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Updated: May 26, 2026

Methods for the Modulation and Analysis of NF-κB-dependent Adult Neurogenesis
Published on: February 13, 2014
n-3 fatty acids prevent impairment of neurogenesis and synaptic plasticity in B-cell activating factor (BAFF)
Rosalia Crupi1, Marco Cambiaghi, Richard Deckelbaum
1Department of Physiology and Pharmacology, CUNY Medical School, New York, NY, USA.
Objective:
Autoimmune-prone B-cell activating factor transgenic mice, a mouse model of systemic lupus erythematosus and Sjögren's syndrome exhibit neuroinflammation, anxiety-like phenotype, deficit in adult hippocampal neurogenesis and impaired neurogenesis-dependent and neurogenesis-independent dentate gyrus long-term potentiation. Given that n-3 polyunsaturated fatty acids regulate hippocampal plasticity and inflammatory responses, we investigated whether n-3 polyunsaturated fatty acids-enriched diet might prevent age-dependent hippocampal changes in B-cell activating factor transgenic mice.
Methods:
B-cell activating factor transgenic mice were fed for 12 weeks with either n-3 polyunsaturated fatty acids-enriched or control diet and we tested the effect of this dietary supplementation on hippocampal inflammation, progenitor cell proliferation and neurogenesis-dependent and neurogenesis-independent long-term potentiation.
Results:
Dietary supplementation with n-3 polyunsaturated fatty acids significantly decreased hippocampal microglial activation and increased the density of bromodeoxyuridine and doublecortin-positive newly-formed cells in the subventricular zone of hippocampus. Furthermore, B-cell activating factor transgenic mice fed with n-3 polyunsaturated fatty acids-enriched diet displayed normal long-term potentiation at the medial perforant pathway/dentate gyrus connections.
Conclusions:
The results indicate that n-3 fatty acids prevent neuroinflammation and deficits of hippocampal plasticity in B-cell activating factor transgenic mice and suggest that increased n-3 fatty acids intake might represent a potential therapeutic option to prevent neuropsychiatric symptoms associated with autoimmune diseases.
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