Evidence map›Paper›PMID 41910845›Full record

ArticleNeurotoxicity research2026

Lipopolysaccharide-induced Neuroimmune Alteration and Memory Decline in Aging Mice: The Role of Augmented Cellular Senescence.

Miracle K Nekabari, Benneth Ben-Azu, Bienose S Chijioke, Daniel T Esuku, Emmanuel O Chidebe, Faith B Friday, Saviour G Usin, Prosper Iwhiwhu, Ayereoghene S Moses, Ovovwe Diakparomre and 1 more

Abstract read
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Article in Neurotoxicity research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Miracle K NekabariDELSU Joint Canada-Israel Neuroscience and Biopsychiatry Laboratory, Department of Pharmacology, Faculty of Allied Health Sciences, College of Health Sciences, Delta State University, Abraka, Delta State, Nigeria.
Benneth Ben-AzuDELSU Joint Canada-Israel Neuroscience and Biopsychiatry Laboratory, Department of Pharmacology, Faculty of Allied Health Sciences, College of Health Sciences, Delta State University, Abraka, Delta State, Nigeria. bben-azu@delsu.edu.ng.ORCID http://orcid.org/0000-0003-3569-3575
Bienose S ChijiokeDELSU Joint Canada-Israel Neuroscience and Biopsychiatry Laboratory, Department of Pharmacology, Faculty of Allied Health Sciences, College of Health Sciences, Delta State University, Abraka, Delta State, Nigeria.
Daniel T EsukuDELSU Joint Canada-Israel Neuroscience and Biopsychiatry Laboratory, Department of Pharmacology, Faculty of Allied Health Sciences, College of Health Sciences, Delta State University, Abraka, Delta State, Nigeria.
Emmanuel O ChidebeDELSU Joint Canada-Israel Neuroscience and Biopsychiatry Laboratory, Department of Pharmacology, Faculty of Allied Health Sciences, College of Health Sciences, Delta State University, Abraka, Delta State, Nigeria.
Faith B FridayDELSU Joint Canada-Israel Neuroscience and Biopsychiatry Laboratory, Department of Pharmacology, Faculty of Allied Health Sciences, College of Health Sciences, Delta State University, Abraka, Delta State, Nigeria.
Saviour G UsinDELSU Joint Canada-Israel Neuroscience and Biopsychiatry Laboratory, Department of Pharmacology, Faculty of Allied Health Sciences, College of Health Sciences, Delta State University, Abraka, Delta State, Nigeria.
Prosper IwhiwhuDELSU Joint Canada-Israel Neuroscience and Biopsychiatry Laboratory, Department of Pharmacology, Faculty of Allied Health Sciences, College of Health Sciences, Delta State University, Abraka, Delta State, Nigeria.
Ayereoghene S MosesDELSU Joint Canada-Israel Neuroscience and Biopsychiatry Laboratory, Department of Pharmacology, Faculty of Allied Health Sciences, College of Health Sciences, Delta State University, Abraka, Delta State, Nigeria.
Ovovwe DiakparomreBiochemistry Unit, Department of Chemical Sciences, University of Delta, Agbor, Delta State, Nigeria.
Onyeka B OnyeukwuBiochemistry Unit, Department of Chemical Sciences, University of Delta, Agbor, Delta State, Nigeria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer’s disease (AD) remains a complex neurodegenerative disorder with multifactorial etiologies, often eluding effective modeling in preclinical studies. However, whether neuroinflammation, exacerbated by accelerated cellular senescence, is central to AD pathology induced by lipopolysaccharide, an endotoxemia agent, remains unknown. This study investigated a combination of lipopolysaccharide (LPS)-induced AD-like neuroinflammation with doxycycline-induced conditioned cellular senescence in mice. Following a 21-day doxycycline (DOXY)-induced cellular senescence in mice, neuroinflammation was induced by LPS from days 15–21. AD-related cognitive decline was investigated through spatial and non-spatial memory tests, oxidative stress, molybdoenzymes, acetylcholinesterase activity, inflammation, amyloid-beta levels, hypoxia-inducible factor (HIF-α) and brain-derived neurotrophic factors (BDNF) in brain regions affected by AD pathology, such as the hippocampus and prefrontal cortex (PFC). Behavioral assessments revealed that both LPS and DOXY independently impaired spatial and non-spatial working memory, locomotor activity, social interaction, and recognition memory, with their interactive treatment exacerbating these deficits significantly. Biochemical analyses revealed synergistic increases in pro-inflammatory cytokines (IL-1β, TNF-α, but not IL-4), oxidative stress markers (malondialdehyde, nitrite), astrocyte activation (GFAP), and amyloid-beta levels, with decreases in antioxidant defenses (GSH, GST, SOD, catalase) in the hippocampus and PFC. The DOXY + LPS group showed higher serum corticosterone levels, increased sulphite-oxidase in the PFC, and increased xanthine-oxidase and acetylcholinesterase in both regions, indicating an amplified stress response and cholinergic dysfunction. Conversely, DOXY + LPS interaction lowered hippocampal-targeted BDNF and HIF-α levels. These findings validate the role of cellular senescence in enhancing LPS-induced neuroinflammation, mimicking complex AD features, and provide a model for testing disease mechanisms and therapeutics.

Indexed as

AgingCellular SenescenceLipopolysaccharidesMemory DisordersNeuroinflammatory DiseasesAlzheimer DiseaseAnimalsDoxycyclineHippocampusMaleMiceOxidative StressDoxycyclineLipopolysaccharidesAlzheimer's diseaseCellular senescenceCognitive impairmentDoxycyclineLipopolysaccharideNeuroinflammationOxidative stress

Identifiers

PMID41910845

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.