Evidence map›Paper›PMID 23321057›Full record

ReviewEpilepsy & behavior : E&B2013

Shared cognitive and behavioral impairments in epilepsy and Alzheimer's disease and potential underlying mechanisms.

Jeannie Chin, Helen E Scharfman

Abstract readReview
In one paragraph

Review in Epilepsy & behavior : E&B, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 5 pooled it
4.2field-weighted citation impact, top 5% 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

67 citing papers in PubMed, 5 syntheses or guidelines pooled it, 128 citations in OpenAlex.

  1. Pooled it
  2. Treatment of epilepsy for people with Alzheimer's disease.The Cochrane database of systematic reviews · 2021
    Pooled it
  3. Pooled it
  4. Treatment of epilepsy for people with Alzheimer's disease.The Cochrane database of systematic reviews · 2018
    Pooled it
  5. Treatment of epilepsy for people with Alzheimer's disease.The Cochrane database of systematic reviews · 2016
    Pooled it
  6. Article
  7. Frontiers in bioengineering and biotechnology · 2026
    Article
  8. Restoration of sFRP3 Preserves the Neural Stem Cell Pool and Spatial Discrimination Ability in a Mouse Model of Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
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  11. Review
  12. Article
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7 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

2 authors at 2 institutions in 1 country.

Jeannie ChinDepartment of Neuroscience and Farber Institute for Neurosciences, Thomas Jefferson University, Philadelphia, PA, USA. Jeannie.Chin@jefferson.edu
Helen E Scharfman
NYU Langone Health · USThomas Jefferson University · US

Funding

PSYCHOSOCIAL COREP30AG008051 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SHAO, YONGZHAO · 1990 to 2019
$36.1M
Ectopic Granule Cells in the Dentate GyrusR21MH090606 · NIMH · NATHAN S. KLINE INSTITUTE FOR PSYCH RES · PI SCHARFMAN, HELEN E · 2011 to 2012
$429k
NIA NIH HHS P30 AG008051NIMH NIH HHS R21 MH090606
6 · The paper itself

Abstract

Seizures in patients with Alzheimer's disease (AD) have been examined by many investigators over the last several decades, and there are diverse opinions about their potential relevance to AD pathophysiology. Some studies suggest that seizures appear to be a fairly uncommon co-morbidity, whereas other studies report a higher incidence of seizures in patients with AD. It was previously thought that seizures play a minor role in AD pathophysiology because of their low frequency, and also because they may only be noticed during late stages of AD, suggesting that seizures are likely to be a consequence of neurodegeneration rather than a contributing factor. However, clinical reports indicate that seizures can occur early in the emergence of AD symptoms, particularly in familial AD. In this case, seizures may be an integral part of the emerging pathophysiology. This view has been supported by evidence of recurrent spontaneous seizures in transgenic mouse models of AD in which familial AD is simulated. Additional data from transgenic animals suggest that there may be a much closer relationship between seizures and AD than previously considered. There is also evidence that seizures facilitate production of amyloid β (Aβ) and can cause impairments in cognition and behavior in both animals and humans. However, whether seizures play a role in the early stages of AD pathogenesis is still debated. Therefore, it is timely to review the similarities and differences between AD and epilepsy, as well as data suggesting that seizures may contribute to cognitive and behavioral dysfunction in AD. Here we focus on AD and temporal lobe epilepsy (TLE), a particular type of epilepsy that involves the temporal lobe, a region that influences behavior and is critical to memory. We also consider potential neurobiological mechanisms that support the view that the causes of seizures in TLE may be related to the causes of cognitive dysfunction in AD. We suggest that similar underlying mechanisms may exist for at least some of the aspects of AD that are also found in TLE.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsCognition DisordersDisease Models, AnimalEpilepsyHumansMental DisordersMiceAmyloid beta-Peptides

Identifiers

PMID23321057
PMCPMC3924321
OpenAlexW2045534779

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.