Evidence map›Paper›PMID 35720097›Full record

ReviewFrontiers in neurology2022

Clinical Manifestations and Molecular Backgrounds of Parkinson's Disease Regarding Genes Identified From Familial and Population Studies.

Kenya Nishioka, Yuzuru Imai, Hiroyo Yoshino, Yuanzhe Li, Manabu Funayama, Nobutaka Hattori

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Common genetic risk for Parkinson's disease and dysfunction of the endo-lysosomal system.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Review
  6. Review
  7. Review
  8. The Role of Immune Dysfunction in Parkinson's Disease Development.International journal of molecular sciences · 2023
    Review
  9. Role of α-synuclein in microglia: autophagy and phagocytosis balance neuroinflammation in Parkinson's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  10. Article
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

6 authors at 1 institution in 1 country.

Kenya NishiokaDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Yuzuru ImaiDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Hiroyo YoshinoResearch Institute for Diseases of Old Age, Graduate School of Medicine, Juntendo University, Tokyo, Japan.
Yuanzhe LiDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Manabu FunayamaDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Nobutaka HattoriDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Juntendo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over the past 20 years, numerous robust analyses have identified over 20 genes related to familial Parkinson's disease (PD), thereby uncovering its molecular underpinnings and giving rise to more sophisticated approaches to investigate its pathogenesis. α-Synuclein is a major component of Lewy bodies (LBs) and behaves in a prion-like manner. The discovery of α-Synuclein enables an in-depth understanding of the pathology behind the generation of LBs and dopaminergic neuronal loss. Understanding the pathophysiological roles of genes identified from PD families is uncovering the molecular mechanisms, such as defects in dopamine biosynthesis and metabolism, excessive oxidative stress, dysfunction of mitochondrial maintenance, and abnormalities in the autophagy-lysosome pathway, involved in PD pathogenesis. This review summarizes the current knowledge on familial PD genes detected by both single-gene analyses obeying the Mendelian inheritance and meta-analyses of genome-wide association studies (GWAS) from genome libraries of PD. Studying the functional role of these genes might potentially elucidate the pathological mechanisms underlying familial PD and sporadic PD and stimulate future investigations to decipher the common pathways between the diseases.

Indexed as

alpha-synucleindopaminefamilial Parkinson's diseasegeneticsGWASLRRK2

Identifiers

PMID35720097
PMCPMC9201061
OpenAlexW4281676652

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.