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Review
. 2025 Jun 21;75(3):81.
doi: 10.1007/s12031-025-02365-0.

The Progress of Cognitive Dysfunction Impairment Caused by Temporal Lobe Epilepsy

Qianqian Wang  1 , Yanguang Geng  1 , Xin Li  1 , Yunhua Hao  2 , Shuqi Huang  3
Affiliations
Review

The Progress of Cognitive Dysfunction Impairment Caused by Temporal Lobe Epilepsy

Qianqian Wang et al. J Mol Neurosci. .

Abstract

Epilepsy is a chronic disease that is characterized primarily by seizures. One of the most common and detrimental comorbidities of epilepsy is cognitive impairment. Approximately, 30-40% of patients with chronic epilepsy experience cognitive impairment, which significantly impacts their daily functioning and quality of life and imposes a heavy burden on both patients and society. Numerous studies have established a correlation between epilepsy and cognitive impairment, showing that epilepsy patients exhibit varying degrees of cognitive deficits influenced by various factors. However, the clinical manifestations, underlying mechanisms, and influencing factors of cognitive impairment in epilepsy patients are still not fully understood. In this review, we aim to summarize and integrate the current understanding of the mechanisms underlying learning and memory impairments in temporal lobe epilepsy (TLE). We summarize the effects of abnormal neuronal discharges, synaptic plasticity alterations, neuroinflammation, and other potential contributors to cognitive dysfunction in TLE.

Keywords: ATF4; BDNF; Cognitive dysfunction; NCAM1; NMDA; Temporal lobe epilepsy.

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Conflict of interest statement

Declarations. During the preparation of this work, the author used LibreChat in order to improve language and readability. After using this tool/service, the author(s) reviewed and edited the content as needed and take(s) full responsibility for the content of the publication. Competing interest: The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Mechanisms and therapeutic targets of TLE-induced cognitive dysfunction
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References

    1. Abarrategui B, Parejo-Carbonell B, Garcia Garcia ME, Di Capua D, Garcia-Morales I (2018) The cognitive phenotype of idiopathic generalized epilepsy. Epilepsy Behav 89:99–104 - PubMed
    1. Ali I, Boets S, Janssens P, Van Eetveldt A, Amhaoul H, Langlois X, Dedeurwaerdere S (2016) Metabotropic glutamate receptor 2/3 density and its relation to the hippocampal neuropathology in a model of temporal lobe epilepsy in rats. Epilepsy Res 127:55–59 - PubMed
    1. Ameri K, Harris AL (2008) Activating transcription factor 4. Int J Biochem Cell Biol 40(1):14–21 - PubMed
    1. Auvin S (2022) Paediatric epilepsy and cognition. Dev Med Child Neurol 64(12):1444–1452 - PubMed
    1. Baleriola J, Walker CA, Jean YY, Crary JF, Troy CM, Nagy PL, Hengst U (2014) Axonally synthesized ATF4 transmits a neurodegenerative signal across brain regions. Cell 158(5):1159–1172 - PMC - PubMed

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