ArticleScientific reports2019
Chronic synaptic insulin resistance after traumatic brain injury abolishes insulin protection from amyloid beta and tau oligomer-induced synaptic dysfunction.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 34 citations in OpenAlex.
- Safety, Efficacy, and Feasibility of Intranasal Insulin for the Treatment of Mild Cognitive Impairment and Alzheimer Disease Dementia: A Randomized Clinical Trial.JAMA neurology · 2020 · on this mapTrial
- Mild and repetitive mild traumatic brain injury: Changes in microglial cells and synapses.Neural regeneration research · 2026Article
- Hippocampal Neural Stem Cell Exosomes Promote Brain Resilience against the Impact of Tau Oligomers.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Amyloid-β oligomers increase the binding and internalization of tau oligomers in human synapses.Acta neuropathologica · 2024Article
- New insights into metabolism dysregulation after TBI.Journal of neuroinflammation · 2024Review
- Influence of metabolic stress and metformin on synaptic protein profile in SH-SY5Y-derived neurons.Physiological reports · 2023Article
- Mechanism and recent updates on insulin-related disorders.World journal of clinical cases · 2023Review
- Cellular and Molecular Pathophysiology of Traumatic Brain Injury: What Have We Learned So Far?Biology · 2023Review
- Liver acts as a metabolic gate for the traumatic brain injury pathology: Protective action of thyroid hormone.Biochimica et biophysica acta. Molecular basis of disease · 2023Article
- Increased Risk of Aging-Related Neurodegenerative Disease after Traumatic Brain Injury.Biomedicines · 2023Review
- Phospholipase D1 Attenuation Therapeutics Promotes Resilience against Synaptotoxicity in 12-Month-Old 3xTg-AD Mouse Model of Progressive Neurodegeneration.International journal of molecular sciences · 2023Article
- Hot Spots for the Use of Intranasal Insulin: Cerebral Ischemia, Brain Injury, Diabetes Mellitus, Endocrine Disorders and Postoperative Delirium.International journal of molecular sciences · 2023Review
- Role of Biliverdin Reductase A in the Regulation of Insulin Signaling in Metabolic and Neurodegenerative Diseases: An Update.International journal of molecular sciences · 2022Review
- Aβ/tau oligomer interplay at human synapses supports shifting therapeutic targets for Alzheimer's disease.Cellular and molecular life sciences : CMLS · 2022Article
- Impaired insulin signalling and allostatic load in Alzheimer disease.Nature reviews. Neuroscience · 2022Review
- Insulin resistance is associated with an unfavorable outcome among non-diabetic patients with isolated moderate-to-severe traumatic brain injury - A propensity score-matched study.Frontiers in neurology · 2022Article
- Concussion/Mild Traumatic Brain Injury (TBI) Induces Brain Insulin Resistance: A Positron Emission Tomography (PET) Scanning Study.International journal of molecular sciences · 2021Article
- Targeting Insulin Resistance to Treat Cognitive Dysfunction.Molecular neurobiology · 2021Review
- Chronic Low Dose Neutron Exposure Results in Altered Neurotransmission Properties of the Hippocampus-Prefrontal Cortex Axis in Both Mice and Rats.International journal of molecular sciences · 2021Article
- PART 3 Bypassing TBI: Metabolic Surgery and the Link Between Obesity and Traumatic Brain Injury-a Review.Obesity surgery · 2021Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is a risk factor for Alzheimer's disease (AD), although the mechanisms contributing to this increased risk are unknown. Insulin resistance is an additional risk factor for AD whereby decreased insulin signaling increases synaptic sensitivity to amyloid beta (Aβ) and tau. Considering this, we used rats that underwent a lateral fluid percussion injury at acute and chronic time-points to investigate whether decreased insulin responsiveness in TBI animals is playing a role in synaptic vulnerability to AD pathology. We detected acute and chronic decreases in insulin responsiveness in isolated hippocampal synaptosomes after TBI. In addition to assessing both Aβ and tau binding on synaptosomes, we performed electrophysiology to assess the dysfunctional impact of Aβ and tau oligomers as well as the protective effect of insulin. While we saw no difference in binding or degree of LTP inhibition by either Aβ or tau oligomers between sham and TBI animals, we found that insulin treatment was able to block oligomer-induced LTP inhibition in sham but not in TBI animals. Since insulin treatment has been discussed as a therapy for AD, this gives valuable insight into therapeutic implications of treating AD patients based on one's history of associated risk factors.
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