Dataset Information

Brain networks and epilepsy development in patients with Alzheimer disease.

ABSTRACT:

Introduction

This study aimed to investigate the association between brain networks and epilepsy development in patients with Alzheimer disease (AD).

Methods

We enrolled patients newly diagnosed with AD at our hospital who underwent three-dimensional T1-weighted magnetic resonance imaging at the time of AD diagnosis and included healthy controls. We obtained the cortical, subcortical, and thalamic nuclei structural volumes using FreeSurfer and applied graph theory to obtain the global brain network and intrinsic thalamic network based on the structural volumes using BRAPH.

Results

We enrolled 25 and 56 patients with AD with and without epilepsy development, respectively. We also included 45 healthy controls. The global brain network differed between the patients with AD and healthy controls. The local efficiency (2.026 vs. 3.185, p = .048) and mean clustering coefficient (0.449 vs. 1.321, p = .024) were lower, whereas the characteristic path length (0.449 vs. 1.321, p = .048) was higher in patients with AD than in healthy controls. Both global and intrinsic thalamic networks were significantly different between AD patients with and without epilepsy development. In the global brain network, local efficiency (1.340 vs. 2.401, p = .045), mean clustering coefficient (0.314 vs. 0.491, p = .045), average degree (27.442 vs. 41.173, p = .045), and assortative coefficient (-0.041 vs. -0.011, p = .045) were lower, whereas the characteristic path length (2.930 vs. 2.118, p = .045) was higher in patients with AD with epilepsy development than in those without. In the intrinsic thalamic network, the mean clustering coefficient (0.646 vs. 0.460, p = .048) was higher, whereas the characteristic path length (1.645 vs. 2.232, p = .048) was lower in patients with AD with epilepsy development than in those without.

Conclusion

We found that the global brain network differs between patients with AD and healthy controls. In addition, we demonstrated significant associations between brain networks (both global brain and intrinsic thalamic networks) and epilepsy development in patients with AD.

SUBMITTER: Lee DA

PROVIDER: S-EPMC10454249 | biostudies-literature | 2023 Aug

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Brain networks and epilepsy development in patients with Alzheimer disease.

Lee Dong Ah DA Lee Ho-Joon HJ Kim Si Eun SE Park Kang Min KM

Brain and behavior 20230707 8

<h4>Introduction</h4>This study aimed to investigate the association between brain networks and epilepsy development in patients with Alzheimer disease (AD).<h4>Methods</h4>We enrolled patients newly diagnosed with AD at our hospital who underwent three-dimensional T1-weighted magnetic resonance imaging at the time of AD diagnosis and included healthy controls. We obtained the cortical, subcortical, and thalamic nuclei structural volumes using FreeSurfer and applied graph theory to obtain the gl ...[more]

PMID: 37416994

Similar Datasets

Project description:Spontaneous mental activity is characterized by dynamic alterations of discrete and stabile brain states called functional microstates that are thought to represent distinct steps of human information processing. Electroencephalography (EEG) directly reflects functioning of brain synapses with a uniquely high temporal resolution, necessary for investigation of brain network dynamics. Since synaptic dysfunction is an early event and best correlate of cognitive status and decline in patients along Alzheimer's disease (AD) continuum, EEG microstates might serve as valuable early markers of AD. The present study investigated differences in EEG microstate topographies and parameters (duration, occurrence and contribution) between a large cohort of healthy elderly (n = 308) and memory clinic patients: subjective cognitive decline (SCD, n = 210); mild cognitive impairment (MCI, n = 230) and AD (n = 197) and how they correlate to conventional cerebrospinal fluid (CSF) markers of AD. Four most representative microstate maps assigned as classes A, B (asymmetrical), C and D (symmetrical) were computed from the resting state EEGs since it has been shown previously that this is sufficient to explain most of the resting state EEG data. Statistically different topography of microstate maps were found between the controls and the patient groups for microstate classes A, C and D. Changes in the topography of microstate class C were associated with the CSF Aβ42 levels, whereas changes in the topography of class B were linked with the CSF p-tau levels. Gradient-like increase in the contribution of asymmetrical (A and B) and gradient-like decrease in the contribution of symmetrical (C and D) maps were observed with the more severe stage of cognitive impairment. Our study demonstrated extensive relationship of resting state EEG microstates topographies and parameters with the stage of cognitive impairment and AD biomarkers. Resting state EEG microstates might therefore serve as functional markers of early disruption of neurocognitive networks in patients along AD continuum.

Project description:Background and objectivesObservational studies suggested a bidirectional relationship between Alzheimer disease (AD) and epilepsies. However, it remains debated whether and in which direction a causal association exists. This study aims to explore the relationship between genetic predisposition to AD, CSF biomarkers of AD (β-amyloid [Aβ] 42 and phosphorylated tau [pTau]), and epilepsies with 2-sample, bidirectional Mendelian randomization (MR) method.MethodsGenetic instruments were obtained from large-scale genome-wide meta-analysis of AD (Ncase/proxy = 111,326, Ncontrol = 677,663), CSF biomarkers of AD (Aβ42 and pTau, N = 13,116), and epilepsy (Ncase = 15,212, Ncontrol = 29,677) of European ancestry. Epilepsy phenotypes included all epilepsy, generalized epilepsy, focal epilepsy, childhood absence epilepsy, juvenile absence epilepsy, juvenile myoclonic epilepsy, generalized epilepsy with tonic-clonic seizures, focal epilepsy with hippocampal sclerosis (focal HS), and lesion-negative focal epilepsy. Main analyses were performed using generalized summary data-based MR. Sensitivity analyses included inverse variance weighted, MR pleiotropy residual sum and outlier, MR-Egger, weighted mode, and weighted median.ResultsFor forward analysis, genetic predisposition to AD was associated with an increased risk of generalized epilepsy (odds ratio [OR] 1.053, 95% CI 1.002-1.105, p = 0.038) and focal HS (OR 1.013, 95% CI 1.004-1.022, p = 0.004). These associations were consistent across sensitivity analyses and replicated using a separate set of genetic instruments from another AD genome-wide association study. For reverse analysis, there was a suggestive effect of focal HS on AD (OR 3.994, 95% CI 1.172-13.613, p = 0.027). In addition, genetically predicted lower CSF Aβ42 was associated with an increased risk of generalized epilepsy (β = 0.090, 95% CI 0.022-0.158, p = 0.010).DiscussionThis MR study supports a causal link between AD, amyloid pathology, and generalized epilepsy. This study also indicates a close association between AD and focal HS. More effort should be made to screen seizure in AD, unravel its clinical implications, and explore its role as a putative modifiable risk factor.

Dataset Information

Brain networks and epilepsy development in patients with Alzheimer disease.

Introduction

Methods

Results

Conclusion

Publications

Brain networks and epilepsy development in patients with Alzheimer disease.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets