Depression can seriously affect the quality of life of epileptic patients and can even lead to suicide. Understanding the regularity, prevention and treatment of depression in patients with epilepsy (PWE) contributes to the improvement of their quality of life. Areas covered: In this paper, we retrospectively analyzed the relevant literature on the pathogenesis, related factors, clinical characteristics, diagnosis and treatment of depression in PWE. A literature search utilized the PubMed, Embase and Google Scholar databases. Expert commentary: PWE often have depression, which can be the result of seizures, antiepileptic drugs (AEDs) or social-demographic factors. It needs to be better understood, and the diagnosis should be more comprehensive for early treatment.

Primary central nervous system lymphoma is an invasive malignant lymphoma confined to the central nervous system. Although patients undergoing first-line treatment can achieve complete response, most of them still relapse within two years. Relapsed lymphoma is derived from occult lymphoma cells, and B cell receptor pathway activation and immune escape are the key mechanisms for the pathogenesis of PCNSL. Most relapses are in the central nervous system, a small number of relapses are isolated systemic relapses, and clinical symptoms occur early and vary. Current treatments for relapse include high-dose methotrexate rechallenge and other regimens of chemotherapy, whole-brain radiation therapy, hematopoietic stem-cell transplantation, targeted therapy and immunotherapy, which have become promising treatments. The overall prognosis of relapsed PCNSL is very poor, although it is affected by many factors. This article summarizes the mechanisms, related factors, clinical features, follow-up, treatment and prognosis of relapsed primary central nervous system lymphoma.

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Aberrantly synchronized neuronal discharges in the brain lead to epilepsy, a devastating neurological disease whose pathogenesis and mechanism are unclear. SAPAP3, a cytoskeletal protein expressed at high levels in the postsynaptic density (PSD) of excitatory synapses, has been well studied in the striatum, but the role of SAPAP3 in epilepsy remains elusive. In this study, we sought to investigate the molecular, cellular, electrophysiological and behavioral consequences of SAPAP3 perturbations in the mouse hippocampus. We identified a significant increase in the SAPAP3 levels in patients with temporal lobe epilepsy (TLE) and in mouse models of epilepsy. In addition, behavioral studies showed that the downregulation of SAPAP3 by shRNA decreased the seizure severity and that the overexpression of SAPAP3 by recombinant SAPAP3 yielded the opposite effect. Moreover, SAPAP3 affected action potentials (APs), miniature excitatory postsynaptic currents (mEPSCs) and N-methyl-D-aspartate receptor (NMDAR)-mediated currents in the CA1 region, which indicated that SAPAP3 plays an important role in excitatory synaptic transmission. Additionally, the levels of the GluN2A protein, which is involved in synaptic function, were perturbed in the hippocampal PSD, and this perturbation was accompanied by ultrastructural morphological changes. These results revealed a previously unknown function of SAPAP3 in epileptogenesis and showed that SAPAP3 may represent a novel target for the treatment of epilepsy.

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