Evidence map›Paper›PMID 31428316›Full record

ReviewTranslational neurodegeneration2019

The interplay of aging, genetics and environmental factors in the pathogenesis of Parkinson's disease.

Shirley Yin-Yu Pang, Philip Wing-Lok Ho, Hui-Fang Liu, Chi-Ting Leung, Lingfei Li, Eunice Eun Seo Chang, David Boyer Ramsden, Shu-Leong Ho

Open access · goldAbstract readReview
In one paragraph

Review in Translational neurodegeneration, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 234 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
234citing papers in PubMed, 6 pooled it
21.6field-weighted citation impact, top 1% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

234 citing papers in PubMed, 6 syntheses or guidelines pooled it, 386 citations in OpenAlex.

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  12. The glymphatic system and Parkinson's disease: a narrative review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
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174 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 3 countries.

Shirley Yin-Yu Pang1Division of Neurology, Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, People's Republic of China.
Philip Wing-Lok Ho1Division of Neurology, Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, People's Republic of China.
Hui-Fang Liu1Division of Neurology, Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, People's Republic of China.
Chi-Ting Leung1Division of Neurology, Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, People's Republic of China.
Lingfei Li1Division of Neurology, Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, People's Republic of China.
Eunice Eun Seo Chang1Division of Neurology, Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, People's Republic of China.
David Boyer Ramsden2Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK.
Shu-Leong Ho1Division of Neurology, Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, People's Republic of China.
Queen Mary Hospital · CNUniversity of Birmingham · GBUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundParkinson's disease (PD) is characterized by dopaminergic neuronal loss in the substantia nigra pars compacta and intracellular inclusions called Lewy bodies (LB). During the course of disease, misfolded α-synuclein, the major constituent of LB, spreads to different regions of the brain in a prion-like fashion, giving rise to successive non-motor and motor symptoms. Etiology is likely multifactorial, and involves interplay among aging, genetic susceptibility and environmental factors. MAIN BODY: The prevalence of PD rises exponentially with age, and aging is associated with impairment of cellular pathways which increases susceptibility of dopaminergic neurons to cell death. However, the majority of those over the age of 80 do not have PD, thus other factors in addition to aging are needed to cause disease. Discovery of neurotoxins which can result in parkinsonism led to efforts in identifying environmental factors which may influence PD risk. Nevertheless, the causality of most environmental factors is not conclusively established, and alternative explanations such as reverse causality and recall bias cannot be excluded. The lack of geographic clusters and conjugal cases also go against environmental toxins as a major cause of PD. Rare mutations as well as common variants in genes such as

conclusionPD is a multifactorial disorder involving interplay of aging, genetics and environmental factors. This has implications on the development of appropriate animal models of PD which take all these factors into account. Common converging pathways likely include mitochondrial dysfunction, impaired autophagy, oxidative stress and neuroinflammation, which are associated with the accumulation and spread of misfolded α-synuclein and neurodegeneration. Understanding the mechanisms involved in the initiation and progression of PD may lead to potential therapeutic targets to prevent PD or modify its course.

Indexed as

AgingEnvironmental toxinsGeneticsParkinson’s disease

Identifiers

PMID31428316
PMCPMC6696688
OpenAlexW2968035162

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.