Activation of PKA/SIRT1 signaling pathway by photobiomodulation therapy reduces Aβ levels in Alzheimer's disease models
Zhang Z, Shen Q, Wu X, Zhang D, Xing D
Aging cell · 114 citas
Cómo se estudió
- Diseño
- Estudio en animales (clasificado por nuestro filtro de IA)
- Estudiado en
- Personas, más trabajo en animales o laboratorio
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- National Natural Science Foundation of China
- Gobierno
- Natural Science Foundation of Guangdong Province
- Subvenciones
- National Natural Science Foundation of China (61361160414); National Natural Science Foundation of China (2014A030313419); National Natural Science Foundation of China (31470072); Natural Science Foundation of Guangdong Province (2014A030313419)
Según 2 financiadores declarados y la declaración de financiación del texto completo.
Publicación
- Publicado
- 2019-10-30 · Aging Cell · vol. 19 · número 1 · pág. e13054
- Editorial
- Wiley
- Citado
- 139 citas · más que el 98% de estudios similares · 9.0× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 40 trabajos
- Acceso
- Acceso abierto (revista) · CC-BY
- Áreas de investigación
- Laser Applications in Dentistry and Medicine · Biochemical effects in animals · Sirtuins and Resveratrol in Medicine
- Palabras clave
- Neuroprotection, Amyloid precursor protein, Neuroscience, Biology, Amyloid precursor protein secretase, Alzheimer's disease, Disease, ADAM10, Amyloid (mycology), Cell biology, Medicine, Internal medicine, Biochemistry, Enzyme
- MeSH
- animals, mice, transgenic, humans, mice, alzheimer disease, disease models, animal, sirtuin 1, amyloid beta-peptides, low-level light therapy
5 autores
- Zhan Zhang🇨🇳South China Normal University
- Qi Shen🇨🇳South China Normal University
- Xiaolei Wu🇨🇳South China Normal University
- Di Zhang🇨🇳South China Normal University
- Da Xing🇨🇳 · autor de correspondenciaSouth China Normal University
Resumen
El texto original del estudio, en el idioma en que se publicó.
A hallmark of Alzheimer's disease (AD) is the accumulation of amyloid-β (Aβ), which correlates significantly with progressive cognitive deficits. Although photobiomodulation therapy (PBMT), as a novel noninvasive physiotherapy strategy, has been proposed to improve neuronal survival, decrease neuron loss, ameliorate dendritic atrophy, and provide overall AD improvement, it remains unknown whether and how this neuroprotective process affects Aβ levels. Here, we report that PBMT reduced Aβ production and plaque formation by shifting amyloid precursor protein (APP) processing toward the nonamyloidogenic pathway, thereby improving memory and cognitive ability in a mouse model of AD. More importantly, a pivotal protein, SIRT1, was involved in this process by specifically up-regulating ADAM10 and down-regulating BACE1, which is dependent on the cAMP/PKA pathway in APP/PS1 primary neurons and SH-SY5Y cells stably expressing human APP Swedish mutation (APPswe). We further found that the activity of the mitochondrial photoacceptor cytochrome c oxidase (CcO) was responsible for PBMT-induced activation of PKA and SIRT1. Together, our research suggests that PBMT as a viable therapeutic strategy has great potential value in improving cognitive ability and combatting AD.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY).
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