ArticleJournal of molecular neuroscience : MN2019
Age- and Nicotine-Associated Gene Expression Changes in the Hippocampus of APP/PS1 Mice.
Article in Journal of molecular neuroscience : MN, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- TUFM: a central regulator in mitochondrial quality control and beyond.Cell death discovery · 2026Review
- Neuronal A2A receptor exacerbates synapse loss and memory deficits in APP/PS1 mice.Brain : a journal of neurology · 2024Article
- SHMT2 Mediates Small-Molecule-Induced Alleviation of Alzheimer Pathology Via the 5'UTR-dependent ADAM10 Translation Initiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- TUFM in health and disease: exploring its multifaceted roles.Frontiers in immunology · 2024Review
- Lipidomic Analysis of Hand Skin Surface Lipids Reveals Smoking-Related Skin Changes.Metabolites · 2023Article
- AP2S1 regulates APP degradation through late endosome-lysosome fusion in cells and APP/PS1 mice.Traffic (Copenhagen, Denmark) · 2023Article
- Metabolome-wide association study onProceedings of the National Academy of Sciences of the United States of America · 2022Article
- CaInternational journal of molecular sciences · 2022Review
- Sex-specific nicotine sensitization and imprinting of self-administration in rats inform GWAS findings on human addiction phenotypes.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- Age-Dependent and Sleep/Seizure-Induced Pathomechanisms of Autosomal Dominant Sleep-Related Hypermotor Epilepsy.International journal of molecular sciences · 2020Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
The etiology of Alzheimer's disease (AD) has been intensively studied. However, little is known about the molecular alterations in early-stage and late-stage AD. Hence, we performed RNA sequencing and assessed differentially expressed genes (DEGs) in the hippocampus of 18-month and 7-month-old APP/PS1 mice. Moreover, the DEGs induced by treatment with nicotine, the nicotinic acetylcholine receptor agonist that is known to improve cognition in AD, were also analyzed in old and young APP/PS1 mice. When comparing old APP/PS1 mice with their younger littermates, we found an upregulation in genes associated with calcium overload, immune response, cancer, and synaptic function; the transcripts of 14 calcium ion channel subtypes were significantly increased in aged mice. In contrast, the downregulated genes in aged mice were associated with ribosomal components, mitochondrial respiratory chain complex, and metabolism. Through comparison with DEGs in normal aging from previous reports, we found that changes in calcium channel genes remained one of the prominent features in aged APP/PS1 mice. Nicotine treatment also induced changes in gene expression. Indeed, nicotine augmented glycerolipid metabolism, but inhibited PI3K and MAPK signaling in young mice. In contrast, nicotine affected genes associated with cell senescence and death in old mice. Our study suggests a potential network connection between calcium overload and cellular signaling, in which additional nicotinic activation might not be beneficial in late-stage AD.
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