It has been described that using noninvasive exposure to 40-Hz white light LED reduces amyloid-beta, a peptide thought to initiate neurotoxic events in Alzheimer's disease (AD). However, the mechanisms remain to be identified. Since AD impairs mitochondrial potassium channels and respiratory chain activity, the objectives of the current study were to determine the effect of 40-Hz white light LED on structure-function of mitoK channel and brain mitochondrial respiratory chain activity, production of reactive oxygen species (ROS), and ΔΨ in AD. Single mitoK channel was considered using a channel incorporated into the bilayer lipid membrane and expression of mitoK-Kir6.1 subunit as a pore-forming subunit of the channel was determined using a western blot analysis in Aβ1-42 toxicity and light-treated rats. Our results indicated a severe decrease in mito-K channel permeation and Kir6.1 subunit expression coming from the Aβ1-42-induced neurotoxicity. Furthermore, we found that Aβ1-42-induced neurotoxicity decreased activities of complexes I and IV and increased ROS production and ΔΨ. Surprisingly, light therapy increased channel permeation and mitoK-Kir6.1 subunit expression. Noninvasive 40-Hz white light LED treatment also increased activities of complexes I and IV and decreased ROS production and ΔΨ up to ~ 70%. Here, we report that brain mito-K channel and respiratory chain are, at least in part, novel targets of 40-Hz white light LED therapy in AD.
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http://dx.doi.org/10.1007/s12035-021-02681-7 | DOI Listing |
Basic Clin Neurosci
July 2024
Neurophysiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Introduction: A 40-Hz white light emitting diode (WLED) has emerged as an alternative nonpharmacological and noninvasive approach to Alzheimer disease (AD). Here, we investigated the therapeutic effects of 40-Hz WLED on psychiatric symptoms (PS) and the contribution of mitochondrial factors in the early stages of sporadic AD (sAD) in rats.
Methods: In male Wistar rats, the AD model was induced via intracerebroventricular (ICV) injection of streptozotocin (STZ).
Sci Rep
November 2024
Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
Schizophrenia (Heidelb)
March 2024
Department of Neuropsychiatry, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
J Alzheimers Dis
January 2024
Cognito Therapeutics, Inc., Cambridge, MA, USA.
Background: Patients with Alzheimer's disease (AD) demonstrate progressive white matter atrophy and myelin loss. Restoring myelin content or preventing demyelination has been suggested as a therapeutic approach for AD.
Objective: Herein, we investigate the effects of non-invasive, combined visual and auditory gamma-sensory stimulation on white matter atrophy and myelin content loss in patients with AD.
Cereb Cortex
January 2024
Department of Neurology, Xuanwu Hospital, Capital Medical University, No. 45 Changchun Street, Xicheng District, Beijing 100053, China.
Repetitive transcranial magnetic stimulation (rTMS) and cognitive training for patients with Alzheimer's disease (AD) can change functional connectivity (FC) within gray matter (GM). However, the role of white matter (WM) and changes of GM-WM FC under these therapies are still unclear. To clarify this problem, we applied 40 Hz rTMS over angular gyrus (AG) concurrent with cognitive training to 15 mild-moderate AD patients and analyzed the resting-state functional magnetic resonance imaging before and after treatment.
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