ArticleBMC neuroscience2007
Calcium-sensitive regulation of monoamine oxidase-A contributes to the production of peroxyradicals in hippocampal cultures: implications for Alzheimer disease-related pathology.
Article in BMC neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 47 citations in OpenAlex.
- Article
- Search for unknown neural link between the masticatory and cognitive brain systems to clarify the involvement of its impairment in the pathogenesis of Alzheimer's disease.Frontiers in cellular neuroscience · 2024Review
- Metabolic Features of Brain Function with Relevance to Clinical Features of Alzheimer and Parkinson Diseases.Molecules (Basel, Switzerland) · 2022Review
- COVID-19 infection and neurodegeneration: Computational evidence for interactions between the SARS-CoV-2 spike protein and monoamine oxidase enzymes.Computational and structural biotechnology journal · 2022Article
- The Aβ(1-38) peptide is a negative regulator of the Aβ(1-42) peptide implicated in Alzheimer disease progression.Scientific reports · 2021Article
- Relationships between Mitochondrial Dysfunction and Neurotransmission Failure in Alzheimer's Disease.Aging and disease · 2020Review
- Exploring the activity of polyamine analogues on polyamine and spermine oxidase: methoctramine, a potent and selective inhibitor of polyamine oxidase.Journal of enzyme inhibition and medicinal chemistry · 2019Article
- Lacidipine attenuates reserpine-induced depression-like behavior and oxido-nitrosative stress in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2019Article
- Monoamine oxidase-A activity is required for clonal tumorsphere formation by human breast tumor cells.Cellular & molecular biology letters · 2019Article
- Can Animal Models Inform on the Relationship between Depression and Alzheimer Disease?Canadian journal of psychiatry. Revue canadienne de psychiatrie · 2019Review
- Type A and B monoamine oxidases distinctly modulate signal transduction pathway and gene expression to regulate brain function and survival of neurons.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- 13 reasons why the brain is susceptible to oxidative stress.Redox biology · 2018Review
- Alzheimer Disease and Selected Risk Factors Disrupt a Co-regulation of Monoamine Oxidase-A/B in the Hippocampus, but Not in the Cortex.Frontiers in neuroscience · 2018Article
- Modulation of monoamine oxidase (MAO) expression in neuropsychiatric disorders: genetic and environmental factors involved in type A MAO expression.Journal of neural transmission (Vienna, Austria : 1996) · 2016Review
- The protective role of Bax inhibitor-1 against chronic mild stress through the inhibition of monoamine oxidase A.Scientific reports · 2013Article
- Aspartic acid substitutions in monoamine oxidase-A reveal both catalytic-dependent and -independent influences on cell viability and proliferation.Journal of neural transmission (Vienna, Austria : 1996) · 2012Article
- Alzheimer disease-related presenilin-1 variants exert distinct effects on monoamine oxidase-A activity in vitro.Journal of neural transmission (Vienna, Austria : 1996) · 2011Article
- MAO-A promoter polymorphism and idiopathic pulmonary arterial hypertension.Journal of genetics · 2010Article
- Calcium and mitochondrial reactive oxygen species generation: how to read the facts.Journal of Alzheimer's disease : JAD · 2010Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCalcium (Ca2+) has recently been shown to selectively increase the activity of monoamine oxidase-A (MAO-A), a mitochondria-bound enzyme that generates peroxyradicals as a natural by-product of the deamination of neurotransmitters such as serotonin. It has also been suggested that increased intracellular free Ca2+ levels as well as MAO-A may be contributing to the oxidative stress associated with Alzheimer disease (AD).
resultsIncubation with Ca2+ selectively increases MAO-A enzymatic activity in protein extracts from mouse hippocampal HT-22 cell cultures. Treatment of HT-22 cultures with the Ca2+ ionophore A23187 also increases MAO-A activity, whereas overexpression of calbindin-D28K (CB-28K), a Ca2+-binding protein in brain that is greatly reduced in AD, decreases MAO-A activity. The effects of A23187 and CB-28K are both independent of any change in MAO-A protein or gene expression. The toxicity (via production of peroxyradicals and/or chromatin condensation) associated with either A23187 or the AD-related beta-amyloid peptide, which also increases free intracellular Ca2+, is attenuated by MAO-A inhibition in HT-22 cells as well as in primary hippocampal cultures.
conclusionThese data suggest that increases in intracellular Ca2+ availability could contribute to a MAO-A-mediated mechanism with a role in AD-related oxidative stress.
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