Epilepsy in Early Onset Alzheimer’s Disease

Haoudy, Sarah; Jonveaux, Thérèse Rivasseau; Puisieux, Salomé; Epstein, Jonathan; Hopes, Lucie; Maillard, Louis; Aron, Olivier; Tyvaert, Louise

doi:10.3233/jad-210681

Cited by 9 publications

(2 citation statements)

References 55 publications

(25 reference statements)

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“…Patients with AD can also have generalized tonic–clonic seizures, as well. In 10 early onset Alzheimer’s disease (EOAD) patients with epilepsy, seizure types included generalized onset tonic-clonic seizures (25%), temporal lobe seizures (25%), myoclonus (25%), focal onset extra-temporal seizures (8%), and other types (17%) ( 37 ).…”

Section: Seizure Semiology and Clinical Course In Alzheimer’s Diseasementioning

confidence: 99%

Alzheimer’s disease and epilepsy: shared neuropathology guides current and future treatment strategies

Lu,

Kouser,

Skylar-Scott

2023

Front. Neurol.

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Epilepsy is a cause of profound disability in patients with Alzheimer’s disease (AD). The risk of being diagnosed with AD increases the risk for epilepsy, and in parallel, a history of epilepsy increases the likelihood of the development of AD. This bi-directional relationship may be due to underlying shared pathophysiologic hallmarks, including decreased cerebrospinal fluid amyloid beta 42 (Aβ42), increased hyperphosphorylated tau protein, and hippocampal hyperexcitability. Additionally, there are practical treatment considerations in patients with co-morbid AD and epilepsy—namely, there is a higher risk of seizures associated with medications commonly prescribed for Alzheimer’s disease patients, including antidepressants and antipsychotics such as trazodone, serotonin norepinephrine reuptake inhibitors (SNRIs), and first-generation neuroleptics. Anti-amyloid antibodies like aducanumab and lecanemab present new and unique considerations in patients with co-morbid AD and epilepsy given the risk of seizures associated with amyloid-related imaging abnormalities (ARIA) seen with this drug class. Finally, we identify and detail five active studies, including two clinical trials of levetiracetam in the respective treatment of cognition and neuropsychiatric features of AD, a study characterizing the prevalence of epilepsy in AD via prolonged EEG monitoring, a study characterizing AD biomarkers in late-onset epilepsy, and a study evaluating hyperexcitability in AD. These ongoing trials may guide future clinical decision-making and the development of novel therapeutics.

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Section: Seizure Semiology and Clinical Course In Alzheimer’s Diseasementioning

confidence: 99%

Alzheimer’s disease and epilepsy: shared neuropathology guides current and future treatment strategies

Lu,

Kouser,

Skylar-Scott

2023

Front. Neurol.

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“…Younger AD patients were found to be more likely to have unprovoked seizures, with a 87-fold increase in the age group of 50–59 years as compared to the age-matched general population [ 18 ]. Epilepsy has been stated as a frequent comorbidity in early-onset AD [ 19 ]. A recent study by Horvath et al confirmed that AD patients with epileptic discharges on EEG and/or epileptic seizures had a dementia onset at a younger age.…”

Section: Introductionmentioning

confidence: 99%

Subclinical epileptiform activity in the Alzheimer continuum: association with disease, cognition and detection method

Nous,

Seynaeve,

Feys

et al. 2024

Alz Res Therapy

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Background Epileptic seizures are an established comorbidity of Alzheimer’s disease (AD). Subclinical epileptiform activity (SEA) as detected by 24-h electroencephalography (EEG) or magneto-encephalography (MEG) has been reported in temporal regions of clinically diagnosed AD patients. Although epileptic activity in AD probably arises in the mesial temporal lobe, electrical activity within this region might not propagate to EEG scalp electrodes and could remain undetected by standard EEG. However, SEA might lead to faster cognitive decline in AD. Aims 1. To estimate the prevalence of SEA and interictal epileptic discharges (IEDs) in a well-defined cohort of participants belonging to the AD continuum, including preclinical AD subjects, as compared with cognitively healthy controls. 2. To evaluate whether long-term-EEG (LTM-EEG), high-density-EEG (hd-EEG) or MEG is superior to detect SEA in AD. 3. To characterise AD patients with SEA based on clinical, neuropsychological and neuroimaging parameters. Methods Subjects (n = 49) belonging to the AD continuum were diagnosed according to the 2011 NIA-AA research criteria, with a high likelihood of underlying AD pathophysiology. Healthy volunteers (n = 24) scored normal on neuropsychological testing and were amyloid negative. None of the participants experienced a seizure before. Subjects underwent LTM-EEG and/or 50-min MEG and/or 50-min hd-EEG to detect IEDs. Results We found an increased prevalence of SEA in AD subjects (31%) as compared to controls (8%) (p = 0.041; Fisher’s exact test), with increasing prevalence over the disease course (50% in dementia, 27% in MCI and 25% in preclinical AD). Although MEG (25%) did not withhold a higher prevalence of SEA in AD as compared to LTM-EEG (19%) and hd-EEG (19%), MEG was significantly superior to detect spikes per 50 min (p = 0.002; Kruskall–Wallis test). AD patients with SEA scored worse on the RBANS visuospatial and attention subset (p = 0.009 and p = 0.05, respectively; Mann–Whitney U test) and had higher left frontal, (left) temporal and (left and right) entorhinal cortex volumes than those without. Conclusion We confirmed that SEA is increased in the AD continuum as compared to controls, with increasing prevalence with AD disease stage. In AD patients, SEA is associated with more severe visuospatial and attention deficits and with increased left frontal, (left) temporal and entorhinal cortex volumes. Trial registration Clinicaltrials.gov, NCT04131491. 12/02/2020.

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Poly (ADP-Ribose) polymerase 1 and parthanatos in neurological diseases: From pathogenesis to therapeutic opportunities

Xu,

Sun,

Zhao

2023

Neurobiology of Disease

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Epilepsy in Early Onset Alzheimer’s Disease

Cited by 9 publications

References 55 publications

Alzheimer’s disease and epilepsy: shared neuropathology guides current and future treatment strategies

Alzheimer’s disease and epilepsy: shared neuropathology guides current and future treatment strategies

Subclinical epileptiform activity in the Alzheimer continuum: association with disease, cognition and detection method

Poly (ADP-Ribose) polymerase 1 and parthanatos in neurological diseases: From pathogenesis to therapeutic opportunities

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