ArticleJournal of Alzheimer's disease : JAD2025
Loss of the mitochondrial protein mitoNEET in mice is associated with cognitive impairments and increased neuroinflammation.
Article in Journal of Alzheimer's disease : JAD, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Extracellular Vesicle-Derived microRNAs as Fluid Biomarkers in Neurodegenerative Diseases: A Systematic Review.Journal of neurochemistry · 2026Pooled it
- The iron-energy metabolism axis in Alzheimer's pathogenesis: from mechanisms to interventions.Cell death discovery · 2026Review
- CDGSH Iron Sulfur Domain 1 Relieves Neuronal Ferroptosis via Activating AMPK Pathway in Alzheimer's Disease.Molecular neurobiology · 2026Article
- Upregulation of mitoNEET disrupts granulosa cell proliferation, apoptosis and mitochondrial homeostasis : a possible pathogenesis of follicular dysplasia in PCOS.Journal of ovarian research · 2026Article
- Proximity labeling unveils potential roles of the Miro2-CISD1 network in mitochondrial dynamics and neuronal differentiation.Communications biology · 2026Article
- Mitochondrial CISD1 Modulates Microglial Metabolic Reprogramming to Drive Stress Susceptibility in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The metabolic engine of cognition: microglia-neuron interactions in health, ageing and disease.Nature metabolism · 2025Review
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10 authors.
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Abstract
backgroundMitochondrial dysfunction is implicated in several neurodegenerative diseases associated with memory and cognitive deficits, including Alzheimer's disease. Changes in bioenergetic function results in reactive oxygen species, oxidative damage and consequently neuroinflammation, which contributes to neuronal cell loss.
objectiveIn this study, we evaluated the impact of the loss of the redox active [2Fe-2S] mitochondrial-associated protein mitoNEET (CISD1) on neuroinflammation and cognition using an age-appropriate preclinical model. While associations between neuroinflammation and poor cognitive impacts have been shown in recent work, little has been done to assess whether loss of mitoNEET is associated with changes in neuroinflammatory markers or negative cognitive-behavioral outcomes.
methodsUsing 9-11-month-old mitoNEET knockout (CISD1-/-) and wild-type mice, we conducted a battery of cognitive tests to assess the impact of mitoNEET loss on performance. We then histologically evaluated the effect of absence of mitoNEET on markers of neuroinflammation in the aged brain.
resultsWe found loss of mitoNEET in mice was associated with a significant reduction in willingness to explore within an open field and impaired short-term spatial working memory in the Y-maze. We also found a significant reduction in novel object recognition memory that was gene-dependent and accompanied by reduced c-fos expression in hippocampus and cortical regions.
conclusionsOur findings indicate that mitoNEET loss is significantly associated with impairments in cognitive-behavioral and neuroinflammatory outcomes; specifically, learning and memory, anxiety-like behaviors, neuroinflammation, and neural activation. This is the first study to demonstrate cognitive-associated behavioral deficits with neuroinflammation in the mitoNEET knockout mouse model.
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