ArticleMolecular neurobiology2018
Evidence for Compromised Insulin Signaling and Neuronal Vulnerability in Experimental Model of Sporadic Alzheimer's Disease.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 47 citations in OpenAlex.
- The effect of canagliflozin on hippocampal dendrite morphology in a model of Alzheimer's disease induced by intracerebroventricular injection of streptozotocin.Brain structure & function · 2026Article
- Differential expression of PPAR isoforms in streptozotocin induced model of sporadic alzheimer's disease in zebrafish.Molecular biology reports · 2026Article
- Emerging role of HIC1 in prostate cancer progression and therapeutic response: A novel perspective.Journal of cell communication and signaling · 2025Article
- Blunted pressor response to peripheral sensory afferent nerve stimulation in intracerebroventricular-streptozotocin injected rats.Autonomic neuroscience : basic & clinical · 2025Article
- The Role of Astrocytes in Synaptic Dysfunction and Memory Deficits in Alzheimer's Disease.Biomolecules · 2025Review
- The mechanism underlying streptozotocin injection for the development of a nontransgenic Alzheimer's disease animal model.Open veterinary journal · 2025Review
- The role of neuron-like cell lines and primary neuron cell models in unraveling the complexity of neurodegenerative diseases: a comprehensive review.Molecular biology reports · 2024Review
- GSK3: A potential target and pending issues for treatment of Alzheimer's disease.CNS neuroscience & therapeutics · 2024Review
- Alzheimer's Disease: Cellular and Pharmacological Aspects.Geriatrics (Basel, Switzerland) · 2024Review
- Co-Culture Models: Key Players in In Vitro Neurotoxicity, Neurodegeneration and BBB Modeling Studies.Biomedicines · 2024Review
- Combined administration of catalpol, puerarin, gastrodin, and borneol modulates the Tlr4/Myd88/NF-κB signaling pathway and alleviates microglia inflammation in Alzheimer's disease.Frontiers in pharmacology · 2024Article
- Hypoglycemic medicines in the treatment of Alzheimer's disease: Pathophysiological links between AD and glucose metabolism.Frontiers in pharmacology · 2023Review
- Andrographolide Attenuates Short-Term Spatial and Recognition Memory Impairment and Neuroinflammation Induced by a Streptozotocin Rat Model of Alzheimer's Disease.Neurotoxicity research · 2022Article
- A Mutant Variant of E2F4 Triggers Multifactorial Therapeutic Effects in 5xFAD Mice.Molecular neurobiology · 2022Article
- Shared cerebral metabolic pathology in non-transgenic animal models of Alzheimer's and Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- Huperzine A ameliorates obesity-related cognitive performance impairments involving neuronal insulin signaling pathway in mice.Acta pharmacologica Sinica · 2020Article
- Mesenchymal Stem Cells Therapy Improved the Streptozotocin-Induced Behavioral and Hippocampal Impairment in Rats.Molecular neurobiology · 2020Article
- Immunotherapies in Huntington's disease and α-Synucleinopathies.Frontiers in immunology · 2020Review
- More Than Mortar: Glia as Architects of Nervous System Development and Disease.Frontiers in cell and developmental biology · 2020Review
- Lack of insulin resistance in response to streptozotocin treatment in neuronal SH-SY5Y cell line.Journal of neural transmission (Vienna, Austria : 1996) · 2020Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Evidence from animal studies categorizes sporadic Alzheimer's disease (sAD) as a metabolic syndrome with accompanying cognitive deficits. Given that glial cells act as "silent partners" to neurons by providing trophic support and defense, the present study investigated the role of glia in sAD pathology. A streptozotocin (STZ)-induced glial-neuronal co-culture model of sAD was used to study the metabolic status of the two cell types. Real time RT-PCR and Western blotting results indicated that amyloid precursor protein (APP) and β-secretase (BACE1) were highly expressed in co-cultured neurons than in monocultures. Increased amyloidogenesis was accompanied by decreased expression of mediators in insulin signaling pathway that included insulin receptor (IR), insulin receptor substrate 2 (IRS2), insulin-like growth factor 2 (IGF2), insulin-like growth factor 1 receptor (IGF1R), total-glycogen synthase kinase 3β (t-GSK3β), and phosphorylated-GSK3β
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