Evidence map›Paper›PMID 20062810›Full record

ArticlePloS one2010

A new target for amyloid beta toxicity validated by standard and high-throughput electrophysiology.

Kucku Varghese, Peter Molnar, Mainak Das, Neelima Bhargava, Stephen Lambert, Mark S Kindy, James J Hickman

Abstract readValidation Study
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
–field-weighted citation impact
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

33 citing papers in PubMed.

  1. Article
  2. Article
  3. Impact Induces Phagocytic Defect in Reactive Microglia.bioRxiv : the preprint server for biology · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Frontiers in pharmacology · 2018
    Article
  16. Review
  17. Article
  18. Oligomerization Alters Binding Affinity Between Amyloid Beta and a Modulator of Peptide Aggregation.The journal of physical chemistry. C, Nanomaterials and interfaces · 2017
    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

7 authors.

Kucku VargheseNanoScience Technology Center, University of Central Florida, Orlando, Florida, United States of America.
Peter Molnar
Mainak Das
Neelima Bhargava
Stephen Lambert
Mark S Kindy
James J Hickman

Funding

High-throughput Electrophysiology for Pathway IdentificationR01EB005459 · NIBIB · UNIVERSITY OF CENTRAL FLORIDA · PI HICKMAN, JAMES J · 2006 to 2008
$1.3M
NIBIB NIH HHS 5R01EB005459NIBIB NIH HHS R01 EB005459
6 · The paper itself

Abstract

backgroundSoluble oligomers of amyloid beta (Abeta) are considered to be one of the major contributing factors to the development of Alzheimer's disease. Most therapeutic development studies have focused on toxicity directly at the synapse. METHODOLOGY/PRINCIPAL

findingsPatch clamp studies detailed here have demonstrated that soluble Abeta can also cause functional toxicity, namely it inhibits spontaneous firing of hippocampal neurons without significant cell death at low concentrations. This toxicity will eventually lead to the loss of the synapse as well, but may precede this loss by a considerable amount of time. In a key technological advance we have reproduced these results utilizing a fast and simple method based on extracellular electrophysiological recording of the temporal electrical activity of cultured hippocampal neurons using multielectrode arrays (MEAs) at low concentrations of Abeta (1-42). We have also shown that this functional deficit can be reversed through use of curcumin, an inhibitor of Abeta oligomerization, using both analysis methods. CONCLUSIONS/SIGNIFICANCE: The MEA recording method utilized here is non-invasive, thus long term chronic measurements are possible and it does not require precise positioning of electrodes, thus it is ideal for functional screens. Even more significantly, we believe we have now identified a new target for drug development for AD based on functional toxicity of hippocampal neurons that could treat neurodegenerative diseases prior to the development of mild cognitive impairment.

Indexed as

Action PotentialsAmyloid beta-PeptidesAnimalsCurcuminHippocampusPatch-Clamp TechniquesRatsSynapsesAmyloid beta-PeptidesCurcumin

Identifiers

PMID20062810
PMCPMC2799531

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.