Therapeutic Potential of Photobiomodulation In Alzheimer’s Disease: A Systematic Review

Cardoso, Fabrízio Dos Santos; Lopes-Martins, Rodrigo Álvaro Brandão; Silva, Sérgio Gomes da

doi:10.34172/jlms.2020.s3

Cited by 22 publications

(16 citation statements)

References 45 publications

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“…Today, photobiomodulation (PBM) therapy has found applications not only in the treatment of chronic wounds but also in the treatment of many diseases, including neurological and musculoskeletal [2]. Also, this noninvasive method is used to reduce pain [3].…”

Section: Introductionmentioning

confidence: 99%

Experimental Study of the Effect of Photobiomodulation Therapy on the Regulation of the Healing Process of Chronic Wounds

Pavlov

Babenko

Kumetchko

et al. 2021

International Journal of Photoenergy

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Currently, wound treatment is an urgent task of medicine around the world. In the process of wound healing, various types of cells are involved under the control and regulation of cytokines and growth factors. Disruption of the synchronization process between the various types of cells and intercellular mediators involved in the restoration of tissue damage can lead to impaired healing and the development of chronic wounds. Photobiomodulation (PBM) therapy promotes platelet activation and aggregation, reduces inflammation and oxidative stress, and accelerates cell migration and proliferation. PBM also induces the production of the extracellular matrix and the release of key growth factors, thereby improving tissue regeneration and accelerating wound healing. The aim of our work was to study the effect of photobiomodulation therapy on the regulation of reparative processes in chronic wounds monitored by biomarkers and platelet aggregation activity. 54 Wistar rats were divided into three groups. Intact animals were not manipulated. In animals of the control and experimental groups, a chronic wound was simulated by reproducing the conditions of local hypoxia and microcirculation disorders. The wounds of the experimental group received PBM therapy. The device Lika-therapist M (Ukraine) was used in a continuous mode at a wavelength of 660 nm, an output power of 10 mW, and an energy density of 1 J/cm2. The wounds of the animals in the control group were treated with sham. The animals were euthanized on days 3, 7, 14, and 28 after the surgery (6 animals, each from the control and experimental groups). Measurements of the levels of interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor alpha (TNF-α), the basic fibroblast growth factor (bFGF), and reactive oxygen species (ROS) were carried out by ELISA. Results revealed the multidirectional effect of PBM therapy on the expression of the studied biomarkers. The results of the histological examination indicated a positive effect of PBM therapy with the applied parameters on the repair processes of chronic wounds. We concluded that the use of PBM therapy made it possible to regulate disturbances in reparative processes by modulating ROS, cytokines, and platelet aggregation activity.

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Section: Introductionmentioning

confidence: 99%

Experimental Study of the Effect of Photobiomodulation Therapy on the Regulation of the Healing Process of Chronic Wounds

Pavlov

Babenko

Kumetchko

et al. 2021

International Journal of Photoenergy

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“…Light therapy, specifically morning blue-enriched light, might be effective for improving sleep quality and cognitive function (60), and evidence indicates that light therapy reduces neuroinflammation and oxidative stress to improve sleep and cognition (61). Indeed, these circadian-based therapies, including sleep behavior modifications (62), are increasingly becoming part of standard of care for AD, and might combat cognitive decline (30).…”

