ReviewMolecular neurobiology2012
From mitochondrial dysfunction to amyloid beta formation: novel insights into the pathogenesis of Alzheimer's disease.
Review in Molecular neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 2 of them syntheses that pooled it.
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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Who cites it
76 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- The cellular model for Alzheimer's disease research: PC12 cells.Frontiers in molecular neuroscience · 2022Pooled it
- Dissecting Complex and Multifactorial Nature of Alzheimer's Disease Pathogenesis: a Clinical, Genomic, and Systems Biology Perspective.Molecular neurobiology · 2016Pooled it
- Sex-specific regulation of angiogenin in Alzheimer's disease.Molecular psychiatry · 2026Article
- Mitochondria-Targeted Nanotherapies in Aging Neurodegenerative Disorders: Emerging Prospects and Clinical Potential.Advanced healthcare materials · 2026Review
- Estrogen Withdrawal-Induced Cognitive Impairment in Menopausal Women: Mechanisms and Prospects for Integrated Interventions.International journal of molecular sciences · 2026Review
- Safranal protects neurons against amyloid beta-induced toxicity.Inflammopharmacology · 2026Article
- The GPCR Connection: Linking Alzheimer's Disease and Glioblastoma.Journal of cellular and molecular medicine · 2026Review
- RNA-binding activity of PHGDH drives amyloid-beta production in a human brain organoid model of sporadic Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Fatty acids alter to the toxicity of islet amyloid polypeptide aggregates in a length and saturation dependent manner.iScience · 2026Article
- Toward common treatment strategies: convergent proteinopathies and mitochondrial dysfunction in Alzheimer's and Parkinson's diseases.Frontiers in neuroscience · 2026Review
- Alzheimer's Disease Etiology Hypotheses and Therapeutic Strategies: A Perspective.International journal of molecular sciences · 2025Review
- Role of Galangin for the Treatment of Alzheimer's Disease: Journey So Far and Road Ahead.Current nutrition reports · 2025Review
- The Hallmarks of Ageing in Microglia.Cellular and molecular neurobiology · 2025Review
- Antioxidant and Anti-Inflammatory Activities of Methanol Extract ofInternational journal of molecular sciences · 2025Article
- Article
- Sigma receptors and mitochondria-associated ER membranes are converging therapeutic targets for Alzheimer's disease.Frontiers in neuroscience · 2025Review
- Nitric oxide donors rescue metabolic and mitochondrial dysfunction in obese Alzheimer's model.Scientific reports · 2024Article
- Characterization of Mitochondrial DNA Methylation of Alzheimer's Disease in Plasma Cell-Free DNA.Diagnostics (Basel, Switzerland) · 2023Article
- Chronic cerebral hypoperfusion: a critical feature in unravelling the etiology of vascular cognitive impairment.Acta neuropathologica communications · 2023Review
- Effects of Exercise Training on Neurotrophic Factors and Blood-Brain Barrier Permeability in Young-Old and Old-Old Women.International journal of environmental research and public health · 2022Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The non-Mendelian sporadic Alzheimer's disease (AD) is the most frequent form of dementia diagnosed worldwide. The most important risk factor to develop sporadic AD is aging itself. Next to hyperphosphorylated Tau, intracellular amyloid beta (Aß) oligomers are known to initiate a cascade of pathological events ranging from mitochondrial dysfunction, synaptic dysfunction, oxidative stress, and loss of calcium regulation, to inflammation. All these events are considered to play an important role in the progressive loss of neurons. The molecular mechanisms determining the balance between Aß production and clearance during the progression of the disease are not well understood. Furthermore, there is cumulating evidence that Aß formation impairs mitochondrial function and that mitochondrial dysfunction is an early event in the pathogenesis of AD. On the other hand, mitochondrial dysfunction, in particular increased formation of mitochondrially derived reactive oxygen species, promote Aß formation. Here, we review these latest findings linking mitochondrial dysfunction and Aß formation. We propose that mitochondrial dysfunction, which is well-known to increase with age, is an initial trigger for Aß production. As Aß itself further accelerates mitochondrial dysfunction and oxidative stress, its formation is self-stimulated. Taken together, a vicious cycle is initiated that originates from mitochondrial dysfunction, implying that AD can be viewed as an age-associated mitochondrial disorder. The proposed mechanism sheds new light on the pathophysiological changes taking place during the progression of AD as well as in the aging process.
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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.