ReviewAging cell2015
Parkinson's disease as a result of aging.
Review in Aging cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis 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
107 citing papers in PubMed, 1 synthesis or guideline pooled it, 218 citations in OpenAlex.
- Effects of Yi Jin Jing on enhancing muscle strength and physical performance in older individuals: a systematic review and meta-analysis.Frontiers in medicine · 2024Pooled it
- Reviving mitochondria to restore the mind: stem cell-based bioenergetic rescue in Parkinson's disease.Neurodegenerative disease management · 2026Review
- Oleuropein regulates neuronal survival and Histone acetylation in Parkinson's disease: cellular and epigenetic insights.Metabolic brain disease · 2026Article
- Unraveling Parkinson's disease: The mystery of mitochondria and the role of aging.Genes & diseases · 2026Review
- Differential Proteomic Landscape of Plasma Neuron-Derived Extracellular Vesicles in Parkinson's Disease with and without RBD: A Pilot Investigation.International journal of nanomedicine · 2026Article
- Single-cell, multi-region profiling of the macaque brain across the lifespan.bioRxiv : the preprint server for biology · 2025Article
- Photochemically synthesized gold nanoparticles conjugated with Boswellic acid inhibit alpha synuclein aggregation and delay fibrillation kinetics.Scientific reports · 2025Article
- Parkinson's disease-linked Kir4.2 mutation R28C leads to loss of ion channel function.The Journal of physiology · 2025Article
- Contextualizing molecular and structural aging across human organs.medRxiv : the preprint server for health sciences · 2025Article
- Review
- Biofilm proficient Bacillus subtilis prevents neurodegeneration in Caenorhabditis elegans Parkinson's disease models via PMK-1/p38 MAPK and SKN-1/Nrf2 signaling.Scientific reports · 2025Article
- Biological age prediction using a DNN model based on pathways of steroidogenesis.Science advances · 2025Article
- Park7 deletion leads to sex-specific transcriptome changes involving NRF2-CYP1B1 axis in mouse midbrain astrocytes.NPJ Parkinson's disease · 2025Article
- Impact of aging on the central and enteric nervous system in a Parkinson's disease mouse model.Frontiers in aging neuroscience · 2025Article
- Neuronal threshold functions: Determining symptom onset in neurological disorders.Progress in neurobiology · 2024Review
- Data-Driven Discovery of Movement-Linked Heterogeneity in Neurodegenerative Diseases.Nature machine intelligence · 2024Article
- The Synergistic Effect Study of Lipopolysaccharide (LPS) and A53T-α-Synuclein: Intranasal LPS Exposure on the A53T-α-Synuclein Transgenic Mouse Model of Parkinson's Disease.Molecular neurobiology · 2024Article
- Nuclear alpha-synuclein accelerates cell senescence and neurodegeneration.Immunity & ageing : I & A · 2024Article
- P7C3 suppresses astrocytic senescence to protect dopaminergic neurons: Implication in the mouse model of Parkinson's disease.CNS neuroscience & therapeutics · 2024Article
- From inflammatory signaling to neuronal damage: Exploring NLR inflammasomes in ageing neurological disorders.Heliyon · 2024Review
47 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
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is generally considered that Parkinson's disease is induced by specific agents that degenerate a clearly defined population of dopaminergic neurons. Data commented in this review suggest that this assumption is not as clear as is often thought and that aging may be critical for Parkinson's disease. Neurons degenerating in Parkinson's disease also degenerate in normal aging, and the different agents involved in the etiology of this illness are also involved in aging. Senescence is a wider phenomenon affecting cells all over the body, whereas Parkinson's disease seems to be restricted to certain brain centers and cell populations. However, reviewed data suggest that Parkinson's disease may be a local expression of aging on cell populations which, by their characteristics (high number of synaptic terminals and mitochondria, unmyelinated axons, etc.), are highly vulnerable to the agents promoting aging. The development of new knowledge about Parkinson's disease could be accelerated if the research on aging and Parkinson's disease were planned together, and the perspective provided by gerontology gains relevance in this field.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.