---
title: "Nitric Oxide Dysregulation Links Metabolic Dysfunction to Cognitive Decline in Type 2 Diabetes"
id: "pubmed-42746741"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42746741"
content_type: "clinical_feed_article"
specialty: "Pharmacology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42746741/"
doi: "10.1042/BST20250325"
published_at: "2026-09-23T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Nitric Oxide Dysregulation Links Metabolic Dysfunction to Cognitive Decline in Type 2 Diabetes
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42746741
- **Specialty:** [Pharmacology](https://medichelpline.com/clinical-feed/pharmacology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42746741/)
- **DOI:** [10.1042/BST20250325](https://doi.org/10.1042%2FBST20250325)
- **Published At:** 2026-09-23T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Type 2 diabetes mellitus (**T2DM**) is increasingly recognised as a driver of cerebrovascular dysfunction and progressive cognitive decline. - The review positions **nitric oxide (•NO)** as a central, pleiotropic messenger that integrates vascular, neuronal, and metabolic functions within the **neurovascular unit (NVU)**. - Under normal physiology, **•NO** couples neuronal activity to blood supply via neurovascular coupling (NVC), modulates endothelial tone through sGC–cGMP–PKG signalling, and supports astrocyte–neuron metabolic interactions and mitochondrial ATP production. - In T2DM, chronic hyperglycaemia and insulin resistance diminish **•NO bioavailability** through multiple mechanisms: increased mitochondrial and NADPH oxidase-derived superoxide, oxidation of the eNOS cofactor BH4 leading to eNOS uncoupling, and impaired PI3K–Akt-mediated eNOS activation. - Reduced **•NO** and increased nitro-oxidative stress shift the cerebrovascular environment toward oxidant-mediated damage, causing endothelial dysfunction and maladaptive vascular remodelling. - The downstream impact includes impaired cerebral blood flow regulation, disrupted **neurovascular coupling**, reduced regional perfusion (notably in metabolically vulnerable regions such as the hippocampus), and a sustained mismatch between energy supply and neuronal demand. - This sustained bioenergetic deficit is linked mechanistically to progressive cognitive impairment in people with **T2DM**. - The review integrates mechanistic evidence but does not report clinical trial outcomes or specific therapeutic protocols in the abstract; details beyond mechanistic links were not reported in the source abstract.
## Clinical Analysis & Structured Key Points
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Affiliations Expand ### Affiliations * 1 Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal. * 2 Faculty of Pharmacy, University of Coimbra, Coimbra, Portugal. * 3 Centre for Innovative Biomedicine and Biotechnology, Coimbra, Portugal. * PMID: **42746741** * PMCID: [ PMC13591264 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC13591264/) * DOI: [ 10.1042/BST20250325 ](https://doi.org/10.1042/bst20250325) Item in Clipboard Review # Nitric oxide as a mechanistic link between metabolic dysfunction and cognitive decline in type 2 diabetes Ana L Marçal et al. Biochem Soc Trans. 2026. Show details Display options Display options Format Abstract PubMed PMID Biochem Soc Trans Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Biochem+Soc+Trans%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Biochem+Soc+Trans%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42746741/) . 2026 Sep 23;54(9):1239-1250. doi: 10.1042/BST20250325. ### Authors [Ana L Marçal](https://pubmed.ncbi.nlm.nih.gov/?term=Mar%C3%A7al+AL&cauthor_id=42746741)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42746741/#short-view-affiliation-1 "Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42746741/#short-view-affiliation-2 "Faculty of Pharmacy, University of Coimbra, Coimbra, Portugal.")[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42746741/#short-view-affiliation-3 "Centre for Innovative Biomedicine and Biotechnology, Coimbra, Portugal."), [João Laranjinha](https://pubmed.ncbi.nlm.nih.gov/?term=Laranjinha+J&cauthor_id=42746741)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42746741/#short-view-affiliation-1 "Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42746741/#short-view-affiliation-2 "Faculty of Pharmacy, University of Coimbra, Coimbra, Portugal.")