ArticleAlzheimer's research & therapy2015
Brivaracetam, but not ethosuximide, reverses memory impairments in an Alzheimer's disease mouse model.
Article in Alzheimer's research & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
What it found
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Who cites it
52 citing papers in PubMed, 95 citations in OpenAlex.
- Spike-wave discharges are uncoupled with cognitive outcome in aged Long-Evans rats.Psychopharmacology · 2026Article
- Cognitive and Neurochemical Effects of Brivaracetam Co-Administered with Ethanol: A Preclinical Study.International journal of molecular sciences · 2026Article
- Levetiracetam prevents Aβ production through SV2a-dependent modulation of APP processing in Alzheimer's disease models.Science translational medicine · 2026Article
- ZCCHC17: a target for synaptic dysfunction and neuronal excitability in Alzheimer's disease.Frontiers in aging neuroscience · 2026Review
- Brivaracitam Ameliorates Increased Inflammation, Oxidative Stress, and Acetylcholinesterase Activity in Ischemic Mice.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2025Article
- Brivaracetam and rufinamide combination increased seizure threshold and improved neurobehavioral deficits in corneal kindling model of epilepsy.Animal models and experimental medicine · 2025Article
- Article
- Hyperfunction of post-synaptic density protein 95 promotes seizure response in early-stage aβ pathology.EMBO reports · 2024Article
- Epilepsy and epileptiform activity in late-onset Alzheimer disease: clinical and pathophysiological advances, gaps and conundrums.Nature reviews. Neurology · 2024Review
- The impact of brivaracetam on cognitive processes and anxiety in various experimental models.Pharmacological reports : PR · 2024Article
- Alzheimer's disease and synapse Loss: What can we learn from induced pluripotent stem Cells?Journal of advanced research · 2023Review
- Alzheimer risk-increasing TREM2 variant causes aberrant cortical synapse density and promotes network hyperexcitability in mouse models.Neurobiology of disease · 2023Article
- Antiseizure Medications in Alzheimer's Disease from Preclinical to Clinical Evidence.International journal of molecular sciences · 2023Review
- A review of cognitive and behavioral outcomes of Brivaracetam.The Kaohsiung journal of medical sciences · 2023Review
- Etiology and Clinical Significance of Network Hyperexcitability in Alzheimer's Disease: Unanswered Questions and Next Steps.Journal of Alzheimer's disease : JAD · 2023Review
- Traditional and Innovative Anti-seizure Medications Targeting Key Physiopathological Mechanisms: Focus on Neurodevelopment and Neurodegeneration.Current neuropharmacology · 2023Article
- Aberrant protein S-nitrosylation contributes to hyperexcitability-induced synaptic damage in Alzheimer's disease: Mechanistic insights and potential therapies.Frontiers in neural circuits · 2023Review
- Higher susceptibility to 6 Hz corneal kindling and lower responsiveness to antiseizure drugs in mouse models of Alzheimer's disease.Epilepsia · 2022Article
- Alzheimer's disease and epilepsy: An increasingly recognized comorbidity.Frontiers in aging neuroscience · 2022Review
- The clinical correlation between Alzheimer's disease and epilepsy.Frontiers in neurology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
introductionRecent studies have shown that several strains of transgenic Alzheimer's disease (AD) mice overexpressing the amyloid precursor protein (APP) have cortical hyperexcitability, and their results have suggested that this aberrant network activity may be a mechanism by which amyloid-β (Aβ) causes more widespread neuronal dysfunction. Specific anticonvulsant therapy reverses memory impairments in various transgenic mouse strains, but it is not known whether reduction of epileptiform activity might serve as a surrogate marker of drug efficacy for memory improvement in AD mouse models.
methodsTransgenic AD mice (APP/PS1 and 3xTg-AD) were chronically implanted with dural electroencephalography electrodes, and epileptiform activity was correlated with spatial memory function and transgene-specific pathology. The antiepileptic drugs ethosuximide and brivaracetam were tested for their ability to suppress epileptiform activity and to reverse memory impairments and synapse loss in APP/PS1 mice.
resultsWe report that in two transgenic mouse models of AD (APP/PS1 and 3xTg-AD), the presence of spike-wave discharges (SWDs) correlated with impairments in spatial memory. Both ethosuximide and brivaracetam reduce mouse SWDs, but only brivaracetam reverses memory impairments in APP/PS1 mice.
conclusionsOur data confirm an intriguing therapeutic role of anticonvulsant drugs targeting synaptic vesicle protein 2A across AD mouse models. Chronic ethosuximide dosing did not reverse spatial memory impairments in APP/PS1 mice, despite reduction of SWDs. Our data indicate that SWDs are not a reliable surrogate marker of appropriate target engagement for reversal of memory dysfunction in APP/PS1 mice.
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Registered trials
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.