期刊
GLIA
卷 70, 期 2, 页码 368-378出版社
WILEY
DOI: 10.1002/glia.24112
关键词
Alzheimer's disease; APP; PS1; astrocyte; astrogliosis; beta amyloid; cortex
资金
- Ayudas para la Movilidad de Investigadores [BA15/00078]
- Ministerio de Ciencia, Innovacion y Universidades [BFU2017-88393-P]
- Ministerio de Economia y Competitividad [BFU2016-80665-P]
- National Institute of Mental Health [R01MH119355]
- National Institute of Neurological Disorders and Stroke [R01NS097312]
- National Institute on Aging [1F31AG057155, 1RF1AG062135]
- National Institute on Drug Abuse [R01DA048822]
- Salvador de Madariaga Program [PRX19/00646]
Research has found that dysfunction of astrocyte networks in AD mice may dysregulate cortical electrical activity, leading to cognitive decline.
Alzheimer's disease (AD) is associated with senile plaques of beta-amyloid (A beta) that affect the function of neurons and astrocytes. Brain activity results from the coordinated function of neurons and astrocytes in astroglial-neuronal networks. However, the effects of A beta on astroglial and neuronal network function remains unknown. Simultaneously monitoring astrocyte calcium and electric neuronal activities, we quantified the impact of A beta on sensory-evoked cortical activity in a mouse model of AD. At rest, cortical astrocytes displayed spontaneous hyperactivity that was related to A beta density. Sensory-evoked astrocyte responsiveness was diminished in AD mice, depending on the density and distance of A beta, and the responses showed altered calcium dynamics. Hence, astrocytes were spontaneously hyperactive but hypo-responsive to sensory stimulation. Finally, AD mice showed sensory-evoked electrical cortical hyperresponsiveness associated with altered astrocyte-neuronal network interplay. Our findings suggest dysfunction of astrocyte networks in AD mice may dysregulate cortical electrical activity and contribute to cognitive decline.
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