Transcranial LED therapy on amyloid-β toxin 25–35 in the hippocampal region of rats

Eltchechem, Camila da Luz; Salgado, Afonso Shiguemi Inoue; Zângaro, Renato Amaro; Pereira, Mário César da Silva; Kerppers, Ivo Ilvan; Silva, L. A. da; Parreira, Rodolfo Borges

doi:10.1007/s10103-017-2156-3

Cited by 40 publications

(40 citation statements)

References 39 publications

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“…da Luz Eltchechem et al [147] also used rats but injected the hippocampus with Aβ25-35 peptide and treated them daily with 627 nm laser for 100 s, 7 J/cm 2 for 21 days. The use of tPBM significantly reduced the Aβ plaques, and improved spatial memory and behavioral and motor skills in treated animals on day 21.…”

Section: Tpbm For Ad In Animal Modelsmentioning

confidence: 99%

Photobiomodulation for Alzheimer’s Disease: Has the Light Dawned?

2019

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Next to cancer, Alzheimer’s disease (AD) and dementia is probably the most worrying health problem facing the Western world today. A large number of clinical trials have failed to show any benefit of the tested drugs in stabilizing or reversing the steady decline in cognitive function that is suffered by dementia patients. Although the pathological features of AD consisting of beta-amyloid plaques and tau tangles are well established, considerable debate exists concerning the genetic or lifestyle factors that predispose individuals to developing dementia. Photobiomodulation (PBM) describes the therapeutic use of red or near-infrared light to stimulate healing, relieve pain and inflammation, and prevent tissue from dying. In recent years PBM has been applied for a diverse range of brain disorders, frequently applied in a non-invasive manner by shining light on the head (transcranial PBM). The present review discusses the mechanisms of action of tPBM in the brain, and summarizes studies that have used tPBM to treat animal models of AD. The results of a limited number of clinical trials that have used tPBM to treat patients with AD and dementia are discussed.

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Section: Tpbm For Ad In Animal Modelsmentioning

confidence: 99%

Photobiomodulation for Alzheimer’s Disease: Has the Light Dawned?

2019

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“…The power to the skin surface was 92 mM, and the power density was 117.2 mW/cm 2 ( Figure S1a). The PBM system was stationary positioned in skin contact at the frontal region in the head of mice; the irradiation was applied once a day for 10 min, at the irradiation dose of 6 J/cm 2 with power of 8.75 mW exposure to the cortex for 30 days (without local temperature increase in the scalp and brain tissue) (Luz Eltchechem et al, 2017). Refer to our previous studies on the transmittance of PBM from the upper part of the exposed brain to the interior of the hippocampus, the transmittance was approximately 30% (Zhang et al, 2020), and then, the hippocampus is required to obtain a dose of 2 J/cm 2 , which indicated that 6 J/cm 2 PBM irradiation is needed.…”

Section: Pbm Treatmentmentioning

confidence: 99%

Photobiomodulation suppresses JNK3 by activation of ERK/MKP7 to attenuate AMPA receptor endocytosis in Alzheimer's disease

Shen

Liu

et al. 2020

Aging Cell

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Alzheimer's disease (AD), a severe age‐related neurodegenerative disorder, lacks effective therapeutic methods at present. Physical approaches such as gamma frequency light flicker that can effectively reduce amyloid load have been reported recently. Our previous research showed that a physical method named photobiomodulation (PBM) therapy rescues Aβ‐induced dendritic atrophy in vitro. However, it remains to be further investigated the mechanism by which PBM affects AD‐related multiple pathological features to improve learning and memory deficits. Here, we found that PBM attenuated Aβ‐induced synaptic dysfunction and neuronal death through MKP7‐dependent suppression of JNK3, a brain‐specific JNK isoform related to neurodegeneration. The results showed PBM‐attenuated amyloid load, AMPA receptor endocytosis, dendrite injury, and inflammatory responses, thereby rescuing memory deficits in APP/PS1 mice. We noted JNK3 phosphorylation was dramatically decreased after PBM treatment in vivo and in vitro. Mechanistically, PBM activated ERK, which subsequently phosphorylated and stabilized MKP7, resulting in JNK3 inactivation. Furthermore, activation of ERK/MKP7 signaling by PBM increased the level of AMPA receptor subunit GluR 1 phosphorylation and attenuated AMPA receptor endocytosis in an AD pathological model. Collectively, these data demonstrated that PBM has potential therapeutic value in reducing multiple pathological features associated with AD, which is achieved by regulating JNK3, thus providing a noninvasive, and drug‐free therapeutic strategy to impede AD progression.

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“…PBM may protect against the neuronal death and mitochondrial dysfunction associated with Alzheimer's disease, which is why this novel treatment has such broad potential (Table 1). In transgenic animal models associated with β-amyloid or tau, PBM reduces cognitive deficits, β-amyloid plaques, tau-associated neurofibrillary tangles, and oxidative stress while increasing the production of adenosine [31][32][33][34][35][36]. Additionally, in vitro studies have shown that PBM decreases β-amyloid plaques while increasing cell survival and ATP production [37].…”

Section: Alzheimer's Disease and Pbmmentioning

confidence: 99%

Photobiomodulation as a treatment for neurodegenerative disorders: current and future trends

Hong

2019

Biomed. Eng. Lett.

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Photobiomodulation (PBM) is a rapidly growing as an innovative therapeutic modality for various types of diseases in recent years. Neuronal degeneration is irreversible process and it is proven to be difficult to slow down or stop the progression. Pharmacologic approaches to slow neuronal degeneration have been studied, but are limited due to concerns about the side effects. Therefore, it is necessary to develop a new therapeutic approach to stabilize neuronal degeneration and achieve neuronal protection against several neurodegenerative diseases. In this review, we have introduced several previous studies showing the positive effect of PBM over neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease and different types of epilepsy. Despite excellent outcomes of animal researches, not many clinical studies are conducted or showed positive outcome of PBM against neurodegenerative disease. To achieve clinical application of PBM against neurodegenerative disorder, determination of exact mechanism and establishment of effective clinical protocol seems to be necessary.

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Transcranial LED therapy on amyloid-β toxin 25–35 in the hippocampal region of rats

Cited by 40 publications

References 39 publications

Photobiomodulation for Alzheimer’s Disease: Has the Light Dawned?

Photobiomodulation for Alzheimer’s Disease: Has the Light Dawned?

Photobiomodulation suppresses JNK3 by activation of ERK/MKP7 to attenuate AMPA receptor endocytosis in Alzheimer's disease

Photobiomodulation as a treatment for neurodegenerative disorders: current and future trends

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