ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
No consistent bioenergetic defects in presynaptic nerve terminals isolated from mouse models of Alzheimer's disease.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. 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, 27 citations in OpenAlex.
- Monocyte abundance and glycolytic reprogramming associate with motivational impairment in depression.Brain, behavior, and immunity · 2026Article
- 13C tracing in synaptosomes reveals that SGLT2 inhibition with dapagliflozin prevents metabolic deficits in the 5X-FAD model of Alzheimer's Disease.bioRxiv : the preprint server for biology · 2025Article
- Glial Cell Metabolic Profile Upon Iron Deficiency: Oligodendroglial and Astroglial Casualties of Bioenergetic Adjustments.Molecular neurobiology · 2023Article
- Hyperphosphorylated Human Tau Accumulates at the Synapse, Localizing on Synaptic Mitochondrial Outer Membranes and Disrupting Respiration in a Mouse Model of Tauopathy.Frontiers in molecular neuroscience · 2022Article
- Contrasting Metabolic Insufficiency in Aging and Dementia.Aging and disease · 2021Review
- Biological sex and DNA repair deficiency drive Alzheimer's disease via systemic metabolic remodeling and brain mitochondrial dysfunction.Acta neuropathologica · 2020Article
- Observational
- Systems biology identifies preserved integrity but impaired metabolism of mitochondria due to a glycolytic defect in Alzheimer's disease neurons.Aging cell · 2019Article
- Early and Late Pathomechanisms in Alzheimer's Disease: From Zinc to Amyloid-β Neurotoxicity.Neurochemical research · 2017Review
- Synaptosomal bioenergetic defects are associated with cognitive impairment in a transgenic rat model of early Alzheimer's disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Nitro-Arachidonic Acid Prevents Angiotensin II-Induced Mitochondrial Dysfunction in a Cell Line of Kidney Proximal Tubular Cells.PloS one · 2016Article
- The role of mitochondrially derived ATP in synaptic vesicle recycling.The Journal of biological chemistry · 2015Article
- Mitochondrial bioenergetics and neuronal survival modelled in primary neuronal culture and isolated nerve terminals.Journal of bioenergetics and biomembranes · 2015Review
- Imaging oxygen in neural cell and tissue models by means of anionic cell-permeable phosphorescent nanoparticles.Cellular and molecular life sciences : CMLS · 2015Article
- Functional mitochondrial analysis in acute brain sections from adult rats reveals mitochondrial dysfunction in a rat model of migraine.American journal of physiology. Cell physiology · 2014Article
- Synaptic activity and bioenergy homeostasis: implications in brain trauma and neurodegenerative diseases.Frontiers in neurology · 2013Review
- SOD2 in mitochondrial dysfunction and neurodegeneration.Free radical biology & medicine · 2013Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Depressed cortical energy supply and impaired synaptic function are predominant associations of Alzheimer's disease (AD). To test the hypothesis that presynaptic bioenergetic deficits are associated with the progression of AD pathogenesis, we compared bioenergetic variables of cortical and hippocampal presynaptic nerve terminals (synaptosomes) from commonly used mouse models with AD-like phenotypes (J20 age 6 months, Tg2576 age 16 months, and APP/PS age 9 and 14 months) to age-matched controls. No consistent bioenergetic deficiencies were detected in synaptosomes from the three models; only APP/PS cortical synaptosomes from 14-month-old mice showed an increase in respiration associated with proton leak. J20 mice were chosen for a highly stringent investigation of mitochondrial function and content. There were no significant differences in the quality of the synaptosomal preparations or the mitochondrial volume fraction. Furthermore, respiratory variables, calcium handling, and membrane potentials of synaptosomes from symptomatic J20 mice under calcium-imposed stress were not consistently impaired. The recovery of marker proteins during synaptosome preparation was the same, ruling out the possibility that the lack of functional bioenergetic defects in synaptosomes from J20 mice was due to the selective loss of damaged synaptosomes during sample preparation. Our results support the conclusion that the intrinsic bioenergetic capacities of presynaptic nerve terminals are maintained in these symptomatic AD mouse models.
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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.