ReviewNeurochemical research2012
Activation of PARP by oxidative stress induced by β-amyloid: implications for Alzheimer's disease.
Review in Neurochemical research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
41 citing papers in PubMed, 74 citations in OpenAlex.
- SGLT2 Inhibitors in Alzheimer's Disease: Biochemical Insights and Therapeutic Potential.International journal of molecular sciences · 2026Review
- The Central Role of Neuronal Cell Death in Alzheimer's Disease Pathobiology.Biomedicines · 2026Review
- Increased nucleotide metabolism alleviates Alzheimer's disease pathology.Cell death & disease · 2025Article
- Poly(ADP-ribose) Polymerase 1 Deficiency Attenuates Amyloid Pathology, Neurodegeneration, and Cognitive Decline in a Familial Alzheimer's Disease Model.bioRxiv : the preprint server for biology · 2025Article
- Proteins Associated with Neurodegenerative Diseases: Link to DNA Repair.Biomedicines · 2024Review
- Effects of amyloid-β-mimicking peptide hydrogel matrix on neuronal progenitor cell phenotype.Acta biomaterialia · 2024Article
- Mitochondrial One-Carbon Metabolism and Alzheimer's Disease.International journal of molecular sciences · 2024Review
- Environmental Toxins and Alzheimer's Disease: a Comprehensive Analysis of Pathogenic Mechanisms and Therapeutic Modulation.Molecular neurobiology · 2024Review
- Low-dose intranasal deferoxamine modulates memory, neuroinflammation, and the neuronal transcriptome in the streptozotocin rodent model of Alzheimer's disease.Frontiers in neuroscience · 2024Article
- Poly-(ADP-ribose) polymerases inhibition by olaparib attenuates activities of the NLRP3 inflammasome and of NF-κB in THP-1 monocytes.PloS one · 2024Article
- Nicotinamide Adenine Dinucleotide (NADAntioxidants & redox signaling · 2023Review
- Regulation of Biomolecular Condensates by Poly(ADP-ribose).Chemical reviews · 2023Review
- Resolving Geroplasticity to the Balance of Rejuvenins and Geriatrins.Aging and disease · 2022Article
- Impact of anthocyanin on genetic stability in mammary adenocarcinoma-induced mice treated with methotrexate.Genes & nutrition · 2022Article
- Neuroprotective Effects of PARP Inhibitors inCells · 2022Article
- NSAIDs Induce Proline Dehydrogenase/Proline Oxidase-Dependent and Independent Apoptosis in MCF7 Breast Cancer Cells.International journal of molecular sciences · 2022Article
- Epigenetic Reprogramming of the Glucose Metabolic Pathways by the Chromatin Effectors During Cancer.Sub-cellular biochemistry · 2022Article
- Cellular functions of the protein kinase ATM and their relevance to human disease.Nature reviews. Molecular cell biology · 2021Review
- Disentangling Mitochondria in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- The interplay between oxidative stress and bioenergetic failure in neuropsychiatric illnesses: can we explain it and can we treat it?Molecular biology reports · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a major neurodegenerative disease of old age, characterised by progressive cognitive impairment, dementia and atrophy of the central nervous system. The pathological hallmarks include the accumulation of the peptide β-amyloid (Aβ) which itself is toxic to neurons in culture. Recently, it has been discovered that Aβ activates the protein poly(ADP-ribosyl) polymerase-1 (PARP-1) specifically in astrocytes, leading indirectly to neuronal cell death. PARP-1 is a DNA repair enzyme, normally activated by single strand breaks associated with oxidative stress, which catalyses the formation of poly ADP-ribose polymers from nicotinamide adenine dinucleotide (NAD(+)). The pathological over activation of PARP-1 causes depletion of NAD(+) and leads to cell death. Here we review the relationship between AD and PARP-1, and explore the role played by astrocytes in neuronal death. AD has so far proven refractory to any effective treatment. Identification of these pathways represents a step towards a greater understanding of the pathophysiology of this devastating disease with the potential to explore novel therapeutic targets.
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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.