Photobiomodulation modulates mitochondrial energy metabolism and ameliorates neurological damage in an APP/PS1 mousmodel of Alzheimer’s disease DOI Creative Commons
Hongli Chen, Na Li, Na Liu

et al.

Alzheimer s Research & Therapy, Journal Year: 2025, Volume and Issue: 17(1)

Published: April 5, 2025

Alzheimer's disease (AD) is a neurodegenerative disease. Amyloid β-protein (Aβ) one of the key pathological features AD, which cytotoxic and can damage neurons, thereby causing cognitive dysfunction. Photobiomodulation (PBM) non-invasive physical therapy that induces changes in intrinsic mechanisms cells tissues through low-power light exposure. Although PBM has been employed treatment effect precise mechanism on AD-induced neurological are still unclear. In vivo experiments, (808 nm, 20 mW/cm2) was used to continuously interfere with APP/PS1 mice for 6 weeks, then their function AD were evaluated. vitro lipopolysaccharide (LPS) induce microglia model inflammation, polarization status phagocytic Aβ ability Hexokinase 2 (HK2) inhibitor 3-bromopyruvate (3BP) study mitochondrial energy metabolism microglia. further ameliorates impairment by alleviating neuroinflammation neuronal apoptosis, attenuating nerve damage. addition, also reduce promoting microglial anti-inflammatory phenotypic polarization; Promotes clearance enhancing engulf Aβ. Among them, regulates inhibits may be related its regulation metabolism, promotion oxidative phosphorylation, inhibition glycolysis. neuroinflammatory response repairing Aβ-induced Mitochondrial plays an important role improving injury mice. This provides theoretical support subsequent application AD.

Language: Английский

Photobiomodulation modulates mitochondrial energy metabolism and ameliorates neurological damage in an APP/PS1 mousmodel of Alzheimer’s disease DOI Creative Commons
Hongli Chen, Na Li, Na Liu

et al.

Alzheimer s Research & Therapy, Journal Year: 2025, Volume and Issue: 17(1)

Published: April 5, 2025

Alzheimer's disease (AD) is a neurodegenerative disease. Amyloid β-protein (Aβ) one of the key pathological features AD, which cytotoxic and can damage neurons, thereby causing cognitive dysfunction. Photobiomodulation (PBM) non-invasive physical therapy that induces changes in intrinsic mechanisms cells tissues through low-power light exposure. Although PBM has been employed treatment effect precise mechanism on AD-induced neurological are still unclear. In vivo experiments, (808 nm, 20 mW/cm2) was used to continuously interfere with APP/PS1 mice for 6 weeks, then their function AD were evaluated. vitro lipopolysaccharide (LPS) induce microglia model inflammation, polarization status phagocytic Aβ ability Hexokinase 2 (HK2) inhibitor 3-bromopyruvate (3BP) study mitochondrial energy metabolism microglia. further ameliorates impairment by alleviating neuroinflammation neuronal apoptosis, attenuating nerve damage. addition, also reduce promoting microglial anti-inflammatory phenotypic polarization; Promotes clearance enhancing engulf Aβ. Among them, regulates inhibits may be related its regulation metabolism, promotion oxidative phosphorylation, inhibition glycolysis. neuroinflammatory response repairing Aβ-induced Mitochondrial plays an important role improving injury mice. This provides theoretical support subsequent application AD.

Language: Английский

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