ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2015
Amyloid β 1-42 induces hypometabolism in human stem cell-derived neuron and astrocyte networks.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 40 citations in OpenAlex.
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- TSPO contributes to neuropathology and cognitive deficits in Alzheimer's disease.Journal of neuroinflammation · 2025Article
- Altered metabolic function induced by Aβ-oligomers and PSEN1 mutations in iPSC-derived astrocytes.Journal of neurochemistry · 2025Article
- Exploring fatty acid metabolism in Alzheimer's disease: the key role of CPT1A.Scientific reports · 2024Article
- Prevention and Treatment Strategies for Alzheimer's Disease: Focusing on Microglia and Astrocytes in Neuroinflammation.Journal of inflammation research · 2024Review
- Lactate metabolism in neurodegenerative diseases.Neural regeneration research · 2024Review
- Metabolic Regulation of Glia and Their Neuroinflammatory Role in Alzheimer's Disease.Cellular and molecular neurobiology · 2022Review
- The effect of citalopram treatment on amyloid-β precursor protein processing and oxidative stress in human hNSC-derived neurons.Translational psychiatry · 2022Article
- Effects of amyloid-β on protein SUMOylation and levels of mitochondrial proteins in primary cortical neurons.IBRO neuroscience reports · 2022Article
- Brain Metabolic Alterations in Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Modelling mitochondrial dysfunction in Alzheimer's disease using human induced pluripotent stem cells.World journal of stem cells · 2019Review
- Article
- Astrocytes and synaptic plasticity in health and disease.Experimental brain research · 2017Review
- Energy crisis precedes global metabolic failure in a novel Caenorhabditis elegans Alzheimer Disease model.Scientific reports · 2016Article
- Impaired fasting glucose is associated with increased regional cerebral amyloid.Neurobiology of aging · 2016Article
- Amyloid-β and Astrocytes Interplay in Amyloid-β Related Disorders.International journal of molecular sciences · 2016Review
- Soluble amyloid-β oligomers as synaptotoxins leading to cognitive impairment in Alzheimer's disease.Frontiers in cellular neuroscience · 2015Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common form of dementia, affecting more than 35 million people worldwide. Brain hypometabolism is a major feature of AD, appearing decades before cognitive decline and pathologic lesions. To date, the majority of studies on hypometabolism in AD have used transgenic animal models or imaging studies of the human brain. As it is almost impossible to validate these findings using human tissue, alternative models are required. In this study, we show that human stem cell-derived neuron and astrocyte cultures treated with oligomers of amyloid beta 1-42 (Aβ1-42) also display a clear hypometabolism, particularly with regard to utilization of substrates such as glucose, pyruvate, lactate, and glutamate. In addition, a significant increase in the glycogen content of cells was also observed. These changes were accompanied by changes in NAD(+)/NADH, ATP, and glutathione levels, suggesting a disruption in the energy-redox axis within these cultures. The high energy demands associated with neuronal functions such as memory formation and protection from oxidative stress put these cells at particular risk from Aβ-induced hypometabolism. Further research using this model may elucidate the mechanisms associated with Aβ-induced hypometabolism.
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