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Metformin attenuates white matter injury and cognitive impairment induced by chronic cerebral hypoperfusion.
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- Author(s): He Y;He Y;He Y; Li Z; Li Z; Shi X; Shi X; Ding J; Ding J; Ding J; Wang X; Wang X; Wang X
- Source:
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism [J Cereb Blood Flow Metab] 2023 Nov; Vol. 43 (2_suppl), pp. 78-94. Date of Electronic Publication: 2023 May 12.- Publication Type:
Journal Article; Research Support, Non-U.S. Gov't- Language:
English - Source:
- Additional Information
- Source: Publisher: SAGE Publications Country of Publication: United States NLM ID: 8112566 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1559-7016 (Electronic) Linking ISSN: 0271678X NLM ISO Abbreviation: J Cereb Blood Flow Metab Subsets: MEDLINE
- Publication Information: Publication: 2016- : Thousand Oaks, CA : SAGE Publications
Original Publication: New York : Raven Press, c1981- - Subject Terms: White Matter* ; Metformin*/pharmacology ; Metformin*/therapeutic use ; Metformin*/metabolism ; Diabetes Mellitus, Type 2*/complications ; Brain Ischemia*/metabolism ; Cognitive Dysfunction*/etiology ; Cognitive Dysfunction*/complications ; Dementia, Vascular*/metabolism ; Carotid Stenosis*/complications ; Carotid Stenosis*/drug therapy ; Carotid Stenosis*/metabolism; Mice ; Animals ; Disease Models, Animal ; Mice, Inbred C57BL
- Abstract: Vascular cognitive impairment and dementia (VCID) is a series of cognitive dysfunction associated with cerebrovascular diseases and currently lacks effective treatments. The white matter, which is essential for neuronal information processing and integration, is nourished by a network of capillaries and is vulnerable to chronic hypoperfusion. Here, we show that metformin, a widely used drug for the treatment of type 2 diabetes, alleviates the white matter damage and improves cognitive impairment in a mouse model of VCID established by bilateral carotid artery stenosis (BCAS)-induced chronic hypoperfusion. Mechanistically, metformin restores the dysfunctions of oligodendrocyte precursor cells (OPCs) under hypoxia. Metformin up-regulates prolyl hydroxylases 2 via activating the AMP-activated protein kinase pathway, leading to hypoxia-inducible factor-1α (HIF-1α) degradation in OPCs. These findings suggest that metformin may have a promising therapeutic role in alleviating cognitive abnormalities by ameliorating white matter damage of VCID.
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Neural Plast. 2021 Dec 3;2021:2412220. (PMID: 34899899) - Contributed Indexing: Keywords: BCAS; VCID; cerebral hypoperfusion; metformin; white matter injury
- Accession Number: 9100L32L2N (Metformin)
- Publication Date: Date Created: 20230513 Date Completed: 20231110 Latest Revision: 20240513
- Publication Date: 20240513
- Accession Number: PMC10638997
- Accession Number: 10.1177/0271678X231175189
- Accession Number: 37177813
- Source:
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