ArticleMolecular neurobiology2016
Hydrogen Sulfide Ameliorates Homocysteine-Induced Alzheimer's Disease-Like Pathology, Blood-Brain Barrier Disruption, and Synaptic Disorder.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 3 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
70 citing papers in PubMed, 3 syntheses or guidelines pooled it, 166 citations in OpenAlex.
- Pooled it
- Recent Advances in Molecular Research on Hydrogen Sulfide (HInternational journal of molecular sciences · 2022Pooled it
- Plasma homocysteine concentrations and risk of intracerebral hemorrhage: a systematic review and meta-analysis.Scientific reports · 2018Pooled it
- Neuroprotective mechanism of hydrogen sulfide in okadaic acid-induced alzheimer-like pathology.GeroScience · 2026Article
- Hydrogen Sulfide: A Multitarget Therapeutic for Neuroinflammation in Neurodegenerative Diseases.Research (Washington, D.C.) · 2026Review
- Changes in plasma hydrogen sulfide are associated with cognitive improvements in schizophrenia patients treated with atypical antipsychotics.Frontiers in psychiatry · 2026Article
- Role and Relationship Between Homocysteine and HMolecular neurobiology · 2025Review
- S-Propargyl-Cysteine Attenuates Stroke Heterogeneity via Promoting Protective Autophagy Across Multiple Neural Cell Types: Insights From Single-Cell Sequencing.CNS neuroscience & therapeutics · 2025Article
- Lower water-soluble vitamins and higher homocysteine are associated with neurodegenerative diseases.Scientific reports · 2025Article
- The involvement of the synaptic vesicle cycle in homocysteine induced neurotoxicity in vitro and in vivo.Scientific reports · 2025Article
- The Role of Purinergic Mechanisms in the Excitability of Trigeminal Afferents of Rats with Prenatal Hyperhomocysteinemia.Biomolecules · 2025Article
- Hydrogen Sulfide Alleviates Schizophrenia-Like Behavior Through Regulating Apoptosis by S-Sulfhydrylation Modification.CNS neuroscience & therapeutics · 2025Article
- Endothelial Dysfunctions in Blood-Brain Barrier Breakdown in Alzheimer's Disease: From Mechanisms to Potential Therapies.CNS neuroscience & therapeutics · 2024Review
- Cystine rather than cysteine is the preferred substrate for β-elimination by cystathionine γ-lyase: implications for dietary methionine restriction.GeroScience · 2024Article
- Novel energy optimizer, meldonium, rapidly restores acute hypobaric hypoxia-induced brain injury by targeting phosphoglycerate kinase 1.Cell communication and signaling : CCS · 2024Article
- Nanomotor-based HBioactive materials · 2024Article
- [High homocysteine level promotes autophagy and apoptosis of mouse hippocampal HT22 cells through the Notch1/Hes1 signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Parkinson's Disease Risk and Hyperhomocysteinemia: The Possible Link.Cellular and molecular neurobiology · 2023Review
- The Role of Hydrogen Sulfide in Regulation of Cell Death following Neurotrauma and Related Neurodegenerative and Psychiatric Diseases.International journal of molecular sciences · 2023Review
- Protective Roles of Hydrogen Sulfide in Alzheimer's Disease and Traumatic Brain Injury.Antioxidants (Basel, Switzerland) · 2023Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Elevated plasma total homocysteine (Hcy) level is associated with an increased risk of Alzheimer's disease (AD). During transsulfuration pathways, Hcy is metabolized into hydrogen sulfide (H2S), which is a synaptic modulator, as well as a neuro-protective agent. However, the role of hydrogen sulfide, as well as N-methyl-D-aspartate receptor (NMDAR) activation, in hyperhomocysteinemia (HHcy) induced blood-brain barrier (BBB) disruption and synaptic dysfunction, leading to AD pathology is not clear. Therefore, we hypothesized that the inhibition of neuronal NMDA-R by H2S and MK801 mitigate the Hcy-induced BBB disruption and synapse dysfunction, in part by decreasing neuronal matrix degradation. Hcy intracerebral (IC) treatment significantly impaired cerebral blood flow (CBF), and cerebral circulation and memory function. Hcy treatment also decreases the expression of cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE) in the brain along with increased expression of NMDA-R (NR1) and synaptosomal Ca(2+) indicating excitotoxicity. Additionally, we found that Hcy treatment increased protein and mRNA expression of intracellular adhesion molecule 1 (ICAM-1), matrix metalloproteinase (MMP)-2, and MMP-9 and also increased MMP-2 and MMP-9 activity in the brain. The increased expression of ICAM-1, glial fibrillary acidic protein (GFAP), and the decreased expression of vascular endothelial (VE)-cadherin and claudin-5 indicates BBB disruption and vascular inflammation. Moreover, we also found decreased expression of microtubule-associated protein 2 (MAP-2), postsynaptic density protein 95 (PSD-95), synapse-associated protein 97 (SAP-97), synaptosomal-associated protein 25 (SNAP-25), synaptophysin, and brain-derived neurotrophic factor (BDNF) showing synapse dysfunction in the hippocampus. Furthermore, NaHS and MK801 treatment ameliorates BBB disruption, CBF, and synapse functions in the mice brain. These results demonstrate a neuro-protective effect of H2S over Hcy-induced cerebrovascular pathology through the NMDA receptor. Our present study clearly signifies the therapeutic ramifications of H2S for cerebrovascular diseases such as Alzheimer's disease. Graphical Abstract ᅟ.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.