Comparison of the neuropsychological mechanisms of 2,6-diisopropylphenol and N-methyl-D-aspartate receptor antagonist against electroconvulsive therapy-induced learning and memory impairment in depressed rats

Background There have been reports of long-term subjective memory worsening after electroconvulsive therapy (ECT). Aims To study the prevalence and risk factors of long-term subjective memory worsening among patients receiving ECT in routine clinical practice. Method Patients (n = 535, of whom 277 were included in the final analysis) were recruited from eight Swedish hospitals. Participants' subjective memory impairment was assessed before ECT and a median of 73 days after ECT using the memory item from the Comprehensive Psychopathological Rating Scale. Participants also rated their pre-ECT expectations and post-ECT evaluations of the effect of ECT on memory on a 7-point scale. We used ordinal regression to identify variables associated with subjective memory worsening and negative evaluations of the effect of ECT on memory. Results Comparisons of pre- and post-ECT assessments showed that subjective memory worsened in 16.2% of participants, remained unchanged in 52.3% and improved in 31.4%. By contrast, when asked to evaluate the effect of ECT on memory after treatment 54.6% reported a negative effect. Subjective memory worsening was associated with negative expectations before ECT, younger age and shorter duration of follow-up. Conclusions Although subjective memory improved more often than it worsened when assessed before and after ECT, a majority of patients reported that ECT had negative effects on their memory when retrospectively asked how ECT had affected it. This might suggest that some patients attribute pre-existing subjective memory impairment to ECT. Clinicians should be aware that negative expectations are associated with subjective worsening of memory after ECT.

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Protective effect of alpha-lipoic acid on bisphenol A-induced learning and memory impairment in developing mice: nNOS and keap1/Nrf2 pathway

Food and Chemical Toxicology ◽

10.1016/j.fct.2021.112307 ◽

2021 ◽

pp. 112307

Author(s):

Dan Wu ◽

Hezuo Liu ◽

Yang Liu ◽

Wei Wei ◽

Qi Sun ◽

...

Keyword(s):

Bisphenol A ◽

Protective Effect ◽

Learning And Memory ◽

Lipoic Acid ◽

Memory Impairment ◽

Alpha Lipoic Acid ◽

Nrf2 Pathway ◽

Developing Mice

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Ferroptosis contributes to isoflurane-induced neurotoxicity and learning and memory impairment

Cell Death Discovery ◽

10.1038/s41420-021-00454-8 ◽

2021 ◽

Vol 7 (1) ◽

Author(s):

Pengfei Liu ◽

Jing Yuan ◽

Yetong Feng ◽

Xin Chen ◽

Guangsuo Wang ◽

...

Keyword(s):

Cell Death ◽

Learning And Memory ◽

Memory Impairment ◽

Close Association ◽

Dimethyl Fumarate ◽

Dependent Manner ◽

Transport Chain ◽

The Relationship

AbstractFerroptosis is a novel type of programmed cell death, which is different from apoptosis and autophagic cell death. Recently, ferroptosis has been indicated to contribute to the in vitro neurotoxicity induced by isoflurane, which is one of the most common anesthetics in clinic. However, the in vivo position of ferroptosis in isoflurane-induced neurotoxicity as well as learning and memory impairment remains unclear. In this study, we mainly explored the relationship between ferroptosis and isoflurane-induced learning and memory, as well as the therapeutic methods in mouse model. Our results indicated that isoflurane induced the ferroptosis in a dose-dependent and time-dependent manner in hippocampus, the organ related with learning and memory ability. In addition, the activity of cytochrome c oxidase/Complex IV in mitochondrial electron transport chain (ETC) was increased by isoflurane, which might further contributed to cysteine deprivation-induced ferroptosis caused by isoflurane exposure. More importantly, isoflurane-induced ferroptosis could be rescued by both ferroptosis inhibitor (ferrostatin-1) and mitochondria activator (dimethyl fumarate), which also showed effective therapeutic action against isoflurane-induced learning and memory impairment. Taken together, our data indicate the close association among ferroptosis, mitochondria and isoflurane, and provide a novel insight into the therapy mode against isoflurane-induced learning and memory impairment.

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