ArticleJournal of Alzheimer's disease : JAD2015
Norepinephrine Protects against Amyloid-β Toxicity via TrkB.
Article in Journal of Alzheimer's disease : JAD, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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The trial behind it
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Who cites it
40 citing papers in PubMed, 59 citations in OpenAlex.
- A phase II study repurposing atomoxetine for neuroprotection in mild cognitive impairment.Brain : a journal of neurology · 2022Trial
- Decreased Length of Locus Coeruleus Norepinephrine Axons and Increased Amyloid Beta Pathology in Male APP/PS1 Mice During Protracted Abstinence From Alcohol.Neurotoxicity research · 2026Article
- Long-term Locus Coeruleus Stimulation Exacerbates Tau Pathology in PS19 Mice.bioRxiv : the preprint server for biology · 2025Article
- Alcohol consumption during early adulthood increases the vulnerability of locus coeruleus neurons and amyloid beta pathology in female APP/PS1 mice.Alcohol (Fayetteville, N.Y.) · 2025Article
- The Locus Coeruleus-Noradrenergic System in the Healthy and Diseased Brain: A Narrative Review.European journal of neurology · 2025Review
- A possible pathway to freezing of gait in Parkinson's disease.Journal of Parkinson's disease · 2025Article
- Neuroprotective actions of norepinephrine in neurological diseases.Pflugers Archiv : European journal of physiology · 2024Review
- Atrophy links lower novelty-related locus coeruleus connectivity to cognitive decline in preclinical AD.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Stabilization and Reduced Cytotoxicity of Amyloid Beta Aggregates in the Presence of Catechol Neurotransmitters.Neurochemical research · 2024Article
- Pain in Parkinson's disease: a neuroanatomy-based approach.Brain communications · 2024Review
- DAT1 and BDNF polymorphisms interact to predict Aβ and tau pathology.Neurobiology of aging · 2024Article
- Search for unknown neural link between the masticatory and cognitive brain systems to clarify the involvement of its impairment in the pathogenesis of Alzheimer's disease.Frontiers in cellular neuroscience · 2024Review
- The effects of locus coeruleus ablation on mouse brain volume and microstructure evaluated by high-field MRI.Frontiers in cellular neuroscience · 2024Article
- Influence of Cortisol on the Fibril Formation Kinetics of Aβ42 Peptide: A Multi-Technical Approach.International journal of molecular sciences · 2022Article
- Pain Modulation from the Locus Coeruleus in a Model of Hydrocephalus: Searching for Oxidative Stress-Induced Noradrenergic Neuroprotection.International journal of molecular sciences · 2022Article
- Understanding How Physical Exercise Improves Alzheimer's Disease: Cholinergic and Monoaminergic Systems.Frontiers in aging neuroscience · 2022Review
- ApoE4 inhibition of VMAT2 in the locus coeruleus exacerbates Tau pathology in Alzheimer's disease.Acta neuropathologica · 2021Article
- Sublingual AKBA Exerts Antidepressant Effects in the Aβ-Treated Mouse Model.Biomolecules · 2021Article
- Alzheimer's disease: An evolving understanding of noradrenergic involvement and the promising future of electroceutical therapies.Clinical and translational medicine · 2021Review
- The Locus Coeruleus in Aging and Alzheimer's Disease: A Postmortem and Brain Imaging Review.Journal of Alzheimer's disease : JAD · 2021Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The locus coeruleus (LC), the brainstem noradrenergic nucleus that is the sole source of norepinephrine (NE) in the forebrain, is one of the first structures affected in Alzheimer's disease (AD). Experimental ablation of the LC exacerbates, while increasing NE abates, AD-like neuropathology and cognitive deficits in animal models of the disease. Some neuroprotective effects of NE appear to be mediated by tropomyosin-related kinase B (TrkB), the canonical receptor for brain-derived neurotrophic factor (BDNF). Here, we report that NE dose-dependently protected primary cortical and LC neurons from amyloid-β (Aβ) toxicity. The neuroprotective effects of NE were fully prevented by the Trk receptor antagonist K252a but only partially attenuated by adrenergic receptor antagonists and not mimicked by adrenergic agonists. Activation of TrkB by NE in cortical and LC neurons was confirmed by immunoblot and immunocytochemistry for phospho-TrkB. These results indicate that NE can activate TrkB and protect against Aβ toxicity, at least in part, via adrenergic receptor-independent mechanisms, and have implications for the consequences of LC degeneration in AD and potential therapies for the disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.