Section: Public Health Implications Of Circadian Disruptionmentioning

confidence: 99%

Circadian disruption and human health

Fishbein¹,

Knutson²,

Zee³

2021

Journal of Clinical Investigation

193

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Circadian (circa, "about," and diem, "day") rhythms are endogenous oscillations with an approximately 24-hour cycle. Circadian rhythms in physiology and behavior are organized by a central "master" clock, the suprachiasmatic nucleus (SCN) located in the anterior hypothalamus, that coordinates alignment between external synchronizing agents with circadian clocks in other brain regions, as well as in peripheral tissues. Circadian rhythms are modulated by endogenous (genetic, physiological) as well as environmental (light) and behavioral (activity, feeding) factors. In this Review, we use "circadian disruption" as a nonspecific umbrella term to describe a disturbance, dysregulation, or problem that negatively affects circadian function, but as Vetter has pointed out, there is a need for clearer terminology and quantification of circadian disruption (1). It is becoming increasingly clear that circadian disruption in humans can result in broad and significant consequences for mental and physical health (2, 3). Furthermore, changes in circadian function are often accompanied by sleep-wake disturbances, which also contribute to poor health outcomes. The interrelationship between circadian rhythms and human disease can create a vicious cycle between disease expression and circadian disruption, as exemplified in immunologic (4, 5), cardiometabolic (6), neurodegenerative, and psychiatric disorders (7). General mechanisms of circadian disruptionIn humans, measures of circadian disruption include the phase (timing), relationship between internal-internal or internal-external rhythms (alignment), the period and amplitude of circadian rhythms. Disturbance of circadian phase alignment and amplitude are the most common measures that have been associated with adverse health consequences. As outlined in Figure 1, circadian disruption can occur at multiple levels, from intrinsic changes at the molecular, cellular, tissue, or system level to misalignment among different organizational levels and/or with behavioral and environmental cycles. The "molecular circadian clock" refers to genes that maintain autoregulatory feedback loops in which oscillating outputs regulate their own expression (circadian locomotor output cycles kaput [CLOCK], brain and muscle ARNTlike [BMAL], period [PER], rev-erb/nuclear receptor subfamily 1, group D [NR1D], and cryptochrome [CRY]; ref. 4). Biomarkers of circadian rhythm and circadian disruptionAlthough the SCN rhythm cannot be directly measured in humans, the timing of melatonin onset and amplitude measured in plasma or saliva, or the melatonin metabolite 6-sulfatoxymelatonin in urine, are gold standard biomarkers of circadian rhythms. The collection of 24-hour urine samples is particularly useful to assess circadian amplitude of melatonin in special populations, such as pediatric patients in whom blood or salivary samples might be difficult to obtain (8), and has been shown to be a useful treatment-responsive biomarker of circadian disruption in neurologic diseases, such as Alzheimer's disease (AD) (9)...

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“…A model providing a mechanistic explanation of the interactions of light with sleep and circadian rhythm patterns resulting in positive effects on mood and cognition has been published (LeGates et al, 2014). A separate review of PBM as a therapeutic modality in treating AD has also been published (Cardoso et al, 2020). Moreover, significant improvements due to the clinical application of tPBM in treating Parkinson's disease patients have been recently reported (Liebert et al, 2021).…”

Section: Photobiomodulationmentioning

confidence: 99%

Is Alzheimer's disease a manifestation of brain quantum decoherence resulting from mitochondrial and microtubular deterioration?

Nichols¹,

Berman²,

Tuszyński³

2023

J. Multiscale Neurosci.

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The etiology of Alzheimer's dementia is, at best multifactorial. Before the emergence of cognitive impairment, symptoms such as thinning of the cortex, accumulation of β-amyloid, and decreased hippocampal volume are common. Hence, the accumulation of β-amyloid and hyperphosphorylated tau fibrillary tangles are two pathological hallmarks in Alzheimer's disease brains, but antibody therapy aimed to decrease β-amyloid has been a failure and, in most optimistic opinions, may delay somewhat disease progression. However, 31-38 % of subjects develop cerebral micro-hemorrhages in aducanumab therapy, an antibody to the amyloid beta plaque by Biogen. Genetics such as Apo E3/E3 have demonstrated defects in the blood-brain barrier in early-onset dementia. Late Onset Alzheimer’s Dementia, has implicated microbe cerebral infections and numerous genetic single nucleotide polymorphisms. However, several cellular biological signatures of Alzheimer's disease have been identified, such as synaptic dysfunction, β-amyloid plaques, hyperphosphorylated tau, cofilin-actin rods, and Hirano bodies which are related to the actin cytoskeleton. Cofilin is one of the most affluent and common actin-binding proteins and plays a role in cell motility, migration, shape, and metabolism. They also play an important role in severing actin filament, nucleating, depolymerizing, and bundling activities. This review summarizes the structure of cofilins appearing after ATP interruptions and deficits in mitochondrial and microtubules and their functional and regulating roles, focusing on the synaptic dysfunction, β-amyloid plaques, hyperphosphorylated tau, cofilin-actin rods, and Hirano bodies of Alzheimer's disease. These findings strengthen our hypothesis that Alzheimer’s dementia is characterized by “Quantum Decoherence” resulting from mitochondrial and microtubular deterioration and responding to near-infrared transcranial photobiomodulation to support mitochondrial and microtubule repair, regrowth and neuronal synaptic renormalization.

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Therapeutic Potential of Photobiomodulation In Alzheimer’s Disease: A Systematic Review

Cited by 22 publications

References 45 publications

Experimental Study of the Effect of Photobiomodulation Therapy on the Regulation of the Healing Process of Chronic Wounds

Experimental Study of the Effect of Photobiomodulation Therapy on the Regulation of the Healing Process of Chronic Wounds

Circadian disruption and human health

Is Alzheimer's disease a manifestation of brain quantum decoherence resulting from mitochondrial and microtubular deterioration?

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