ArticleFrontiers in cellular neuroscience2015
Monomeric ß-amyloid interacts with type-1 insulin-like growth factor receptors to provide energy supply to neurons.
Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- The Amyloid-β Pathway in Alzheimer's Disease.Molecular psychiatry · 2021Pooled it
- Structural Assessment of Fibrillated Beta Amyloid to Reveal the Potential Epitopes for Alzheimer's Disease.Cell biochemistry and biophysics · 2026Article
- KLVFF Functionalized Graphene Oxide for AβSmall (Weinheim an der Bergstrasse, Germany) · 2025Article
- Acute targeting of N-terminal tau protein has long-lasting beneficial effects in Tg2576 APP/Aβ mouse model by reducing cognitive impairment, cerebral Aβ-amyloidosis, synaptic remodeling and microgliosis later in life.Acta neuropathologica communications · 2025Article
- Semax, a Copper Chelator Peptide, Decreases the Cu(II)-Catalyzed ROS Production and Cytotoxicity of aβ by Metal Ion Stripping and Redox Silencing.Bioinorganic chemistry and applications · 2025Article
- Why Is Iron Deficiency/Anemia Linked to Alzheimer's Disease and Its Comorbidities, and How Is It Prevented?Biomedicines · 2023Review
- Exploring the Role of Hsp60 in Alzheimer's Disease and Type 2 Diabetes: Suggestion for Common Drug Targeting.International journal of molecular sciences · 2023Review
- Amyloid β-based therapy for Alzheimer's disease: challenges, successes and future.Signal transduction and targeted therapy · 2023Review
- AβACS chemical neuroscience · 2023Article
- Biological Mechanism-based Neurology and Psychiatry: A BACE1/2 and Downstream Pathway Model.Current neuropharmacology · 2023Article
- Therapeutic effects of phlorotannins in the treatment of neurodegenerative disorders.Frontiers in molecular neuroscience · 2023Review
- The therapeutic potential of carnosine: Focus on cellular and molecular mechanisms.Current research in pharmacology and drug discovery · 2023Review
- Alzheimer's disease: an axonal injury disease?Frontiers in aging neuroscience · 2023Review
- Blood-brain barrier penetrating neprilysin degrades monomeric amyloid-beta in a mouse model of Alzheimer's disease.Alzheimer's research & therapy · 2022Article
- A Brain-Targeting Bispecific-Multivalent Antibody Clears Soluble Amyloid-Beta Aggregates in Alzheimer's Disease Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Physiological Roles of Monomeric Amyloid-β and Implications for Alzheimer's Disease Therapeutics.Experimental neurobiology · 2022Review
- The Pleiotropic Potential of BDNF beyond Neurons: Implication for a Healthy Mind in a Healthy Body.Life (Basel, Switzerland) · 2021Review
- Suppression of a core metabolic enzyme dihydrolipoamide dehydrogenase (Genes & diseases · 2021Article
- β-amyloid monomers drive up neuronal aerobic glycolysis in response to energy stressors.Aging · 2021Article
- Novel Peptide-Calix[4]arene Conjugate Inhibits Aβ Aggregation and Rescues Neurons from Aβ's Oligomers CytotoxicityACS chemical neuroscience · 2021Article
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Authors and funding
17 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ß-amyloid (Aß1-42) is produced by proteolytic cleavage of the transmembrane type-1 protein, amyloid precursor protein. Under pathological conditions, Aß1-42self-aggregates into oligomers, which cause synaptic dysfunction and neuronal loss, and are considered the culprit of Alzheimer's disease (AD). However, Aß1-42 is mainly monomeric at physiological concentrations, and the precise role of monomeric Aß1-42 in neuronal function is largely unknown. We report that the monomer of Aß1-42 activates type-1 insulin-like growth factor receptors and enhances glucose uptake in neurons and peripheral cells by promoting the translocation of the Glut3 glucose transporter from the cytosol to the plasma membrane. In neurons, activity-dependent glucose uptake was blunted after blocking endogenous Aß production, and re-established in the presence of cerebrospinal fluid Aß. APP-null neurons failed to enhance depolarization-stimulated glucose uptake unless exogenous monomeric Aß1-42 was added. These data suggest that Aß1-42 monomers were critical for maintaining neuronal glucose homeostasis. Accordingly, exogenous Aß1-42 monomers were able to rescue the low levels of glucose consumption observed in brain slices from AD mutant mice.
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