Cited by 213Alzheimer's disease research and treatmentsNicotinic Acetylcholine Receptors StudyDementia and Cognitive Impairment Research

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Chronic nicotine administration exacerbates tau pathology in a transgenic model of Alzheimer's disease

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Oddo, Salvatore, Caccamo, Antonella, Green, Kim N., Liang, Kevin, Tran, Levina, Chen, Yiling, Leslie, Frances M., LaFerla, Frank M.·2005·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.0408500102PMC PMC549455

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Abstract

The association between nicotinic acetylcholine receptor (nAChR) dysfunction and cognitive decline in Alzheimer's disease (AD) has been widely exploited for its therapeutic potential. The effects of chronic nicotine exposure on Aβ accumulation have been studied in both humans and animal models, but its therapeutic efficacy for AD neuropathology is still unresolved. To date, no in vivo studies have addressed the consequences of activating nAChRs on tau pathology. To determine the effects of chronic nicotine administration on Aβ and tau pathology, we chronically administrated nicotine to a transgenic model of AD (3xTg-AD) in their drinking water. Here, we show that chronic nicotine intake causes an up-regulation of nicotinic receptors, which correlated with a marked increase in the aggregation and phosphorylation state of tau. These data show that nicotine exacerbates tau pathology in vivo . The increase in tau phosphorylation appears to be due to the activation of p38-mitogen-activated protein kinase, which is known to phosphorylate tau in vivo and in vitro . We also show that the 3xTg-AD mice have an age-dependent reduction of α7nAChRs compared with age-matched nontransgenic mice in specific brain regions. The reduction of α7nAChRs is first apparent at 6 months of age and is restricted to brain regions that show intraneuronal Aβ 42 accumulation. Finally, this study highlights the importance of testing compounds designed to ameliorate AD pathology in a model with both neuropathological lesions because of the differential effects it can have on either Aβ or tau.

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Authors: Oddo, S., Caccamo, A., Green, K. N., Liang, K., Tran, L., Chen, Y., Leslie, F. M., & LaFerla, F. M.
Affiliations: University of California, Irvine (US)
Departments of Neurobiology and Behavior and Pharmacology, University of California, Irvine, CA 92697
ORCID: Oddo, Salvatore
Caccamo, Antonella
Green, Kim N.
Leslie, Frances M.
LaFerla, Frank M.
Venue: Proceedings of the National Academy of Sciences
Publisher: National Academy of Sciences
Published: 2005-02-10
Volume: 102
Issue: 8
Pages: 3046-3051
ISSN: 0027-8424 (ISSN-L)
1091-6490
DOI: 10.1073/pnas.0408500102
PMC: PMC549455
OpenAlex: W2139557860
Cited by: 211
References: 47
Citations by year: 2026: 2 · 2025: 9 · 2024: 9 · 2023: 7 · 2022: 7 · 2021: 6 · 2020: 6 · 2019: 7 · 2018: 6 · 2017: 5 · 2016: 8 · 2015: 5 · 2014: 14 · 2013: 14 · 2012: 11
FWCI: 10.43
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Proceedings of the National Academy of Sciences (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Alzheimer's Association
National Institute on Aging (AG0212982)
National Institute on Drug Abuse (DA-10612, R01DA010612)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: chronic nicotine administration, tau pathology, Alzheimer's disease, nicotinic acetylcholine receptors, alpha7 nicotinic acetylcholine receptor, tau phosphorylation, p38 MAPK, amyloid-beta deposition, 3xTg-AD mice
MeSH terms: Age Factors, Alzheimer Disease, Animals, Calcium, Disease Models, Animal, Mice, Transgenic, Nicotine, Phosphorylation, Receptors, Nicotinic, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, tau Proteins, Mice, alpha7 Nicotinic Acetylcholine Receptor

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Chronic nicotine administration exacerbates tau pathology in a transgenic model of Alzheimer's disease

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