ArticleNeurochemical research2012
Amyloid-β protein modulates insulin signaling in presynaptic terminals.
Article in Neurochemical research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 44 citations in OpenAlex.
- Insulin and IGF signaling in the brain: multilevel regulation of synaptic and network homeostasis.Frontiers in endocrinology · 2026Review
- The protective role of carnosine against type 2 diabetes-induced cognitive impairment.Food science & nutrition · 2024Review
- Association between pre-diabetes or diabetes and cognitive impairment in a community-dwelling older population: Bushehr Elderly Health (BEH) program.Journal of diabetes and metabolic disorders · 2024Article
- Article
- Design, Synthesis, and Preliminary Evaluation of [Bioconjugate chemistry · 2022Article
- Aβ-Induced Alterations in Membrane Lipids Occur before Synaptic Loss Appears.International journal of molecular sciences · 2022Article
- Review of Advanced Drug Trials Focusing on the Reduction of Brain Beta-Amyloid to Prevent and Treat Dementia.Journal of experimental pharmacology · 2022Review
- From Metabolic Syndrome to Neurological Diseases: Role of Autophagy.Frontiers in cell and developmental biology · 2021Review
- The seed ofPharmaceutical biology · 2020Article
- Insulin resistance and impaired lipid metabolism as a potential link between diabetes and Alzheimer's disease.Drug development research · 2020Review
- Icariin Attenuates Amyloid-β (Aβ)-Induced Neuronal Insulin Resistance Through PTEN Downregulation.Frontiers in pharmacology · 2020Article
- Intra- and extracellular β-amyloid overexpression via adeno-associated virus-mediated gene transfer impairs memory and synaptic plasticity in the hippocampus.Scientific reports · 2019Article
- Aβ inhibits SREBP-2 activation through Akt inhibition.Journal of lipid research · 2018Article
- Article
- Streptozotocin Intracerebroventricular-Induced Neurotoxicity and Brain Insulin Resistance: a Therapeutic Intervention for Treatment of Sporadic Alzheimer's Disease (sAD)-Like Pathology.Molecular neurobiology · 2016Review
- Diabetes and Cognitive Impairment.Current diabetes reports · 2016Review
- The rise and fall of insulin signaling in Alzheimer's disease.Metabolic brain disease · 2016Review
- The Essential Role of Soluble Aβ Oligomers in Alzheimer's Disease.Molecular neurobiology · 2016Review
- The neuroprotective effects of the anti-diabetic drug linagliptin against Aβ-induced neurotoxicity.Neural regeneration research · 2016Article
- Aggregation propensity of neuronal receptors: potential implications in neurodegenerative disorders.Future science OA · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptic loss is a major neuropathological correlate of memory decline as a result of Alzheimer's disease (AD). This phenomenon appears to be aggravated by soluble amyloid-β (Aβ) oligomers causing presynaptic terminals to be particularly vulnerable to damage. Furthermore, insulin is known to participate in synaptic plasticity through the activation of the insulin receptor (IR) and the PI3K signaling pathway, while low concentrations of soluble Aβ and Aβ oligomers aberrantly modulate IR function in cultured neurons. To further examine how Aβ and insulin interact in the pathology of AD, the present work analyzes the effect of insulin and Aβ in the activation of the IR/PI3K pathway in synaptosomes. We found that insulin increased mitochondrial activity and IR/Akt phosphorylation in synaptosomes taken from both hippocampus and cortex. Also, pretreatment with Aβ antagonized insulin's effect on hippocampal synaptosomes, but not vice versa. These results show that Aβ can reduce responsiveness to insulin. Combined with evidence that insulin desensitization can increase the risk of developing AD, our results suggest that the initial mechanism that impairs synaptic maintenance in AD might start with Aβ changes in insulin sensitivity.
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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.