ReviewCells2023
Reappraisal of the Concept of Accelerated Aging in Neurodegeneration and Beyond.
Review in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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
6 citing papers in PubMed.
- When Age Is More Than a Number: Acceleration of Brain Aging in Neurodegenerative Diseases.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2025Article
- Association between eGDR and accelerated aging: the mediating role of ePWV.Diabetology & metabolic syndrome · 2025Article
- The Hallmarks of Ageing in Human Immunodeficiency Virus Infection and the Impact of Antiretroviral Therapy on Telomeres: A Molecular Perspective.Current issues in molecular biology · 2025Review
- Pancreatic Volume in Thalassemia: Determinants and Association with Alterations of Glucose Metabolism.Diagnostics (Basel, Switzerland) · 2025Article
- An Update on Neuroaging on Earth and in Spaceflight.International journal of molecular sciences · 2025Review
- HEALTHY AGING: THE PROMISE, AND PERILS, OF GEROSCIENCE.Transactions of the American Clinical and Climatological Association · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGenetic and epigenetic changes, oxidative stress and inflammation influence the rate of aging, which diseases, lifestyle and environmental factors can further accelerate. In accelerated aging (AA), the biological age exceeds the chronological age.
objectiveThe objective of this study is to reappraise the AA concept critically, considering its weaknesses and limitations.
methodsWe reviewed more than 300 recent articles dealing with the physiology of brain aging and neurodegeneration pathophysiology.
results(1) Application of the AA concept to individual organs outside the brain is challenging as organs of different systems age at different rates. (2) There is a need to consider the deceleration of aging due to the potential use of the individual structure-functional reserves. The latter can be restored by pharmacological and/or cognitive therapy, environment, etc. (3) The AA concept lacks both standardised terminology and methodology. (4) Changes in specific molecular biomarkers (MBM) reflect aging-related processes; however, numerous MBM candidates should be validated to consolidate the AA theory. (5) The exact nature of many potential causal factors, biological outcomes and interactions between the former and the latter remain largely unclear.
conclusionsAlthough AA is commonly recognised as a perspective theory, it still suffers from a number of gaps and limitations that assume the necessity for an updated AA concept.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.