Impact of noradrenergic inhibition on neuroinflammation and pathophysiology in mouse models of Alzheimer’s disease

被引：1

作者：

Andrew K. Evans ^{[1
]}

Heui Hye Park ^{[1
]}

Claire E. Woods ^{[1
]}

Rachel K. Lam ^{[1
]}

Daniel Ryskamp Rijsketic ^{[1
]}

Christine Xu ^{[2
]}

Emily K. Chu ^{[1
]}

Peter Ciari ^{[1
]}

Sarah Blumenfeld ^{[1
]}

Laura M. Vidano ^{[1
]}

Nay Lui Saw ^{[1
]}

Boris D. Heifets ^{[1
]}

Mehrdad Shamloo ^{[2
]}

机构：

[1] Stanford University School of Medicine,Department of Neurosurgery

[2] Stanford University School of Medicine,Department of Anesthesiology, Perioperative, and Pain Medicine

[3] Stanford University School of Medicine,Department of Psychiatry and Behavioral Sciences

来源：

Journal of Neuroinflammation | / 21卷 / 1期

关键词：

Alzheimer’s Disease; Norepinephrine; Locus coeruleus; Beta-adrenergic receptor; Beta-blocker; Neuroinflammation; iDISCO+; Amyloid beta; Microglia;

D O I：

10.1186/s12974-024-03306-1

中图分类号：

学科分类号：

摘要：

Norepinephrine (NE) modulates cognitive function, arousal, attention, and responses to novelty and stress, and it also regulates neuroinflammation. We previously demonstrated behavioral and immunomodulatory effects of beta-adrenergic pharmacology in mouse models of Alzheimer’s disease (AD). The current studies were designed to block noradrenergic signaling in 5XFAD mice through (1) chemogenetic inhibition of the locus coeruleus (LC), (2) pharmacologic blocking of β-adrenergic receptors, and (3) conditional deletion of β1- or β2-adrenergic receptors (adrb1 or adrb2) in microglia.

引用

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