The generation effect (GE) is a phenomenon in which material that is produced by an individual is learned and remembered better than information that is provided to that individual. The current study examined the potential benefits of self-generation on learning and memory in individuals with traumatic brain injury (TBI) and multiple sclerosis (MS). The impact of cognitive impairment on the benefits of self-generation was also examined. Subjects consisted of 18 individuals with TBI and 31 individuals with clinically definite MS. Both the TBI and MS groups recalled significantly more words in the self-generated condition versus the provided condition. Those impaired in the domains of working memory, episodic memory, or executive functioning demonstrated a significant benefit from self-generation (all ps < .05). Furthermore, although individuals with impairments in multiple cognitive domains recalled fewer words overall compared to those with no or one impaired cognitive domain, this group demonstrated a large effect size in the difference in recall for generated versus provided words. Results demonstrate that people with cognitive impairments can benefit from self-generation to improve learning and memory. Future research should focus on how to amplify the benefit of the GE for impaired groups, apply it to everyday functional tasks, and sustain its effect over time.
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http://dx.doi.org/10.1080/09602010600751160 | DOI Listing |
Proc Natl Acad Sci U S A
February 2025
Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA 94158.
The ε4 variant of human apolipoprotein E () is a key genetic risk factor for neurodegeneration in Alzheimer's disease and elevated all-cause mortality in humans. Understanding the factors and mechanisms that can mitigate the harmful effects of has significant implications. In this study, we find that inactivating the VHL-1 (Von Hippel-Lindau) protein can suppress mortality, neural and behavioral pathologies caused by transgenic human in .
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
January 2025
Department of Pharmacology, ISF College of Pharmacy, Ghal Kalan, GT Road, Moga, 142001, Punjab, India.
In examining the enduring consequences of diabetes, recent research has focused on the anticipated outcomes of the condition. Specifically, cognitive impairment has been linked to diabetes mellitus dating back to the discovery of insulin. This study delves into the neuroprotective effects of TZP, i.
View Article and Find Full Text PDFJ Neurophysiol
January 2025
Department of Psychology, University of Wisconsin-Milwaukee, Milwaukee WI, USA.
The hippocampus has a known role in learning and memory, with the ventral subregion supporting many learning tasks involving affective responding, including fear conditioning. Altered neuronal intrinsic excitability reflects experience-dependent plasticity that supports learning-related behavioral changes. Such changes have previously been observed in the dorsal hippocampus following fear conditioning, but little work has examined the effect of fear conditioning on ventral hippocampal intrinsic plasticity.
View Article and Find Full Text PDFJ Cell Mol Med
January 2025
Department of Anesthesia, Fujian Medical University Union Hospital, Fuzhou, China.
In this study, we aimed to explore the sex-specific effects and mechanisms of sevoflurane exposure on the neural development of pubertal rats on the basis of M1/M2 microglial cell polarisation and related signalling pathways. A total of 48 rat pups (24 males and 24 females) were assigned to the 0- or 2-h sevoflurane exposure group on the seventh day after birth. The Morris water maze (MWM) test was subsequently conducted on the 32nd to 38th days after birth.
View Article and Find Full Text PDFFront Neurosci
January 2025
HealthPartners Institute, Neuroscience Research, HealthPartners Neuroscience Center, Saint Paul, MN, United States.
Introduction: Intranasal (IN) deferoxamine (DFO) has emerged over the past decade as a promising therapeutic in preclinical experiments across neurodegenerative and neurovascular diseases. As an antioxidant iron chelator, its mechanisms are multimodal, involving the binding of brain iron and the consequent engagement of several pathways to counter pathogenesis across multiple diseases. We and other research groups have shown that IN DFO rescues cognitive impairment in several rodent models of Alzheimer Disease (AD).
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