ArticleNeurology2024
Association of Seizure Foci and Location of Tau and Amyloid Deposition and Brain Atrophy in Patients With Alzheimer Disease and Seizures.
Article in Neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- mTORC2-NaChannels (Austin, Tex.) · 2026Article
- Input-output curves demonstrate motor cortex hyperexcitability associated with cognitive impairment in Alzheimer's disease.Neurobiology of aging · 2026Article
- A comprehensive German claims data analysis of care pathways, risk factors and comorbidities among acetylcholinesterase inhibitor initiators in Alzheimer's disease.Scientific reports · 2026Article
- Patient-Derived PSEN1 Cerebral Organoids Revealed Parallel Development of Amyloid-β Accumulation and Network Dysfunction.Cellular and molecular neurobiology · 2026Article
- Calbindin-D28k deficiency mediates tau-driven hippocampal hyperexcitement and cognitive impairment.Translational neurodegeneration · 2026Article
- Tau accumulation increases the susceptibility to effective seizures of electroconvulsive therapy.Translational psychiatry · 2026Article
- Epilepsy and Alzheimer Disease: Epidemiologic, Clinical, Molecular, and Neuropathologic Convergences and Divergences.Neurology. Clinical practice · 2026Review
- Mesial temporal shape asymmetry as a neuro-imaging correlate of epilepsy in mild cognitive impairment and dementia.Brain communications · 2026Article
- Every-Other-Day Feeding Prevents the Loss of Parvalbumin-Expressing Neurons in the Cerebral Cortex of Female 5xFAD Mice.Molecular neurobiology · 2025Article
- Hemispheric asymmetries in resting-state connectivity: insights from healthy controls and implications for neurological disorders.Brain structure & function · 2025Article
- Hyperactive neuronal networks enhance tau spread in an Alzheimer's disease mouse model.bioRxiv : the preprint server for biology · 2025Article
- Hemispheric asymmetry of tau pathology is related to asymmetric amyloid deposition in Alzheimer's Disease.Nature communications · 2025Article
- Distinct manifestations of excitatory-inhibitory imbalance associated with amyloid-β and tau in patients with Alzheimer's disease.Nature communications · 2025Article
- High-frequency oscillations >250 Hz in people with Down syndrome and associated Alzheimer's disease dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- The Bidirectional Relationship Between Epilepsy and Alzheimer's Disease.Current neurology and neuroscience reports · 2025Review
- Association of Seizure Foci and Location of Tau and Amyloid Deposition and Brain Atrophy in Patients With Alzheimer Disease and Seizures.Neurology · 2025Article
- A case report about focal status epilepticus as first presentation in Alzheimer's disease: finding the culprit.BMC neurology · 2024Article
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Corrections and comments
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12 authors.
Funding
Abstract
BACKGROUND AND
objectivesAlzheimer disease (AD) is associated with a 2 to 3-fold increased risk of developing late-onset focal epilepsy, yet it remains unclear how development of focal epilepsy in AD is related to AD pathology. The objective of this study was to examine spatial relationships between the epileptogenic zone and tau deposition, amyloid deposition, and brain atrophy in individuals with AD who developed late-onset, otherwise unexplained focal epilepsy. We hypothesized that if network hyperexcitability is mechanistically linked to AD pathology, then there would be increased tau and amyloid deposition within the epileptogenic hemisphere.
methodsIn this cross-sectional study, we performed tau and amyloid PET imaging, brain MRI, and overnight scalp EEG in individuals with early clinical stages of AD who developed late-onset, otherwise unexplained focal epilepsy (AD-Ep). Participants were referred from epilepsy and memory disorders clinics at our institutions. We determined epilepsy localization based on EEG findings and seizure semiology. We quantified tau deposition, amyloid deposition, and atrophy across brain regions and calculated asymmetry indices for these measures. We compared findings in AD-Ep with those in a control AD group without epilepsy (AD-NoEp).
resultsThe AD-Ep group included 8 individuals with a mean age of 69.5 ± 4.2 years at PET imaging. The AD-NoEp group included 14 individuals with a mean age of 71.7 ± 9.8 years at PET imaging. In AD-Ep, we found a highly asymmetric pattern of tau deposition, with significantly greater tau in the epileptogenic hemisphere. Amyloid deposition and cortical atrophy were also greater in the epileptogenic hemisphere, although the magnitudes of asymmetry were reduced compared with tau. Compared with AD-NoEp, the AD-Ep group had significantly greater tau asymmetry and trends toward greater asymmetry of amyloid and atrophy. AD-Ep also had significantly greater amyloid burden bilaterally and trends toward greater tau burden within the epileptogenic hemisphere, compared with AD-NoEp. DISCUSSION: Our results reveal a spatial association between the epileptogenic focus and tau deposition, amyloid deposition, and neurodegeneration in early clinical stages of AD. Within the limitations of a cross-sectional study with small sample sizes, these findings contribute to our understanding of the clinicopathologic heterogeneity of AD, demonstrating an association between focal epilepsy and lateralized pathology in AD.
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