Temporal Lobe Epilepsy with Late Onset: Brain Atrophy and AD Biomarkers
Overview
This study examined cortical atrophy patterns and cerebrospinal fluid (CSF) biomarkers of Alzheimer's disease (AD) in patients with late-onset temporal lobe epilepsy (LO-TLE) of unknown origin. LO-TLE patients showed normal CSF amyloid-β and tau levels and no significant brain atrophy compared to healthy controls, contrasting with patients with mild cognitive impairment (MCI) due to AD.
Background
Epilepsy incidence peaks in childhood and after age 50, with late-onset epilepsies (LOEs) increasing due to aging populations. While many LOEs have structural causes, up to 20% lack identifiable etiology and are termed late-onset epilepsy of unknown etiology (LOEU). LOEU, especially temporal lobe forms (LO-TLE), may overlap with neurodegenerative diseases such as AD, as some patients show AD-like CSF biomarker changes and increased risk of dementia. However, the relationship between LO-TLE, brain atrophy, and AD biomarkers remains unclear.
Data Highlights
Group
Number of Patients
Mean Disease Duration (years)
CSF Biomarkers (Aβ, pTau, tTau)
Cortical Atrophy
LO-TLE
20
1.8
Normal values
No significant difference vs. healthy controls
MCI-AD
25
Not specified
Abnormal (decreased Aβ, increased pTau)
Widespread cortico-subcortical atrophy
MCI-noAD
25
Not specified
Normal
Widespread cortico-subcortical atrophy
Healthy Controls
25
N/A
Normal
Baseline reference
Key Findings
LO-TLE patients had normal CSF amyloid-β and tau protein levels, distinct from MCI patients with AD pathology.
No significant differences in cortical thickness or subcortical volumes were observed between LO-TLE patients and healthy controls.
MCI patients, both with and without AD biomarkers, exhibited widespread cortico-subcortical atrophy compared to LO-TLE and controls.
LO-TLE patients had a short disease duration (mean 1.8 years) at the time of assessment.
Findings suggest LO-TLE of unknown origin is not associated with early AD-like neurodegeneration.
Clinical Implications
In patients presenting with late-onset temporal lobe epilepsy without cognitive impairment, normal CSF AD biomarkers and absence of significant brain atrophy may help differentiate LO-TLE from early neurodegenerative processes such as AD. This distinction is important for prognosis and management, indicating that LO-TLE may not represent a prodromal phase of AD in all cases. Routine assessment of CSF biomarkers and MRI morphometry can aid in clinical characterization.
Conclusion
LO-TLE patients with short disease duration exhibit normal AD biomarker profiles and brain morphometry comparable to healthy older adults, suggesting that LO-TLE of unknown etiology is distinct from AD-related neurodegeneration. These findings support the need for biological phenotyping to guide diagnosis and management.
