Near infrared light mitigates cerebellar pathology in transgenic mouse models of dementia

Purushothuman, Sivaraman; Johnstone, Daniel M.; Nandasena, Charith; Eersel, Janet van; Ittner, Lars M.; Mitrofanis, John; Stone, Jonathan

doi:10.1016/j.neulet.2015.02.037

Cited by 60 publications

(56 citation statements)

References 28 publications

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“…In transgenic mouse models of dementia, the cerebellar pathology of dementia is maintained (Franco et al, 2011;Purushothuman et al, 2015). Our results showed that LIMK1 was detected in the NFL and EPL of the olfactory bulb in WT mice and the App/PS +/-mouse model of AD.…”

Section: Discussionmentioning

confidence: 62%

Distribution of LIM domain kinase 1 in the olfactory bulb, cerebral cortex, hippocampus, and cerebellum of the App/PS+/- mice

Liu

et al. 2015

Genet. Mol. Res.

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ABSTRACT. LIM domain kinase 1 (LIMK1), an actin-binding kinase, can phosphorylate and inactivate its substrates, and can regulate long-term memory and synaptic plasticity. Both β-amyloid precursor protein (App) and presenilin (PS) are functional degeneration factors during early neuronal development, and are considered as potential factors that contribute to the development of Alzheimer's disease (AD). However, hardly any information is available about the distribution and expression of LIMK1. Thus, using the App and PS deficient mice, the role of LIMK1 was demonstrated in the absence of App and PS. Our results showed that LIMK1 was present in the nerve fiber layer and external plexiform layer of the olfactory bulb, as well as in the mitral cells and Purkinje cells of the cerebellum in App and PS deficient mice. Additionally, LIMK1 was concentrated in the granule cell layer of the olfactory bulb and cerebellum and LIMK1 positive cells were located in the CA1 region of the hippocampus. Our study indicates that there is a connection between LIMK1 and AD in the mouse model of AD. This might explain neurological problems such as cerebellar ataxia, impaired long-term memory, and impaired synaptic plasticity observed in AD.

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Section: Discussionmentioning

confidence: 62%

Distribution of LIM domain kinase 1 in the olfactory bulb, cerebral cortex, hippocampus, and cerebellum of the App/PS+/- mice

Liu

et al. 2015

Genet. Mol. Res.

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“…After one month of treatment, NIR mitigated AD-related pathologies. 28 The mechanisms associated with NIR e®ect on AD mouse are typically mediated via ATP generation to increase and improve mitochondrial function. 29 Taboada et al used 808 nm in APP transgenic mice, which increased the ATP levels as well as percent oxygen consumption.…”

Section: Discussionmentioning

confidence: 99%

Near infra-red light treatment of Alzheimer’s disease

Han

Wang

Xue

et al. 2017

J. Innov. Opt. Health Sci.

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Alzheimer's disease (AD) is a chronic neurodegenerative disease. The symptoms include memory and spatial learning di±culties, language disorders, and loss of motivation, which get worse over time, eventually ending in death. No e®ective treatments are available for AD, currently. Current treatments only attenuate symptoms temporarily and are associated with severe side e®ects. Near infra-red (NIR) light has been studied for a long time. We investigated the e®ect of NIR on AD using a transgenic mouse model, which was obtained by co-injecting two vectors carrying AD mutations in amyloid precursor protein (APP) and presenilin-1 (PSEN1) into C57BL/6J mice. The irradiation equipment consisted of an accommodating box and an LED array. The wavelength of NIR light emitted from LED was between 1040 nm and 1090 nm. The power density delivered at the level of the mice was approximately 15 mW/cm 2 . Firstly, we treated the mice with NIR for 40 days. Then, the irradiation was suspended for 28 days. Finally, another 15 days treatment was brought to mice. We conducted Morris water maze and immuno°uorescence analysis to evaluate the e®ects of treatment. Immuno°uorescence analysis was based on measuring the quantity of plaques in mouse brain slices. Our results show that NIR light improves memory and spatial learning ability and reduces plaques moderately. NIR light represents a potential treatment for AD.

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“…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%

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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Near infrared light mitigates cerebellar pathology in transgenic mouse models of dementia

Cited by 60 publications

References 28 publications

Distribution of LIM domain kinase 1 in the olfactory bulb, cerebral cortex, hippocampus, and cerebellum of the App/PS+/- mice

Distribution of LIM domain kinase 1 in the olfactory bulb, cerebral cortex, hippocampus, and cerebellum of the App/PS+/- mice

Near infra-red light treatment of Alzheimer’s disease

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

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