ArticleNeurobiology of disease2007
Changes in inflammatory processes associated with selective vulnerability following mild impairment of oxidative metabolism.
Article in Neurobiology of disease, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 58 citations in OpenAlex.
- Exploring the Therapeutic Potential of Benfotiamine in a Sporadic Alzheimer's-Like Disease Rat Model: Insights into Insulin Signaling and Cognitive function.ACS chemical neuroscience · 2024Article
- Stem Cell Therapy and Thiamine Deficiency-Induced Brain Damage.Neurochemical research · 2024Review
- The importance of thiamine (vitamin B1) in humans.Bioscience reports · 2023Article
- Total flavonoids extracted fromFrontiers in pharmacology · 2023Article
- The significance of glycolysis index and its correlations with immune infiltrates in Alzheimer's disease.Frontiers in immunology · 2022Article
- Midline Thalamic Damage Associated with Alcohol-Use Disorders: Disruption of Distinct Thalamocortical Pathways and Function.Neuropsychology review · 2021Review
- Neuroprotective Effects of Thiamine and Precursors with Higher Bioavailability: Focus on Benfotiamine and Dibenzoylthiamine.International journal of molecular sciences · 2021Review
- Preliminary Evidence for a Relationship between Elevated Plasma TNFα and Smaller Subcortical White Matter Volume in HCV Infection Irrespective of HIV or AUD Comorbidity.International journal of molecular sciences · 2021Article
- Region-selective permeability of the blood-brain barrier to α-aminoisobutyric acid during thiamine deficiency and following its reversal.Metabolic brain disease · 2021Article
- Supplemental thiamine as a practical, potential way to prevent Alzheimer's disease from commencing.Alzheimer's & dementia (New York, N. Y.) · 2021Article
- Dynamics of Internalization and Intracellular Interaction of Tau Antibodies and Human Pathological Tau Protein in a Human Neuron-Like Model.Frontiers in neurology · 2020Article
- A Pivotal Role for Thiamine Deficiency in the Expression of Neuroinflammation Markers in Models of Alcohol-Related Brain Damage.Alcoholism, clinical and experimental research · 2019Article
- Enterohemorrhagic Escherichia coli infection inhibits colonic thiamin pyrophosphate uptake via transcriptional mechanism.PloS one · 2019Article
- Molecular mechanisms involved in the adaptive regulation of the colonic thiamin pyrophosphate uptake process.American journal of physiology. Cell physiology · 2017Article
- Affinity of Tau antibodies for solubilized pathological Tau species but not their immunogen or insoluble Tau aggregates predicts in vivo and ex vivo efficacy.Molecular neurodegeneration · 2016Article
- PKR downregulation prevents neurodegeneration and β-amyloid production in a thiamine-deficient model.Cell death & disease · 2015Article
- Associations between in vivo neuroimaging and postmortem brain cytokine markers in a rodent model of Wernicke's encephalopathy.Experimental neurology · 2014Article
- miR-21 improves the neurological outcome after traumatic brain injury in rats.Scientific reports · 2014Article
- A rat model for chronic spinal nerve root compression.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2014Article
- Autophagy alleviates neurodegeneration caused by mild impairment of oxidative metabolism.Journal of neurochemistry · 2013Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Abnormalities in oxidative metabolism and reductions of thiamine-dependent enzymes accompany many age-related neurodegenerative diseases. Thiamine deficiency (TD) produces a cascade of events including mild impairment of oxidative metabolism, activation of microglia, astrocytes and endothelial cells that leads to neuronal loss in select brain regions. The earliest changes occur in a small, well-defined brain region, the submedial thalamic nucleus (SmTN). In the present study, a micropunch technique was used to evaluate quantitatively the selective regional changes in mRNA and protein levels. To test whether this method can distinguish between changes in vulnerable and non-vulnerable regions, markers for neuronal loss (NeuN) and endothelial cells (eNOS) and inflammation (IL-1beta, IL-6 and TNF-alpha) in SmTN and cortex of control and TD mice were assessed. TD significantly reduced NeuN and increased CD11b, GFAP and ICAM-1 immunoreactivity in SmTN as revealed by immunocytochemistry. When assessed on samples obtained by the micropunch method, NeuN protein declined (-49%), while increased mRNA levels were observed for eNOS (3.7-fold), IL-1beta (43-fold), IL-6 (44-fold) and TNF-alpha (64-fold) in SmTN with TD. The only TD-induced change that occurred in cortex with TD was an increase in TNF-alpha (22-fold) mRNA levels. Immunocytochemical analysis revealed that IL-1beta, IL-6 and TNF-alpha protein levels increased in TD brains and colocalized with glial markers. The consistency of these quantitative results with immunocytochemical measurements validates the micropunch technique. The results demonstrate that TD induces quantitative, distinct inflammatory responses and oxidative stress in vulnerable and non-vulnerable regions that may underlie selective vulnerability.
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