[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42746741/#short-view-affiliation-3 "Centre for Innovative Biomedicine and Biotechnology, Coimbra, Portugal."), [Cátia F Lourenço](https://pubmed.ncbi.nlm.nih.gov/?term=Louren%C3%A7o+CF&cauthor_id=42746741)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42746741/#short-view-affiliation-1 "Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42746741/#short-view-affiliation-2 "Faculty of Pharmacy, University of Coimbra, Coimbra, Portugal.")[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42746741/#short-view-affiliation-3 "Centre for Innovative Biomedicine and Biotechnology, Coimbra, Portugal.") ### Affiliations * 1 Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal. * 2 Faculty of Pharmacy, University of Coimbra, Coimbra, Portugal. * 3 Centre for Innovative Biomedicine and Biotechnology, Coimbra, Portugal. * PMID: **42746741** * PMCID: [ PMC13591264 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC13591264/) * DOI: [ 10.1042/BST20250325 ](https://doi.org/10.1042/bst20250325) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID ## Abstract Type 2 diabetes mellitus (T2DM) is increasingly recognised as a driver of cerebrovascular dysfunction and cognitive decline, yet the molecular mechanisms underlying this association remain incompletely understood. Here, we review and support a key mechanistic role for nitric oxide (•NO), a pleiotropic diffusible messenger that integrates vascular, neuronal, and metabolic functions within the neurovascular unit (NVU). Under physiological conditions, •NO integrates vascular and metabolic responses by coupling blood supply to neuronal activity and fine-tuning cellular energy metabolism. In T2DM, chronic hyperglycemia and insulin resistance converge to reduce •NO bioavailability through multiple mechanisms: mitochondrial and NADPH oxidase-derived superoxide production, endothelial nitric oxide synthases (eNOS) uncoupling via BH4 oxidation, and impaired PI3K-Akt-dependent eNOS activation. The resulting redox imbalance shifts the cerebrovascular environment towards oxidant-mediated damage, compromising the functional and structural integrity of the NVU. This translates into impaired cerebral blood flow regulation and maladaptive remodelling of the cerebrovascular network, ultimately disrupting neurovascular coupling (NVC) and reducing regional cerebral perfusion. Together, impaired perfusion and disrupted NVC result in a sustained mismatch between energy supply and neuronal demand, particularly in metabolically vulnerable regions such as the hippocampus, ultimately leading to progressive cognitive impairment. In sum, the present review integrates current mechanistic evidence positioning •NO dysregulation as a central driver of neurovascular and metabolic dysfunction in T2DM, linking impaired cerebral perfusion, disrupted NVC, and structural vascular remodelling to cognitive decline. **Keywords:** Cerebrovascular dysfunction; Neurovascular coupling; Nitric oxide; Type 2 diabetes mellitus. © 2026 The Author(s). [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement The authors declare that there are no competing interests associated with the manuscript. ## Figures [ ![Figure 1](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d66/13591264/681bba0fd4aa/bst-54-bst20250325-g1.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d66/13591264/0957a77cd838/bst-54-bst20250325-g1.webp) ** Figure 1. Nitric oxide-mediated neurovascular coupling and… ** ** Figure 1. Nitric oxide-mediated neurovascular coupling and astrocyte–neuron metabolic support in the healthy NVC ** Neuronal… **Figure 1. Nitric oxide-mediated neurovascular coupling and astrocyte–neuron metabolic support in the healthy NVC** Neuronal activity induces Ca2+-dependent nNOS activation and •NO production, which diffuses to nearby vessels to promote vasodilation via the sGC-cGMP-PKG pathway. Endothelial •NO, generated through shear stress and PI3K-Akt signalling, further contributes to vascular tone regulation. In parallel, •NO modulates astrocytic glycolysis and lactate shuttling to neurons, supporting mitochondrial ATP production and matching energy supply to neuronal demand. [ ![Figure 2](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d66/13591264/da5ab362cae5/bst-54-bst20250325-g2.