ReviewLife (Basel, Switzerland)2021
The Causal Role of Lipoxidative Damage in Mitochondrial Bioenergetic Dysfunction Linked to Alzheimer's Disease Pathology.
Review in Life (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Capturing silent oxidative stress in early Alzheimer's disease: prediction of CSF biomarkers from sleep qEEG data.GeroScience · 2026Article
- Multilayer metabolomic integration reveals bioenergetic disruption in Long COVID.Journal of translational medicine · 2026Article
- Synaptic mitochondrial dysfunction and Alzheimer's disease: from molecular mechanisms to therapeutic strategies.Frontiers in pharmacology · 2026Review
- Metabolic Profiling of Brain Tissue and Brain-Derived Extracellular Vesicles in Alzheimer's Disease.Journal of extracellular vesicles · 2025Article
- Application of Isotope Dilution Gas Chromatography-Mass Spectrometry Using Selected Ion-Monitoring to Evaluate Nonenzymatic Protein Damage in Cerebrospinal Fluid.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Inflammatory and Redox Blood Gene Expression Fingerprint of Severe Obstructive Sleep Apnoea in Patients With Mild Alzheimer's Disease.Journal of inflammation research · 2025Article
- The shift in the fatty acid composition of the circulating lipidome in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Cerebrospinal fluid neutral lipids predict progression from mild cognitive impairment to Alzheimer's disease.GeroScience · 2024Article
- Lipidomic Alterations in the Cerebral Cortex and White Matter in Sporadic Alzheimer's Disease.Aging and disease · 2023Article
- Changes in Plasma Neutral and Ether-Linked Lipids Are Associated with The Pathology and Progression of Alzheimer's Disease.Aging and disease · 2023Article
- Article
- mTOR Complex 1 Content and Regulation Is Adapted to Animal Longevity.International journal of molecular sciences · 2022Review
- Evaluation of mRNA expression level of the ATP synthase membrane subunit c locus 1 (Biochemistry and biophysics reports · 2022Article
- Selective brain regional changes in lipid profile with human aging.GeroScience · 2022Article
- Impaired Mitochondrial Bioenergetics under Pathological Conditions.Life (Basel, Switzerland) · 2022Article
- Inhibitory Effect of Trihydroxy Isoflavone on Neuronal Apoptosis in Natural Aging Rats.Disease markers · 2022Article
- XJB-5-131 Is a Mild Uncoupler of Oxidative Phosphorylation.Journal of Huntington's disease · 2022Article
- Alzheimer's disease is an inherent, natural part of human brain aging: an integrated perspective.Free neuropathology · 2022Article
- The interplay among oxidative stress, brain insulin resistance and AMPK dysfunction contribute to neurodegeneration in type 2 diabetes and Alzheimer disease.Free radical biology & medicine · 2021Review
- Insights into the Pathogenesis of Neurodegenerative Diseases: Focus on Mitochondrial Dysfunction and Oxidative Stress.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Current shreds of evidence point to the entorhinal cortex (EC) as the origin of the Alzheimer's disease (AD) pathology in the cerebrum. Compared with other cortical areas, the neurons from this brain region possess an inherent selective vulnerability derived from particular oxidative stress conditions that favor increased mitochondrial molecular damage with early bioenergetic involvement. This alteration of energy metabolism is the starting point for subsequent changes in a multitude of cell mechanisms, leading to neuronal dysfunction and, ultimately, cell death. These events are induced by changes that come with age, creating the substrate for the alteration of several neuronal pathways that will evolve toward neurodegeneration and, consequently, the development of AD pathology. In this context, the present review will focus on description of the biological mechanisms that confer vulnerability specifically to neurons of the entorhinal cortex, the changes induced by the aging process in this brain region, and the alterations at the mitochondrial level as the earliest mechanism for the development of AD pathology. Current findings allow us to propose the existence of an altered allostatic mechanism at the entorhinal cortex whose core is made up of mitochondrial oxidative stress, lipid metabolism, and energy production, and which, in a positive loop, evolves to neurodegeneration, laying the basis for the onset and progression of AD pathology.
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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.