ArticleAging cell2025
Age-Dependent Regulation of Hippocampal Inflammation by the Mitochondrial Translocator Protein in Mice.
Article in Aging cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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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.
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Who cites it
3 citing papers in PubMed.
- Article
- Age-dependent neuroprotection and inflammatory responses to mild therapeutic hypothermia following cardiac arrest.Resuscitation plus · 2026Article
- The translocator protein antagonist ONO-2952 attenuates neuroinflammation and neuronal apoptosis in an epilepsy rat model.Frontiers in neurology · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
The mitochondrial translocator protein (TSPO) is a biomarker of inflammation associated with neurodegenerative diseases, widely regarded to be upregulated in the aging brain. Here we investigated the interaction between aging and TSPO immunomodulatory function in the mouse hippocampus, a region severely affected in Alzheimer's Disease (AD). Surprisingly, we found that TSPO levels were decreased in brain innate immune populations in aging. Aging resulted in a reversal of TSPO knockout transcriptional signatures following inflammatory insult. TSPO deletion drastically exacerbated inflammatory transcriptional responses in the aging hippocampus, while dampening inflammation in the young hippocampus. This age-dependent effect of TSPO was linked to NF-kβ and interferon regulatory transcriptional networks. Drugs that disrupt the cell cycle and induce DNA damage, such as heat shock protein and topoisomerase inhibitors, were identified to mimic the inflammatory transcriptional signature characterizing aging in TSPO knockout mice most closely. These findings indicate that TSPO plays a protective role in brain aging. This TSPO-aging interaction is an important consideration in the interpretation of TSPO-targeted biomarker and therapeutic studies, as well as in vitro studies that cannot model the aging brain.
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Registered trials
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.