Evidence map›Paper›PMID 21199444›Full record

ReviewCNS neuroscience & therapeutics2011

Parkinson's disease dementia and potential therapeutic strategies.

John N Caviness, LihFen Lue, Charles H Adler, Douglas G Walker

Open access · bronzeAbstract readReview
In one paragraph

Review in CNS neuroscience & therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. The Neuroprotective Effects ofInternational journal of molecular sciences · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Ethanol Extract ofInternational journal of molecular sciences · 2021
    Article
  10. Article
  11. Cortical phosphorylated α-Synuclein levels correlate with brain wave spectra in Parkinson's disease.Movement disorders : official journal of the Movement Disorder Society · 2016
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Cumulative exposure to lead and cognition in persons with Parkinson's disease.Movement disorders : official journal of the Movement Disorder Society · 2013
    Article
  19. Article
  20. 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

4 authors at 2 institutions in 1 country.

John N CavinessMayo Clinic College of Medicine, Mayo Clinic, USA. jcaviness@mayo.edu
LihFen Lue
Charles H Adler
Douglas G Walker
Banner Sun Health Research Institute · USMayo Clinic in Arizona · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dementia in Parkinson's disease (PD-D) has only been acknowledged in the recent three decades, but research in this field has accelerated. The purpose of this review was to discuss advances in PD-D regarding biomarker correlates and potential therapeutic targets. Attention and executive dysfunction, memory deficits that improve with cueing, and visual hallucinations are characteristic in PD-D. PD-D dramatically increases the disability and misery of the disease. Current treatment for PD-D is symptomatic, modest, and only transiently effective. There is wide agreement that more effective treatment is needed, but this will require more knowledge about PD-D pathophysiology. Advances in the pathogenesis of PD have focused on the substantia nigra, which is the location from where the pathophysiology of motor symptoms primarily arises in initial stages. In contradistinction, pathology studies have suggested that cognitive decline correlates with cortical and subcortical-cortical projection pathway abnormalities. There is evidence that substantia nigra mechanisms, including protein aggregation of α-synuclein (e.g., Lewy bodies) may also play a role in cortical neuron degeneration. Other different mechanisms, such as Alzheimer's disease pathology (e.g., Aβ aggregation) may be operant for PD-D. Biomarkers of various types are being proposed for the study of PD-D as well as for objective measures of PD-D prediction and progression. Therapeutic targets are currently derived mostly from general PD neurodegeneration research rather than cortical PD neurodegeneration per se. Protein aggregation, genes that are associated with PD, oxidative stress, inflammation, and trophic factors constitute the major classes of therapeutic targets for PD-D. More research is needed on the specific aspects of cortical dysfunction and degeneration that create PD-D.

Indexed as

BiomarkersBrainDementiaHumansParkinson DiseaseBiomarkers

Identifiers

PMID21199444
PMCPMC6493795
OpenAlexW1582425028

What OpenQuestion holds

Textmetadata
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.