New Insights on Temporal Lobe Epilepsy Based on Plasticity-Related Network Changes and High-Order Statistics

Abstract

Epilepsy is a disorder of the brain characterized by the predisposition to generate recurrent unprovoked seizures, which involves reshaping of neuronal circuitries based on intense neuronal activity. In this review, we first detailed the regulation of plasticity-associated genes, such as ARC, GAP-43, PSD-95, synapsin, and synaptophysin. Indeed, reshaping of neuronal connectivity after the primary, acute epileptogenesis event increases the excitability of the temporal lobe. Herein, we also discussed the heterogeneity of neuronal populations regarding the number of synaptic connections, which in the theoretical field is commonly referred as degree. Employing integrate-and-fire neuronal model, we determined that in addition to increased synaptic strength, degree correlations might play essential and unsuspected roles in the control of network activity. Indeed, assortativity, which can be described as a condition where high-degree correlations are observed, increases the excitability of neural networks. In this review, we summarized recent topics in the field, and data were discussed according to newly developed or unusual tools, as provided by mathematical graph analysis and high-order statistics. With this, we were able to present new foundations for the pathological activity observed in temporal lobe epilepsy.

Celastrol Attenuates Learning and Memory Deficits in an Alzheimer’s Disease Rat Model

“…Previous studies have shown that transsynaptic Nrx1b-NL1 interactions enhance the PSD95-dependent recruitment of postsynaptic molecules in the hippocampus [33][34][35]. Additionally, synaptic protein synapsin and postsynaptic protein PSD95 are indicators of synaptic structure and have previously been used to evaluate neuroplasticity [36]. Therefore, we observed the expression of neurexins, neuroligins, synapsin, and PSD95.…”

Cortical microstructural gradients capture memory network reorganization in temporal lobe epilepsy

“…For instance, different growth-associated proteins are predominantly expressed in limbic and association cortices during adulthood relative to primary sensory and motor cortices 91,104,105 . However, this increased plasticity may render limbic areas more vulnerable to pathology 91 and create a favourable context for the emergence of more widespread microstructural anomalies and associated epileptogenic networks within these regions 106 . For instance, animal models of TLE have shown that increased plasticity (e.g., indexed by the increased expression of molecules such as GAP-43) may contribute to the development of epileptogenic networks and the early stages of mossy fibre sprouting [107][108][109] .…”

Dynamic Network Connectivity Reveals Markers of Response to Deep Brain Stimulation in Parkinson’s Disease

“…As a measure of network resilience, assortativity may be interpreted as the ability of the brain to efficiently transfer information throughout the entire network. While assortativity has been found to decline in multiple sclerosis and neurodegenerative diseases; (Bahrami and Hossem-Zadeh, 2015;Llufriu et al, 2019) it has also been noted to be elevated in pathologies with hyperexcitable states, such as epilepsy and chronic insomnia (Kinjo et al, 2018;Li et al, 2018;Lim et al, 2019). While use of network assortativity has been limited in PD, one study reported a positive correlation between assortativity and cognitive performance in PD (Lin et al, 2018).…”