Cited by 1,297Neuroscience and Neuropharmacology ResearchAlzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

Molecular mechanisms of excitotoxicity and their relevance to pathogenesis of neurodegenerative diseases

Open access
Dong, Xiao-xia, Wang, Yan, Qin, Zheng-hong·2009·Acta Pharmacologica Sinica

Abstract

A pivotal role for excitotoxicity in neurodegenerative diseases is gaining increasingly more acceptance, but the underlying mechanisms through which it participates in neurodegeneration still need further investigation. Excessive activation of glutamate receptors by excitatory amino acids leads to a number of deleterious consequences, including impairment of calcium buffering, generation of free radicals, activation of the mitochondrial permeability transition and secondary excitotoxicity. Recent studies implicate excitotoxicity in a variety of neuropathological conditions, suggesting that neurodegenerative diseases with distinct genetic etiologies may share excitotoxicity as a common pathogenic pathway. Thus, understanding the pathways involved in excitotoxicity is of critical importance for the future clinical treatment of many neurodegenerative diseases. This review discusses the current understanding of excitotoxic mechanisms and how they are involved in the pathogenesis of neurodegenerative diseases.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1038/aps.2009.24

Cites

98 of 98 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 4

  1. Qin ZH, Wang Y, Nakai M, Chase TN. Activation of transcription factor NF-κB contributes to excitotoxin-induced apoptosis. Mol Pharmacol 1998; 53: 33-42.
  2. Liang ZQ, Wang XX, Wang Y, Chen RW, Chuang DM, Chase TN, et al. NF-κB-dependent cyclin D1 induction associated with N-methyl-D-aspartate receptor-mediated apoptosis in rat striatum. J Neurosci Res 2007; 85: 1295-309.
  3. Qin ZH, Chen RW, Wang Y, Nakai M, Chuang DM, Chase TN. NF-κB nuclear translocation up-regulates c-Myc and p53 during N-methyl-D-aspartate receptor-mediatedapoptosis. J Neurosci 1999; 19: 4023-33.
  4. Kooncumchoo P, Sharma S, Porter J, Govitrapong P, Ebadi M. Coenzyme Q (10) provides neuroprotection in iron-induced apo- ptosis in dopamine neurons. J Mol Neurosci 2006; 28: 125-41.

Cited by

Sorted by citations

Authors
Dong, X.-X., Wang, Y., & Qin, Z.-H.
Affiliations
Soochow University (CN)
Corresponding author
Qin, Zheng-hong
Venue
Acta Pharmacologica Sinica
Published
2009-04
Volume
30
Issue
4
Pages
379-387
ISSN
  • 0253-9756 (ISSN-L)
  • 1671-4083
  • 1745-7254
OpenAlex
W2005614483
Cited by
1,297
References
98
Citations by year
2026: 85 · 2025: 113 · 2024: 136 · 2023: 114 · 2022: 127 · 2021: 125 · 2020: 113 · 2019: 85 · 2018: 64 · 2017: 55 · 2016: 72 · 2015: 35 · 2014: 35 · 2013: 38 · 2012: 37
FWCI
2.86
Type
journal article
Language
en
Open access
Locations
  • Acta Pharmacologica Sinica (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Natural Science Foundation of China (30772560)
  • Government of Jiangsu Province
  • Soochow University
  • Specialized Research Fund for the Doctoral Program of Higher Education of China
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
excitotoxicity, neurodegenerative diseases, glutamate receptors, excitatory amino acids, calcium buffering, free radicals, mitochondrial permeability transition, neurodegeneration pathogenesis
MeSH terms
Alzheimer Disease, Animals, Autophagy, Calcium, Chlorides, Humans, Huntington Disease, Nitric Oxide, Receptors, N-Methyl-D-Aspartate, Apoptosis, Reactive Oxygen Species, Receptors, Glutamate, Receptors, AMPA, Oxidative Stress, Glutamic Acid, Neurodegenerative Diseases

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review