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Cited by 246

The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.

Calcium and Mitochondrial Reactive Oxygen Species Generation: How to Read the Facts

Open access
Adam-Vizi, Vera, Starkov, Anatoly A.·2010·Journal of Alzheimer's Disease

Abstract

A number of recent discoveries indicate that abnormal Ca2+ signaling, oxidative stress, and mitochondrial dysfunction are involved in the neuronal damage in Alzheimer's disease. However, the literature on the interactions between these factors is controversial especially in the interpretation of the cause-effect relationship between mitochondrial damage induced by Ca2+ overload and the production of reactive oxygen species (ROS). In this review, we survey the experimental observations on the Ca2+-induced mitochondrial ROS production, explain the sources of controversy in interpreting these results, and discuss the different molecular mechanisms underlying the effect of Ca2+ on the ROS emission by brain mitochondria.

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Crossref · 10.3233/jad-2010-100465

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Metadata

Authors
Adam-Vizi, V., & Starkov, A. A.
Venue
Journal of Alzheimer's Disease
Published
2010-06-03
Volume
20
Issue
s2
Pages
S413-S426
ISSN
  • 1387-2877 (ISSN-L)
  • 1875-8908
OpenAlex
W1509344561
Cited by
246
References
24
FWCI
2.72
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Calcium and Mitochondrial Reactive Oxygen Species Generation: How to Read the Facts. https://app.cochat.ai/papers/10.3233/jad-2010-100465
The paper
Adam-Vizi, V., & Starkov, A. A. (2010). Calcium and Mitochondrial Reactive Oxygen Species Generation: How to Read the Facts. Journal of Alzheimer's Disease. https://doi.org/10.3233/jad-2010-100465

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.