Evidence map›Paper›PMID 40890882›Full record

ArticleAlzheimer's research & therapy2025

Disruption of electrophysiological rhythms and memory impairment in an Alzheimer's transgenic rat model.

Xiaoxiao Tao, Udaya Kumar, Miaomiao Wang, Kapil Manglani, Cansheng Zhu, Mychica R Jones, Alexander Bombino, Anatol Bragin, Gregory Cole, Keith Vossel and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Alzheimer's research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

13 authors.

Xiaoxiao TaoDepartment of Biomedical Engineering, University of North Texas, Denton, TX, 76207, USA.
Udaya KumarDepartment of Neurology, University of California, Los Angeles, CA, 90095, USA.
Miaomiao WangDepartment of Biomedical Engineering, University of North Texas, Denton, TX, 76207, USA.
Kapil ManglaniGeriatric Research, Education and Clinical Center, Veterans Greater Los Angeles Healthcare System, Los Angeles, CA, 90073, USA.
Cansheng ZhuGeriatric Research, Education and Clinical Center, Veterans Greater Los Angeles Healthcare System, Los Angeles, CA, 90073, USA.
Mychica R JonesGeriatric Research, Education and Clinical Center, Veterans Greater Los Angeles Healthcare System, Los Angeles, CA, 90073, USA.
Alexander BombinoGeriatric Research, Education and Clinical Center, Veterans Greater Los Angeles Healthcare System, Los Angeles, CA, 90073, USA.
Anatol BraginDepartment of Neurology, University of California, Los Angeles, CA, 90095, USA.
Gregory ColeDepartment of Neurology, University of California, Los Angeles, CA, 90095, USA.
Keith VosselDepartment of Neurology, University of California, Los Angeles, CA, 90095, USA.
Jerome EngelDepartment of Neurology, University of California, Los Angeles, CA, 90095, USA.
Sally A FrautschyDepartment of Neurology, University of California, Los Angeles, CA, 90095, USA. sfrautschy@mednet.ucla.edu.
Lin LiDepartment of Biomedical Engineering, University of North Texas, Denton, TX, 76207, USA. Lin.li@unt.edu.

Funding

IN VIVO STUDIES OF THE EPILEPTIC HIPPOCAMPUSR01NS033310 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI JEROME NONE ENGEL, Richard Staba · 1994 to 2026
$7.5M
Metabolic and Vascular Factors in tau pathogenesisR01AG066212 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FRAUTSCHY, SALLY ANN · 2020 to 2024
$3.4M
Preventing Seizures and Associated Memory Loss in Alzheimer's Disease by Blocking Tau Interactions with SH3-containing Proteins.R01AG058820 · NIA · UNIVERSITY OF MINNESOTA · PI VOSSEL, KEITH ALAN · 2019 to 2023
$1.9M
New approach for identification pHFO networks to predict epileptogenesisR16NS131108 · NINDS · UNIVERSITY OF NORTH TEXAS · PI Lin Li · 2022 to 2026
$1.3M
BLRD VA I01 BX004332BLRD VA I01 BX005919National Institute of Aging R01-AG058820NIA NIH HHS R01 AG058820NIA NIH HHS R01 AG066212NIA NIH HHS R01AG066212NINDS NIH HHS 1R16-NS131108-01NINDS NIH HHS R01 NS033310NINDS NIH HHS R01-NS033310NINDS NIH HHS R16 NS131108VA Merit 1 I01 BX005919-01VA Merit BX004332-01
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is one of the most prevalent causes of dementia, characterized by progressive memory loss and cognitive decline. Abnormal electrophysiological patterns, especially interictal epileptiform discharges (IEDs) and high-frequency oscillations (HFOs), have been observed in mouse models of AD and are suggested to contribute to cognitive dysfunction. However, comprehensive evaluations of IEDs across different brain regions are limited, and their impact on cognitive performance and neuropathology remains unclear, particularly in more complex AD models with relevant comorbidities. To address this gap, our study aims to clarify how IEDs and HFOs contribute to cognitive decline and neuropathology in AD, potentially informing the development of new biomarkers for early detection.

methodsWe investigate these effects in an AD (PS1/APP) rat model (FAD+) with coexisting hypertension-associated small vessel disease (SVD), as well as in their transgene-negative littermates (FAD-). We conducted behavioral experiments at 6, 8, and 11 months of animal age, alongside neural signal recordings at 8 and 11 months. AD pathology (neuritic plaques and hyperphosphorylated tau) and novel biomarkers (14-3-3γ) or biomarkers common to both disorders (neuropeptide Y, astrocyte and microglia) were evaluated at the end of the experiment.

resultsSeizures were observed in three out of 14 FAD + rats. IED rates were significantly greater in FAD + rats compared to FAD- at all tested periods, correlating with changes in neuropathological biomarkers. Furthermore, coupling strength between IEDs and HFOs was significantly elevated in FAD + rats, especially during the later stages of disease progression. In addition, FAD + rats exhibited deficits in both learning and recall abilities at both ages, which correlated most strongly with increased IED-HFO coupling strength. No such correlation was observed in the FAD- group.

conclusionOur findings suggest that pathological synchronization between IEDs and HFOs in the hippocampus, along with neuropathological changes in both the hippocampus and entorhinal cortex, may contribute to memory dysfunction in AD, highlighting a potential mechanistic link between epileptiform activity, AD biomarker changes, and cognitive decline.

Indexed as

Alzheimer DiseaseBrainMemory DisordersAnimalsDisease Models, AnimalElectroencephalographyMaleRatsRats, TransgenicAlzheimer’s diseaseAβ-immunoreactive plaquesHigh-frequency oscillationsInterictal epileptic spikespTau217 pathology

Identifiers

PMID40890882
PMCPMC12403914

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Registered trials

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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.