Evidence map›Paper›PMID 33929683›Full record

ReviewNeurochemical research2021

Alzheimer's Disease and Epilepsy: A Perspective on the Opportunities for Overlapping Therapeutic Innovation.

Leanne Lehmann, Alexandria Lo, Kevin M Knox, Melissa Barker-Haliski

Open access · hybridAbstract readReview
In one paragraph

Review in Neurochemical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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  6. bioRxiv : the preprint server for biology · 2026
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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 1 institution in 1 country.

Leanne Lehmann *Undergraduate Neuroscience Program, University of Washington, Seattle, WA, 98195, USA.
Alexandria Lo *Department of Public Health-Global Health, School of Public Health, University of Washington, Seattle, WA, 98195, USA.
Kevin M KnoxDepartment of Pharmacy, School of Pharmacy, University of Washington, Seattle, WA, 98195, USA.
Melissa Barker-HaliskiDepartment of Pharmacy, School of Pharmacy, University of Washington, Seattle, WA, 98195, USA. mhaliski@uw.edu.ORCID http://orcid.org/0000-0002-8175-0553
University of Washington · US

Funding

Transform Dissemination and Implementation Science in CTSA ProgramsUL1TR002319 · NCATS · UNIVERSITY OF WASHINGTON · PI John K. Amory · 2017 to 2026
$100.0M
NCCIH Supplement to NCATS/CTSA Program for KL2 Scholars - M. SoddersKL2TR002317 · NCATS · UNIVERSITY OF WASHINGTON · PI Christy Michelle McKinney · 2017 to 2026
$14.5M
Impact of Chronic Seizures on Neuropsychiatric Comorbidities in AD-Associated ModelsR01AG067788 · NIA · UNIVERSITY OF WASHINGTON · PI BARKER-HALISKI, MELISSA LEIGH · 2020 to 2024
$1.9M
National Institute on Aging (US) 1R01AG067788NCATS NIH HHS 5UL1TR002319NCATS NIH HHS KL2 TR002317NCATS NIH HHS UL1 TR002319NIA NIH HHS R01 AG067788
6 · The paper itself

Abstract

Early-onset Alzheimer's disease (AD) is associated with variants in amyloid precursor protein (APP) and presenilin (PSEN) 1 and 2. It is increasingly recognized that patients with AD experience undiagnosed focal seizures. These AD patients with reported seizures may have worsened disease trajectory. Seizures in epilepsy can also lead to cognitive deficits, neuroinflammation, and neurodegeneration. Epilepsy is roughly three times more common in individuals aged 65 and older. Due to the numerous available antiseizure drugs (ASDs), treatment of seizures has been proposed to reduce the burden of AD. More work is needed to establish the functional impact of seizures in AD to determine whether ASDs could be a rational therapeutic strategy. The efficacy of ASDs in aged animals is not routinely studied, despite the fact that the elderly represents the fastest growing demographic with epilepsy. This leaves a particular gap in understanding the discrete pathophysiological overlap between hyperexcitability and aging, and AD more specifically. Most of our preclinical knowledge of hyperexcitability in AD has come from mouse models that overexpress APP. While these studies have been invaluable, other drivers underlie AD, e.g. PSEN2. A diversity of animal models should be more frequently integrated into the study of hyperexcitability in AD, which could be particularly beneficial to identify novel therapies. Specifically, AD-associated risk genes, in particular PSENs, altogether represent underexplored contributors to hyperexcitability. This review assesses the available studies of ASDs administration in clinical AD populations and preclinical studies with AD-associated models and offers a perspective on the opportunities for further therapeutic innovation.

Indexed as

AgingAlzheimer DiseaseAnimalsAnticonvulsantsComorbidityEpilepsyHumansMutationPresenilin-1Presenilin-2SeizuresAnticonvulsantsPresenilin-1Presenilin-2Alzheimer’s diseaseAnimal modelsAntiseizure drugsCognitive declineEpilepsy

Identifiers

PMID33929683
PMCPMC8254705
OpenAlexW3158179630

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.