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Analyzing nicotine action against amyloid toxicity by NMR-pharmacometabolomics: an exploratory study

ABSTRACT:

Alzheimer's disease (AD) is the primary neurodegenerative disease spread worldwide. One of the main histopathological hallmarks of AD is amyloid plaque deposition in the brain. Despite some epidemiological studies demonstrating that cigarette smoke is a factor in predisposing people to AD, nicotine, the principal alkaloid of Nicotiana Tobacco, has been widely studied for its ability to improve cognitive performance, both in animal models and in human studies.

Several hypotheses have been proposed to explain the mechanism of action underlying the beneficial effect of Nicotine in AD; however, this is still questioned.

To have new insights into the molecular mechanism underlying the neuroprotective action of Nicotine in Alzheimer's disease, we performed an NMR metabolomic analysis of SH-SY5Y neuroblastoma cells treated with Aβ (1-42) in the presence of nicotine. Our data show that the neuroprotective action of nicotine resides in its ability to restore the systemic unbalanced metabolism associated with AD. In particular, nicotine reverses most Aβ (1-42)-induced metabolic impairments, including those related to amino acid metabolism, especially those involved in neurotransmission, as well as alterations in energy metabolism and membrane phospholipid metabolism.

INSTRUMENT(S): Nuclear Magnetic Resonance (NMR) -

PROVIDER: MTBLS12706 | MetaboLights | 2026-06-26

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS12706_NMR___metabolite_profiling-1.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS12706_NMR___metabolite_profiling-1_v2_maf.tsv	Tabular
	s_MTBLS12706.txt	Txt

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Project description:Alzheimer's disease (AD) is a chronic neurodegenerative disorder characterized by progressive deterioration of cognitive function. Evidence suggests a role for epigenetic regulation, in particular the cytosine modifications 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC,) in AD. 5hmC is highly enriched in the nervous system and displays neurodevelopment and age-related changes. To determine the role of 5hmC in AD, we performed genome-wide analyses of 5hmC in DNA from prefrontal cortex of post-mortem AD as well as RNA-Seq to correlate changes in methylation status with transcriptional changes. We also utilized the existing AD fly model to further test the functional significance of these epigenetically altered loci. We identified 325 genes containing differentially hydroxymethylated loci (DhMLs) in both the discovery and replication datasets, and these are enriched for pathways involved in neuron projection development and neurogenesis. Of the 325 genes identified, 140 also showed changes in gene expression by RNA-Seq. Proteins encoded by genes identified in the current analysis form direct protein-protein interactions with AD-associated genes, expanding the network of genes implicated in AD. Furthermore, we identified AD-associated single nucleotide polymorphisms (SNPs) located within or near DhMLs, suggesting that these SNPs may identify regions of epigenetic gene regulation that play a role in AD pathogenesis. Finally using the existing AD fly model we showed that some of these genes could modulate the toxicity associated with AD. Our data implicate neuron projection development and neurogenesis pathways as potential targets in AD. These results indicate that incorporating epigenomic and transcriptomic data with GWAS data can expand the known network of genes involved in disease pathogenesis. Combination of epigenome profiling and Drosophila model enables us to identify the epigenetic modifiers of Alzheimer's disease. University of Kentucky Alzheimer's Disease Research Center (3 control, 3 Alzheimer's) and Emory University Alzheimer's Disease Research Center (2 control, 2 Alzheimer's)

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Analyzing nicotine action against amyloid toxicity by NMR-pharmacometabolomics: an exploratory study

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