Evidence map›Paper›PMID 20828718›Full record

ArticleJournal of psychiatric research2011

Biochemical studies in Normal Pressure Hydrocephalus (NPH) patients: change in CSF levels of amyloid precursor protein (APP), amyloid-beta (Aβ) peptide and phospho-tau.

Balmiki Ray, Patricio F Reyes, Debomoy K Lahiri

Abstract read
In one paragraph

Article in Journal of psychiatric research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 3 pooled it
0.7field-weighted citation impact, top 36% 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

24 citing papers in PubMed, 3 syntheses or guidelines pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. Guideline
  3. Pooled it
  4. Article
  5. Review
  6. Article
  7. Cerebrospinal Fluid Biomarkers in iNPH: A Narrative Review.Diagnostics (Basel, Switzerland) · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Cerebrospinal fluid biomarkers profile of idiopathic normal pressure hydrocephalus.Journal of neural transmission (Vienna, Austria : 1996) · 2018
    Review
  15. Observational
  16. Article
  17. Article
  18. 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

3 authors at 2 institutions in 1 country.

Balmiki RayDepartment of Psychiatry, Institute of Psychiatric Research, Indiana University School of Medicine, 791 Union Drive, Indianapolis, IN 46202, USA.
Patricio F Reyes
Debomoy K Lahiri
Indiana University School of MedicineMinnesota Wire (United States) · US

Funding

Regulation of APP Pathway Gene Promoters in Alzheimer'sR01AG018379 · NIA · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2000 to 2011
$3.1M
Mechanisms of Cholinesterase Inhibitors on Beta-amyloidR01AG018884 · NIA · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2002 to 2012
$2.9M
NONCHOLINERGIC FUNCTIONS OF CHOLINESTERASE INHIBITORSR03AG014882 · NIA · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 1997 to 1997
–
NIA NIH HHS AG18379NIA NIH HHS AG18884NIA NIH HHS R01 AG018379NIA NIH HHS R01 AG018884NIA NIH HHS R03 AG014882
6 · The paper itself

Abstract

Normal Pressure Hydrocephalus (NPH) is one of the causes of dementia of the elderly characterized by impaired mental function, gait difficulties and urinary incontinence. Previously, it was proposed that some of the NPH patients may develop Alzheimer's disease (AD) like pathology. Aim of this study was to compare levels of different CSF biomarkers, including total secreted β-amyloid precursor protein (sAPP), sAPP-alpha form (sAPPα), amyloid-beta (Aβ) peptide, total-tau protein and hyperphosphorylated-tau protein in subjects from NPH and Non-NPH Control (NNC). CSF was collected from 23 NPH patients and 13 Non-NPH controls by lumber puncture. Western blot analysis was performed to measure levels of sAPP-total. ELISA was used separately to determine levels of sAPPα, Aβ peptide, total-tau and phospho-tau proteins. We found a significant decrease in levels of total secreted APP, sAPPα and Aβ (1-42) in the CSF sample of NPH patients vs. NNC. We did not observe any change in levels of total-tau or phospho-tau in NPH vs. NNC subjects. Notably, phospho-tau level was significantly increased in the NPH patients, who were suffering from the disease for more than one year, vs. NNC. Among five biomarkers studied, decreased sAPP, sAPPα and Aβ (1-42) levels in CSF can be molecular markers to distinguish NPH cases from NNC. Disease severity can also be assessed by increased levels of CSF phospho-tau protein and the ratio of phospho-tau to Aβ (1-42), which might be a useful tool for predicting conversion of NPH individuals to other neurodegenerative disorders including Alzheimer's disease (AD).

Indexed as

Amyloid beta-PeptidesAmyloid beta-Protein PrecursorEnzyme-Linked Immunosorbent AssayFemaleHumansHydrocephalus, Normal PressureMalePeptide FragmentsPhosphorylationStatistics, Nonparametrictau ProteinsAmyloid beta-Peptidesamyloid beta-protein (1-40)amyloid beta-protein (1-42)Amyloid beta-Protein PrecursorPeptide Fragmentstau Proteins

Identifiers

PMID20828718
PMCPMC3813465
OpenAlexW2014240369

What OpenQuestion holds

Textmetadata
LicenceTDM
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.