Cited by 305Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

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Locus Ceruleus Degeneration Promotes Alzheimer Pathogenesis in Amyloid Precursor Protein 23 Transgenic Mice

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Heneka, Michael T., Ramanathan, Mutiah, Jacobs, Andreas H., Dumitrescu-Ozimek, Lucia, Bilkei-Gorzo, Andras, Debeir, Thomas, Sastre, Magdalena, Galldiks, Norbert, Zimmer, Andreas, Hoehn, Mathias, Heiss, Wolf-Dieter, Klockgether, Thomas, Staufenbiel, Matthias·2006·The Journal of Neuroscience

DOI 10.1523/jneurosci.4236-05.2006PMC PMC6675491

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Abstract

Locus ceruleus (LC) degeneration and loss of cortical noradrenergic innervation occur early in Alzheimer’s disease (AD). Although this has been known for several decades, the contribution of LC degeneration to AD pathogenesis remains unclear. We induced LC degeneration with N-(2-chloroethyl)-N-ethyl-bromo-benzylamine (dsp4) in amyloid precursor protein 23 (APP23) transgenic mice with a low amyloid load. Then 6 months later the LC projection areas showed a robust elevation of glial inflammation along with augmented amyloid plaque deposits. Moreover, neurodegeneration and neuronal loss significantly increased. Importantly, the paraventricular thalamus, a nonprojection area, remained unaffected. Radial arm maze and social partner recognition tests revealed increased memory deficits while high-resolution magnetic resonance imaging-guided micro-positron emission tomography demonstrated reduced cerebral glucose metabolism, disturbed neuronal integrity, and attenuated acetylcholinesterase activity. Nontransgenic mice with LC degeneration were devoid of these alterations. Our data demonstrate that the degeneration of LC affects morphology, metabolism, and function of amyloid plaque-containing higher brain regions in APP23 mice. We postulate that LC degeneration substantially contributes to AD development.

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Authors: Heneka, M. T., Ramanathan, M., Jacobs, A. H., Dumitrescu-Ozimek, L., Bilkei-Gorzo, A., Debeir, T., Sastre, M., Galldiks, N., Zimmer, A., Hoehn, M., Heiss, W.-D., Klockgether, T., & Staufenbiel, M.
Affiliations: University of Bonn (DE)
ORCID: Heneka, Michael T.
Sastre, Magdalena
Galldiks, Norbert
Zimmer, Andreas
Hoehn, Mathias
Heiss, Wolf-Dieter
Klockgether, Thomas
Venue: The Journal of Neuroscience
Publisher: Society for Neuroscience
Published: 2006-02-01
Volume: 26
Issue: 5
Pages: 1343-1354
ISSN: 0270-6474 (ISSN-L)
1529-2401
DOI: 10.1523/jneurosci.4236-05.2006
PMC: PMC6675491
OpenAlex: W2118414216
Cited by: 305
References: 54
Citations by year: 2026: 9 · 2025: 9 · 2024: 18 · 2023: 21 · 2022: 23 · 2021: 18 · 2020: 16 · 2019: 16 · 2018: 12 · 2017: 20 · 2016: 9 · 2015: 17 · 2014: 11 · 2013: 17 · 2012: 19
FWCI: 7.31
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-sa
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 181 d)
Locations: Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Open Repository and Bibliography (University of Luxembourg) (submittedVersion, other-oa)
Max Planck Institute for Plasma Physics (submittedVersion)
MPG.PuRe (Max Planck Society) (submittedVersion)
Funders: Deutsche Forschungsgemeinschaft (SFB400)
International Brain Research Organization
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: Alzheimer's disease pathogenesis, glial inflammation, amyloid plaques, neurodegeneration, memory impairment, brain glucose metabolism, acetylcholinesterase activity, paraventricular thalamus, cholinergic hypothesis
MeSH terms: Alzheimer Disease, Animals, Astrocytes, Brain, Cognition Disorders, Female, Locus Coeruleus, Mice, Transgenic, Nerve Degeneration, Norepinephrine, Amyloid beta-Protein Precursor, Microglia, Peroxynitrous Acid, Positron-Emission Tomography, Vesicular Acetylcholine Transport Proteins, Mice, Nitric Oxide Synthase Type II, Plaque, Amyloid

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Locus Ceruleus Degeneration Promotes Alzheimer Pathogenesis in Amyloid Precursor Protein 23 Transgenic Mice

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