) [24][25][26][27][28][29][30][31][32]. Because red or NIR light can effectively penetrate into brain tissues [33,34], it can be noninvasive and play a beneficial role in increasing ATP biosynthesis and neurogenesis [1,2].…”

Section: Introductionmentioning

confidence: 99%

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Transcranial Low-Level Laser Therapy for Depression and Alzheimer’s Disease

Chang¹,

Ren²,

Wang³

et al. 2018

Neuropsychiatry

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There is no effective therapy in patients with depression and Alzheimer's disease (AD). The need for novel treatments offers researchers the opportunity to explore new technology for these disorders. Transcranial low-level laser therapy (LLLT) is a novel therapeutic approach based on laser irradiation to biological tissue, and it has been used to treat brain disorders. Although there are certain therapeutic options for depression and AD, there is little treatment available as non-invasive physical therapy. In this mini-review, we focus on a growing body of evidence surrounding the therapeutic effects of LLLT for depression and AD. Transcranial LLLT can enhance ATP biosynthesis, regulate mitochondrial homeostasis, and facilitate neurogenesis and/or neuroplasticity. However, the cellular and molecular mechanisms underlying the treatment of LLLT on these disorders are still at early stages. Clinical trials on depression and AD by transcranial LLLT are critical for future studies.

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Section: The Mechanisms Of Lllt In Depression Lllt Might Increase Thementioning

confidence: 99%

Section: Lllt Regulates/modulates Multiple Intracellular Down-stream mentioning

confidence: 99%

Section: Conclusion and Perspectivementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Transcranial Low-Level Laser Therapy for Depression and Alzheimer’s Disease

Chang¹,

Ren²,

Wang³

et al. 2018

Neuropsychiatry

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“…14 Moreover, it has been reported that LPLI can signi¯cantly prevent cell apoptosis induced by A in PC12 cells through activation of Akt/GSK3 signaling. 15 LPLI can e±ciently penetrate into biological tissues including the central nervous system, producing noninvasive bene¯cial photobiomodulation e®ects such as promoting nerve regeneration and increasing ATP synthesis. 16 All the evidence suggests that LPLI regulates di®erent biological processes through diverse signaling pathways in many cell types and ultimately a®ects cell physiological processes.…”

Section: Introductionmentioning

confidence: 99%

Photoactivation of GLUT4 translocation promotes glucose uptake via PI3-K/Akt2 signaling in 3T3-L1 adipocytes

Huang

Gong

Jiang

et al. 2014

J. Innov. Opt. Health Sci.

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Insulin resistance is a hallmark of the metabolic syndrome and type 2 diabetes. Dysfunction of PI-3K/Akt signaling was involved in insulin resistance. Glucose transporter 4 (GLUT4) is a key factor for glucose uptake in muscle and adipose tissues, which is closely regulated by PI-3K/Akt signaling in response to insulin treatment. Low-power laser irradiation (LPLI) has been shown to regulate various physiological processes and induce the synthesis or release of multiple molecules such as growth factors, which (especially red and near infrared light) is mainly through the activation of mitochondrial respiratory chain and the initiation of intracellular signaling pathways. Nevertheless, it is unclear whether LPLI could promote glucose uptake through activation of PI-3K/Akt/GLUT4 signaling in 3T3L-1 adipocytes. In this study, we investigated how LPLI promoted glucose uptake through activation of PI-3K/Akt/GLUT4 signaling pathway. Here, we showed that GLUT4 was localized to the Golgi apparatus and translocated from cytoplasm to cytomembrane upon LPLI treatment in 3T3L-1 adipocytes, which enhanced glucose uptake. Moreover, we found that glucose uptake was mediated by the PI3-K/Akt2 signaling, but not Akt1 upon LPLI treatment with Akt isoforms gene silence and PI3-K/Akt inhibitors. Collectively, our results indicate that PI3-K/Akt2/GLUT4 signaling act as the key regulators for improvement of glucose uptake under LPLI treatment in 3T3L-1 adipocytes. More importantly, our¯ndings suggest that activation of PI3-K/Akt2/GLUT4 signaling by LPLI may provide guidance in practical applications for promotion of glucose uptake in insulin-resistant adipose tissue.

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Neurological Conditions

Godine¹

2017

Laser Therapy in Veterinary Medicine

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Photobiomodulation by low-power laser irradiation attenuates Aβ-induced cell apoptosis through the Akt/GSK3β/β-catenin pathway

Cited by 94 publications

References 49 publications

Transcranial Low-Level Laser Therapy for Depression and Alzheimer’s Disease

Transcranial Low-Level Laser Therapy for Depression and Alzheimer’s Disease

Photoactivation of GLUT4 translocation promotes glucose uptake via PI3-K/Akt2 signaling in 3T3-L1 adipocytes

Neurological Conditions

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