ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2005
Normal brain ageing: models and mechanisms.
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 115 citations in OpenAlex.
- Creatine and Cognition in Aging: A Systematic Review of Evidence in Older Adults.Nutrition reviews · 2026Pooled it
- Effects of creatine supplementation on cognitive function of healthy individuals: A systematic review of randomized controlled trials.Experimental gerontology · 2018Pooled it
- Vitamin C enhances theAnimal biotechnology · 2024Article
- Neural ageing and synaptic plasticity: prioritizing brain health in healthy longevity.Frontiers in aging neuroscience · 2024Review
- Mitochondrial dysfunction in neurodegenerative disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Review
- Reactive Oxygen Species Damage Bovine Endometrial Epithelial Cells via the Cytochrome C-mPTP Pathway.Antioxidants (Basel, Switzerland) · 2023Article
- Mitochondrial permeability transition pore-dependent necrosis.Journal of molecular and cellular cardiology · 2023Review
- Visual Function and Survival of Injured Retinal Ganglion Cells in Aged Rbfox1 Knockout Animals.Cells · 2022Article
- A Perspective: Challenges in Dementia Research.Medicina (Kaunas, Lithuania) · 2022Article
- Does cognitive aging follow an orchid and dandelion phenomenon?Frontiers in aging neuroscience · 2022Article
- Down-regulation of EPB41L4A-AS1 mediated the brain aging and neurodegenerative diseases via damaging synthesis of NADCell & bioscience · 2021Article
- Review
- Astrocyte Intracellular CaNeurotoxicity research · 2021Article
- Dietary Antioxidants and the Mitochondrial Quality Control: Their Potential Roles in Parkinson's Disease Treatment.Antioxidants (Basel, Switzerland) · 2020Review
- Mitochondrial Dysfunction in Kidney Disease and Uremic Sarcopenia.Frontiers in physiology · 2020Review
- Honey as an antioxidant therapy to reduce cognitive ageing.Iranian journal of basic medical sciences · 2019Review
- Glutamate and ATP at the Interface Between Signaling and Metabolism in Astroglia: Examples from Pathology.Neurochemical research · 2017Review
- Mammalian Target of Rapamycin: Its Role in Early Neural Development and in Adult and Aged Brain Function.Frontiers in cellular neuroscience · 2016Review
- Reactive Oxygen Species: Physiological and Physiopathological Effects on Synaptic Plasticity.Journal of experimental neuroscience · 2016Review
- In vivo imaging of axonal transport of mitochondria in the diseased and aged mammalian CNS.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Normal ageing is associated with a degree of decline in a number of cognitive functions. Apart from the issues raised by the current attempts to expand the lifespan, understanding the mechanisms and the detailed metabolic interactions involved in the process of normal neuronal ageing continues to be a challenge. One model, supported by a significant amount of experimental evidence, views the cellular ageing as a metabolic state characterized by an altered function of the metabolic triad: mitochondria-reactive oxygen species (ROS)-intracellular Ca2+. The perturbation in the relationship between the members of this metabolic triad generate a state of decreased homeostatic reserve, in which the aged neurons could maintain adequate function during normal activity, as demonstrated by the fact that normal ageing is not associated with widespread neuronal loss, but become increasingly vulnerable to the effects of excessive metabolic loads, usually associated with trauma, ischaemia or neurodegenerative processes. This review will concentrate on some of the evidence showing altered mitochondrial function with ageing and also discuss some of the functional consequences that would result from such events, such as alterations in mitochondrial Ca2+ homeostasis, ATP production and generation of ROS.
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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.