Evidence map›Paper›PMID 29515352›Full record

ReviewFrontiers in neuroscience2018

The Role of Insulin/IGF-1/PI3K/Akt/GSK3β Signaling in Parkinson's Disease Dementia.

Liying Yang, Hongyan Wang, Lijun Liu, Anmu Xie

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed, 4 pooled it
13.3field-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

116 citing papers in PubMed, 4 syntheses or guidelines pooled it, 224 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Type 2 Diabetes as a Determinant of Parkinson's Disease Risk and Progression.Movement disorders : official journal of the Movement Disorder Society · 2021
    Pooled it
  5. Trial
  6. Review
  7. 8-Gingerol Mitigates MPPNeurochemical research · 2026
    Article
  8. Review
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  20. Contribution of insulin‑like growth factor‑1 to tendon repair (Review).International journal of molecular medicine · 2025
    Review

56 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

4 authors at 2 institutions in 1 country.

Liying YangDepartment of Neurology, Affiliated Hospital of Qingdao University, Qingdao, China.
Hongyan WangDepartment of Neurology, Qingdao Municipal Hospital, Qingdao, China.
Lijun LiuDepartment of Neurology, Affiliated Hospital of Qingdao University, Qingdao, China.
Anmu XieDepartment of Neurology, Affiliated Hospital of Qingdao University, Qingdao, China.
Affiliated Hospital of Qingdao University · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dementia, a condition that frequently afflicts patients in advanced stages of Parkinson's disease (PD), results in decreased quality of life and survival time. Nevertheless, the pathological mechanisms underlying Parkinson's disease dementia (PDD) are not completely understood. The symptoms characteristic of PDD may be the result of functional and structural deficiencies. The present study implicates the accumulation of Lewy bodies in the cortex and limbic system as a potent trigger in the development of PDD. In addition, significant Alzheimer-type pathologies, including amyloid-β (Aβ) plaques and NFTs, are observed in almost half of PDD patients. Interestingly, links between PDD pathogenesis and the mechanisms underlying the development of insulin resistance have begun to emerge. Furthermore, previous studies have demonstrated that insulin treatment reduces amyloid plaques in Alzheimer's disease (AD), and normalizes the production and functionality of dopamine and ameliorates motor impairments in 6-OHDA-induced rat PD models. GSK3β, a downstream substrate of PI3K/Akt signaling following induction by insulin and IGF-1, exerts an influence on AD and PD physiopathology. The genetic overexpression of GSK3β in cortex and hippocampus results in signs of neurodegeneration and spatial learning deficits in

Indexed as

AktGlycogen synthase kinase β (GSK3β)insulinInsulin-like growth factor (IGF-I)Parkinson's disease dementia (PDD)phosphoinositide 3 kinase (PI3k)tauα-synuclein

Identifiers

PMID29515352
PMCPMC5826217
OpenAlexW2793678678

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.