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Epilepsy and Alzheimer Disease: Epidemiologic, Clinical, Molecular, and Neuropathologic Convergences and Divergences
Devinsky O, Leitner DF, Kamondi A, Wisniewski T.. Neurology. Clinical practice, 2026-02-26
Topic: Amyloid, tau and blood-test diagnosis
Purpose of review Alzheimer disease (AD) and epilepsy are major causes of neurologic disability and are reciprocally related: epileptiform discharges, subclinical seizures, and epilepsy are more prevalent in patients with AD compared with controls; progressive cognitive impairment commonly afflicts epilepsy patients; and late-onset epilepsy patients have higher rates of new-onset dementia. Recent findings Epidemiologic studies support shared risk factors (e.g., genetic variants, vascular disease, sleep disorders, microbiome) with notable divergences. AD and epilepsy have some overlapping anatomic (e.g., hippocampus, entorhinal, and association cortex), clinical (e.g., memory, attentional, and executive) impairments, and neuropathologic (e.g., amyloid, tau, neurofibrillary tangles) features.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Devinsky, O., Leitner, D. F., Kamondi, A., & Wisniewski, T. (2026). Epilepsy and Alzheimer Disease: Epidemiologic, Clinical, Molecular, and Neuropathologic Convergences and Divergences. Neurology. Clinical practice. https://doi.org/10.1212/cpj.0000000000200589
Vancouver
Devinsky O, Leitner DF, Kamondi A, Wisniewski T. Epilepsy and Alzheimer Disease: Epidemiologic, Clinical, Molecular, and Neuropathologic Convergences and Divergences. Neurology. Clinical practice. 2026. doi:10.1212/cpj.0000000000200589. PMID: 41766754.
BibTeX
@article{devinsky2026-41766754,
author = {Devinsky, O. and Leitner, D. F. and Kamondi, A. and Wisniewski, T.},
title = {{Epilepsy and Alzheimer Disease: Epidemiologic, Clinical, Molecular, and Neuropathologic Convergences and Divergences}},
journal = {Neurology. Clinical practice},
year = {2026},
doi = {10.1212/cpj.0000000000200589},
pmid = {41766754},
url = {https://doi.org/10.1212/cpj.0000000000200589}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- Recent findings Epidemiologic studies support shared risk factors (e.g., genetic variants, vascular disease, sleep disorders, microbiome) with notable divergences.
- AD and epilepsy have some overlapping anatomic (e.g., hippocampus, entorhinal, and association cortex), clinical (e.g., memory, attentional, and executive) impairments, and neuropathologic (e.g., amyloid, tau, neurofibrillary tangles) features.
- Shared clinical and translational challenges include underlying mechanisms (e.g., genetic variants, neuroinflammation, metabolic and mitochondrial dysfunction, excitatory/inhibitory imbalance, microbiome, and sociodemographic factors) and identifying valid and reliable biomarkers (e.g., total tau and phosphorylated tau (p-tau), amyloid deposition, Aβ42/Aβ40 ratio) to assess disease progression, predict outcomes, and assess potentially disease-modifying interventions.
- Summary Identifying convergences and divergences between epilepsy and AD may inform our understanding.
Why it matters
This review describes shared risk factors and overlapping brain, clinical, and pathological features between Alzheimer's disease and epilepsy, along with notable differences. It does not report any treatment, cure, or prevention, and the shared mechanisms remain unresolved challenges.
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Study details
- Evidence strengthLow
How this study scored 39/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neurology. Clinical practice) |
| Journal's citation record | 0 / 4 | Neurology Clinical Practice: journal h-index 60 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 5 / 5 | 2026 — within 1 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 1 / 7 | Cited 2 times (OpenAlex, 2026-10-10) |
| Citations per year | 1 / 5 | 1.0 citations a year over 2 year(s) since 2026 |
| Impact for its field and year | 4 / 6 | Cited 9.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 0 / 4 | Cited 2 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Thomas Wısnıewskı: h-index 93 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | New York University: institution h-index 1,612 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 41766754) |
| Free to read | 2 / 2 | Free to read |
| Total | 39 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1212/cpj.0000000000200589
- PubMed: 41766754
- Original source →
- Free full text: Neurology Clinical Practice →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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