ArticleInternational journal of cell biology2012
Mitochondrial- and endoplasmic reticulum-associated oxidative stress in Alzheimer's disease: from pathogenesis to biomarkers.
Article in International journal of cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 146 citations in OpenAlex.
- Effects of Moderate Aerobic Exercise on Cognitive Abilities and Redox State Biomarkers in Older Adults.Oxidative medicine and cellular longevity · 2016Trial
- Amyloid-beta fibrils as active contributors to synaptic dysfunction in Alzheimer's disease.Acta pharmacologica Sinica · 2026Article
- The Glial Autophagy-Lysosomal-Inflammation Axis in Alzheimer's Disease: a Unifying Mechanistic Framework.Molecular neurobiology · 2026Review
- Review
- Pioglitazone protects against trimethyltin hippocampal injury by reducing pyroptosis, mitochondrial dysregulation and ER stress.Scientific reports · 2026Article
- From Food Additives to Neurodegeneration: The Emerging Role of Polyphosphates in Tauopathies.ACS chemical neuroscience · 2026Review
- Therapeutic Potential of Select Berry Varieties in Mitigating Cognitive Decline via Oxidative Stress and Insulin Resistance in AlClBrain and behavior · 2026Article
- Tangeretin prevents cardiac failure induced by reperfusion/ischaemia by inhibiting apoptosis, endoplasmic reticulum stress, and JNK/ERK pathway.Archives of medical science : AMS · 2026Article
- Targeting Cathepsins in Neurodegeneration: Biochemical Advances.Biomedicines · 2025Review
- Impaired Synaptic Plasticity Mechanisms in Alzheimer's Disease.Metabolic brain disease · 2025Review
- Nandrolone Abuse Prior to Head Trauma Mitigates Endoplasmic Reticulum Stress, Mitochondrial Bioenergetic Deficits, and Markers of Neurodegeneration.Molecular neurobiology · 2025Article
- The Role of Zinc in the Development of Vascular Dementia and Parkinson's Disease and the Potential of Carnosine as Their Therapeutic Agent.Biomedicines · 2024Review
- Oxidative Stress, Endoplasmic Reticulum Stress and Apoptosis in the Pathology of Alzheimer's Disease.Cell biochemistry and biophysics · 2024Review
- Neuroprotective mechanisms of luteolin in glutamate-induced oxidative stress and autophagy-mediated neuronal cell death.Scientific reports · 2024Article
- Targeted Treatment Strategies for Mitochondria Dysfunction: Correlation with Neurological Disorders.Current drug targets · 2024Review
- The neuroprotective effects of peracetylated chitosan oligosaccharides against β-amyloid-induced cognitive deficits in rats.Marine life science & technology · 2023Article
- Dendrimers and Derivatives as Multifunctional Nanotherapeutics for Alzheimer's Disease.Pharmaceutics · 2023Review
- Quinolinic Acid Induces Alterations in Neuronal Subcellular Compartments, Blocks Autophagy Flux and Activates Necroptosis and Apoptosis in Rat Striatum.Molecular neurobiology · 2022Article
- The Credible Role of Curcumin in Oxidative Stress-Mediated Mitochondrial Dysfunction in Mammals.Biomolecules · 2022Review
- Artificial Intelligence Predictor for Alzheimer's Disease Trained on Blood Transcriptome: The Role of Oxidative Stress.International journal of molecular sciences · 2022Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common cause of dementia in the elderly, affecting several million of people worldwide. Pathological changes in the AD brain include the presence of amyloid plaques, neurofibrillary tangles, loss of neurons and synapses, and oxidative damage. These changes strongly associate with mitochondrial dysfunction and stress of the endoplasmic reticulum (ER). Mitochondrial dysfunction is intimately linked to the production of reactive oxygen species (ROS) and mitochondrial-driven apoptosis, which appear to be aggravated in the brain of AD patients. Concomitantly, mitochondria are closely associated with ER, and the deleterious crosstalk between both organelles has been shown to be involved in neuronal degeneration in AD. Stimuli that enhance expression of normal and/or folding-defective proteins activate an adaptive unfolded protein response (UPR) that, if unresolved, can cause apoptotic cell death. ER stress also induces the generation of ROS that, together with mitochondrial ROS and decreased activity of several antioxidant defenses, promotes chronic oxidative stress. In this paper we discuss the critical role of mitochondrial and ER dysfunction in oxidative injury in AD cellular and animal models, as well as in biological fluids from AD patients. Progress in developing peripheral and cerebrospinal fluid biomarkers related to oxidative stress will also be summarized.
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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.