ArticleBrain research2019
Complex noradrenergic dysfunction in Alzheimer's disease: Low norepinephrine input is not always to blame.
Article in Brain research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
43 citing papers in PubMed, 63 citations in OpenAlex.
- Altered locus coeruleus links to atrophy and hypometabolism in individuals with high Alzheimer's disease biomarkers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Trial
- Systems biology of Alzheimer's Disease: a scoping review of key pathways and mechanisms.Molecular neurodegeneration · 2026Article
- Central cytometabolic functional vascular coupling in health and disease.npj metabolic health and disease · 2025Review
- Eye movement evidence for locus coeruleus-noradrenaline system contributions to age differences in attention.Psychology and aging · 2025Article
- Cerebrospinal fluid NPTX2 and [Alzheimer's research & therapy · 2025Article
- Long-term Locus Coeruleus Stimulation Exacerbates Tau Pathology in PS19 Mice.bioRxiv : the preprint server for biology · 2025Article
- Pleiotropic prodrugs for both symptomatic and disease-modifying treatment of Alzheimer's disease.Acta pharmaceutica Sinica. B · 2025Article
- Article
- Beyond the brain: early autonomic dysfunction in Alzheimer's disease.Acta neuropathologica communications · 2025Article
- Long-term exposure to excessive norepinephrine in the brain induces tau aggregation, neuronal death, and cognitive deficits in early tau transgenic mice.Aging cell · 2025Article
- Monoamine alterations in Alzheimer's disease and their implications in comorbid neuropsychiatric symptoms.GeroScience · 2025Review
- Deciphering the Role of Adrenergic Receptors in Alzheimer's Disease: Paving the Way for Innovative Therapies.Biomolecules · 2025Review
- Monoamine signaling and neuroinflammation: mechanistic connections and implications for neuropsychiatric disorders.Frontiers in immunology · 2025Review
- Eye movements reveal age differences in how arousal modulates saliency priority but not attention processing speed.bioRxiv : the preprint server for biology · 2024Article
- Adrenoceptor Desensitization: Current Understanding of Mechanisms.Pharmacological reviews · 2024Review
- Relationship between SLC6A2 gene polymorphisms and brain volume in Han Chinese adults who lost their sole child.BMC psychiatry · 2024Article
- Advances in Understanding and Managing Alzheimer's Disease: From Pathophysiology to Innovative Therapeutic Strategies.Current drug targets · 2024Review
- Profiling Chemobiological Connection between Natural Product and Target Space Based on Systematic Analysis.International journal of molecular sciences · 2023Article
- Two-photon fluorescence imaging and specifically biosensing of norepinephrine on a 100-ms timescale.Nature communications · 2023Article
- Cerebrospinal fluid and positron-emission tomography biomarkers for noradrenergic dysfunction in neurodegenerative diseases: a systematic review and meta-analysis.Brain communications · 2023Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The locus coeruleus-noradrenergic (LC-NA) system supplies the cerebral cortex with norepinephrine, a key modulator of cognition. Neurodegeneration of the LC is an early hallmark of Alzheimer's disease (AD). In this article, we analyze current literature to understand whether NA degeneration in AD simply leads to a loss of norepinephrine input to the cortex. With reported adaptive changes in the LC-NA system at the anatomical, cellular, and molecular levels in AD, existing evidence support a seemingly sustained level of extracellular NE in the cortex, at least at early stages of the long course of AD. We postulate that loss of the integrity of the NA system, rather than mere loss of NE input, is a key contributor to AD pathogenesis. A thorough understanding of NA dysfunction in AD has a large impact on both our comprehension and treatment of this devastating 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.