It has been shown that applying transcranial direct current stimulation (tDCS) over the dorsolateral prefrontal cortex (DLPFC) influences declarative memory processes. This study investigates the efficacy of tDCS on emotional memory consolidation, especially experimental fear conditioning. We applied an auditory fear-conditioning paradigm, in which two differently colored squares (blue and yellow) were presented as conditioned stimuli (CS) and an auditory stimulus as unconditioned stimulus (UCS). Sixty-nine participants were randomly assigned into three groups: anodal, cathodal, and sham stimulation. The participants of the two active groups (i.e., anodal and cathodal) received tDCS over the left DLPFC for 12 min after fear conditioning. The effect of fear conditioning and consolidation (24 h later) was measured by assessing the skin conductance response (SCR) to the CS. The results provide evidence that cathodal stimulation of the left DLPFC leads to an inhibitory effect on fear memory consolidation compared to anodal and sham stimulation, as indicated by decreased SCRs to CS+ presentation during extinction training at day 2. In conclusion, current work suggests that cathodal stimulation interferes with processes of fear memory consolidation.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3781351 | PMC |
http://dx.doi.org/10.3389/fpsyt.2013.00107 | DOI Listing |
J Transl Med
January 2025
Research Unit NeuroBiology of Diabetes, Helmholtz Munich, Ingolstädter Landstraße 1, 85764, Neuherberg, Germany.
Background: Obese subjects undergoing weight loss often fear the Yoyo dieting effect, which involves regaining or even surpassing their initial weight. To date, our understanding of such long-term obesity and weight cycling effects is still limited and often based on only short-term murine weight gain and loss studies. This study aimed to investigate the long-term impacts of weight cycling on glycemic control and metabolic health, focusing on adipose tissue, liver, and hypothalamus.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Background: The prevalence of sepsis and delirium in the elderly is a risk factor for subsequent diagnosis of Alzheimer's disease and related dementias (ADRD). Post-sepsis impairments include changes in memory, attention, emotional function, and neuromuscular strength. Studies have shown a link between the prolonged activation of microglia after infection.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Mayo Clinic Florida, Jacksonville, FL, USA.
Background: We previously identified the novel mechanism of pathological tau transfer via extracellular vesicles (EVs) in Alzheimer's disease (AD). Targeting EV secretion to mitigate tau transfer is therefore a promising therapeutic approach for AD. P2X purinoreceptor 7 (P2RX7), an ATP-gated cationic channel, regulates microvesicle shedding or secretion of multivesicular body-derived exosomes.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Utah, Salt Lake City, UT, USA.
Background: Neurodegenerative disorders such as Alzheimer's Disease (AD) are increasingly associated with irregular lipid accumulation. Dysfunction in the catabolism of sphingolipids leads to many neurodegenerative disorders but has only recently garnered interest in AD. Excess ceramide deposition has been observed in Aβ-plaques, plasma, and cerebrospinal fluid in AD patients and AD mouse models.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Iowa, Iowa City, IA, USA.
Background: Sorbs2 is a cytoskeletal adaptor protein that is expressed in hippocampal neurons, but its mechanistic role in these cells is not yet fully understood.
Method: We created two groups of mice for our study: whole-body Sorbs2-Knockout (KO) mice and Sorbs2-Flox mice, which had neuronal knockout via AAV-PHP.eB-hSyn1-Cre virus injection.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!