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d66/13591264/5e7c34c2d2cb/bst-54-bst20250325-g2.webp) ** Figure 2. Shift of • NO-dependent neurovascular… ** ** Figure 2. Shift of • NO-dependent neurovascular function in T2DM ** In the healthy neurovascular unit ( **…** **Figure 2. Shift of •NO-dependent neurovascular function in T2DM ** In the healthy neurovascular unit (**A**), •NO supports endothelial function, astrocytic metabolism, and neuronal signalling, maintaining NVC and adequate cerebral blood flow. In T2DM (**B**), reduced •NO bioavailability and increased nitro-oxidative stress disrupt these processes, leading to endothelial dysfunction, impaired astrocyte-neuron metabolic coupling, mitochondrial dysfunction, and ultimately neurovascular uncoupling and bioenergetic deficit. [See this image and copyright information in PMC](https://pubmed.ncbi.nlm.nih.gov/42746741/) ## Similar articles * [ Impairment of neurovascular coupling in the hippocampus due to decreased nitric oxide bioavailability supports early cognitive dysfunction in type 2 diabetic rats. ](https://pubmed.ncbi.nlm.nih.gov/36372286/) Gonçalves JS, Seiça RM, Laranjinha J, Lourenço CF.Gonçalves JS, et al.Free Radic Biol Med. 2022 Nov 20;193(Pt 2):669-675. doi: 10.1016/j.freeradbiomed.2022.11.009. Epub 2022 Nov 11.Free Radic Biol Med. 2022.PMID: 36372286Review. * [ mTOR Attenuation with Rapamycin Reverses Neurovascular Uncoupling and Memory Deficits in Mice Modeling Alzheimer's Disease. ](https://pubmed.ncbi.nlm.nih.gov/33888602/) Van Skike CE, Hussong SA, Hernandez SF, Banh AQ, DeRosa N, Galvan V.Van Skike CE, et al.J Neurosci. 2021 May 12;41(19):4305-4320. doi: 10.1523/JNEUROSCI.2144-20.2021. Epub 2021 Apr 22.J Neurosci. 2021.PMID: 33888602Free PMC article. * [ The Unexpected Role of the Endothelial Nitric Oxide Synthase at the Neurovascular Unit: Beyond the Regulation of Cerebral Blood Flow. ](https://pubmed.ncbi.nlm.nih.gov/39201757/) Scarpellino G, Brunetti V, Berra-Romani R, De Sarro G, Guerra G, Soda T, Moccia F.Scarpellino G, et al.Int J Mol Sci. 2024 Aug 21;25(16):9071. doi: 10.3390/ijms25169071.Int J Mol Sci. 2024.PMID: 39201757Free PMC article.Review. * [ Treatment with the poly(ADP-ribose) polymerase inhibitor PJ-34 improves cerebromicrovascular endothelial function, neurovascular coupling responses and cognitive performance in aged mice, supporting the NAD+ depletion hypothesis of neurovascular aging. ](https://pubmed.ncbi.nlm.nih.gov/31679124/) Tarantini S, Yabluchanskiy A, Csipo T, Fulop G, Kiss T, Balasubramanian P, DelFavero J, Ahire C, Ungvari A, Nyúl-Tóth Á, Farkas E, Benyo Z, Tóth A, Csiszar A, Ungvari Z.Tarantini S, et al.Geroscience. 2019 Oct;41(5):533-542. doi: 10.1007/s11357-019-00101-2. Epub 2019 Nov 2.Geroscience. 2019.PMID: 31679124Free PMC article. * [ Benefits of Dietary Nitrate in Cognitive Decline Associated With Type 2 Diabetes: Pathways and Therapeutic Potential. ](https://pubmed.ncbi.nlm.nih.gov/42126395/) Gonçalves JS, Marçal A, Laranjinha J, Lourenço CF.Gonçalves JS, et al.Eur J Clin Invest. 2026 May;56(5):e70223. doi: 10.1111/eci.70223.Eur J Clin Invest. 2026.PMID: 42126395Review. [ See all similar articles ](https://pubmed.ncbi.nlm.nih.gov/?linkname=pubmed_pubmed&from_uid=42746741) ## References 1. 1. (International Diabetes Federation (2025) IDF Diabetes Atlas. 11th edition Brussels, Belgium: Available from: 2. 1. de Galan B.E. (2024) Diabetes and brain disorders, a new role for insulin? Neurosci. Biobehav. Rev. 163, 105775. 10.1016/j.neubiorev.2024.105775 - [DOI](https://doi.org/10.1016/j.neubiorev.2024.105775) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/38901787/) 3. 1. Heni M. (2024) The insulin resistant brain: impact on whole-body metabolism and body fat distribution. Diabetologia 67, 1181–1191 10.1007/s00125-024-06104-9 - [DOI](https://doi.org/10.1007/s00125-024-06104-9) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC11153284/) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/38363340/) 4. 1. Claassen J.A.H.R., Thijssen D.H.J., Panerai R.B. and Faraci F.M. (2021) Regulation of cerebral blood flowin humans: Physiology and clinical implications of autoregulation. Physiol. Rev. 101, 1487–1559 10.1152/physrev.00022.2020 - [DOI](https://doi.org/10.1152/physrev.00022.2020) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC8576366/) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/33769101/) 5. 1. Mokhber N., Shariatzadeh A., Avan A., Saber H., Babaei G.S., Chaimowitz [G.et](http://G.et) al. (2021) Cerebral blood flow changes during aging process and in cognitive disorders: A review. Neuroradiol. 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