ArticleJournal of neuroinflammation2024
Prolactin deficiency drives diabetes-associated cognitive dysfunction by inducing microglia-mediated synaptic loss.
Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Microglia-specific NLRP3 inhibition mitigates hippocampal neuroinflammation and cognitive deficits after hemorrhagic shock with resuscitation.Behavioral and brain functions : BBF · 2026Article
- Reconstituting central nervous system niche cues partially restores homeostatic-like features in cultured murine primary microglia.Scientific reports · 2026Article
- How organs react under fasting or glucose-insulin status: a self-controlled study usingEuropean journal of nuclear medicine and molecular imaging · 2026Article
- The relationships between diabetic male infertility, diabetic cognitive impairment, and the neuroendocrine-immune network: A review.Medicine · 2026Review
- Altered tear fluid protein expression in persons with mild cognitive impairment.Journal of Alzheimer's disease : JAD · 2026Article
- The novel IDO-1 inhibitor 3-047 combined with icaritin ameliorates neuroinflammation and diabetes-associated cognitive dysfunction with suppression of TLR4/MyD88/NF-κB signaling.Frontiers in immunology · 2026Article
- Border-associated macrophages: an emerging perspective from physiological basis and multi-disease roles to the mechanism of vascular cognitive impairment and dementia.Journal of neuroinflammation · 2025Review
- Microbiota-host crosstalk: the role of short-term dietary restriction in neurological and metabolic dysregulation.NPJ biofilms and microbiomes · 2025Article
- Tanshinone IIA suppresses the proliferation and fibrosis of mesangial cell in diabetic nephropathy though WTAP-mediated mScientific reports · 2025Article
- Underexplored Connections Between Diabetes, Hypomanic States and Insecure Attachment.Psychology research and behavior management · 2025Review
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8 authors.
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Abstract
backgroundDiabetes-associated cognitive dysfunction, characterized by hippocampal synaptic loss as an early pathological feature, seriously threatens patients' quality of life. Synapses are dynamic structures, and hormones play important roles in modulating the formation and elimination of synapses. The pituitary, the master gland of the body, releases several hormones with multiple roles in hippocampal synaptic regulation. In this study, we aimed to explore the relationship between pituitary hormones and cognitive decline in diabetes.
methodsA total of 744 patients with type 2 diabetes (T2DM) (445 men and 299 postmenopausal women) who underwent serum pituitary hormone level assessments, comprehensive cognitive evaluations and MRI scans were enrolled. Dynamic diet interventions were applied in both chow diet-fed mice and high-fat diet (HFD)-fed diabetic mice. The cognitive performance and hippocampal pathology of prolactin (PRL)-knockout mice, neuronal prolactin receptor (PRLR)-specific knockout mice and microglial PRLR-specific knockout mice were assessed. Microglial PRLR-specific knockout mice were fed an HFD to model diabetes. Diabetic mice received an intracerebroventricular infusion of recombinant PRL protein or vehicle.
resultsThis clinical study revealed that decreased PRL levels were associated with cognitive impairment and hippocampal damage in T2DM patients. In diabetic mice, PRL levels diminished before hippocampal synaptic loss and cognitive decline occurred. PRL loss could directly cause cognitive dysfunction and decreased hippocampal synaptic density. Knockout of PRLR in microglia, rather than neurons, induced hippocampal synaptic loss and cognitive impairment. Furthermore, blockade of PRL/PRLR signaling in microglia exacerbated abnormal microglial phagocytosis of synapses, further aggravating hippocampal synaptic loss and cognitive impairment in diabetic mice. Moreover, PRL infusion reduced microglia-mediated synaptic loss, thereby alleviating cognitive impairment in diabetic mice.
conclusionPRL is associated with cognitive dysfunction and hippocampal damage in T2DM patients. In diabetes, a decrease in PRL level drives hippocampal synaptic loss and cognitive impairment by increasing microglia-mediated synapse engulfment. Restoration of PRL levels ameliorates cognitive dysfunction and hippocampal synaptic loss in diabetic mice.
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