Facing a Long-Term Memory Loss

2011 ◽  
Vol 39 (2) ◽  
pp. 53-54
Author(s):  
Kevin Mccarty
Keyword(s):  
Memory Loss ◽  
Long Term Memory ◽  
Term Memory

scholarly journals Methamphetamine Inhibits Long-Term Memory Acquisition and Synaptic Plasticity by Evoking Endoplasmic Reticulum Stress

2021 ◽  
Vol 14 ◽  
Author(s):  
Guang Chen ◽  
Xiaoning Wei ◽  
Xiang Xu ◽  
Gang Yu ◽  
Zheng Yong ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Synaptic Plasticity ◽  
Er Stress ◽  
Memory Loss ◽  
Translation Initiation Factor ◽  
Long Term Memory ◽  
Term Memory ◽  
Expression Levels ◽  
Memory Acquisition

Methamphetamine (MA), an illicit drug abused worldwide, leads to cognitive impairment and memory loss. However, the detailed mechanisms of MA-induced neurologic impairment are still unclear. The present study aimed to investigate the mechanisms of MA-induced inhibition of memory acquisition from the perspective of endoplasmic reticulum (ER) stress. ER stress, caused by the accumulation of wrongly folded proteins in the ER, is important for new protein synthesis, which further influence the formation of long-term memory. A subacute MA poisoning model of mice was established and several behavioral experiments were performed, including elevated plus maze, Morris water maze, electro-stimulus Y-maze, and novel object recognition tasks. The present results suggested that 4 days exposure to MA induced significant memory loss. Whereas, this damage to memory formation could be protected when mice were pre-treated with ER stress inhibitor, tauroursodeoxycholic acid (TUDCA). The results of Western blotting showed that subacute exposure to MA increased the expression levels of ER stress marker proteins, such as binding immunoglobulin protein, phosphorylated eukaryotic translation initiation factor 2α, cyclic AMP-dependent transcription factor (ATF)-4, ATF-6, and CCAAT-enhancer binding protein homologous protein. Meanwhile, the enhanced expression levels of these proteins were reversed by TUDCA, indicating that MA administration induced memory loss by evoking ER stress in the hippocampus. We also found that MA inhibited the induction of long-term potentiation (LTP) in the hippocampus. Nevertheless, LTP could be induced when mice were pre-treated with TUDCA. In conclusion, MA inhibited long-term memory acquisition and synaptic plasticity via ER stress.

scholarly journals Prophylactic Subacute Administration of Zinc Increases CCL2, CCR2, FGF2, and IGF-1 Expression and Prevents the Long-Term Memory Loss in a Rat Model of Cerebral Hypoxia-Ischemia

2015 ◽  
Vol 2015 ◽  
pp. 1-15 ◽  
Author(s):  
Victor Manuel Blanco-Alvarez ◽  
Guadalupe Soto-Rodriguez ◽  
Juan Antonio Gonzalez-Barrios ◽  
Daniel Martinez-Fong ◽  
Eduardo Brambila ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Growth Factors ◽  
Neural Plasticity ◽  
Memory Loss ◽  
Male Rats ◽  
Long Term Memory ◽  
Cerebral Hypoxia ◽  
Term Memory ◽  
Hypoxia Ischemia

Prophylactic subacute administration of zinc decreases lipoperoxidation and cell death following a transient cerebral hypoxia-ischemia, thus suggesting neuroprotective and preconditioning effects. Chemokines and growth factors are also involved in the neuroprotective effect in hypoxia-ischemia. We explored whether zinc prevents the cerebral cortex-hippocampus injury through regulation of CCL2, CCR2, FGF2, and IGF-1 expression following a 10 min of common carotid artery occlusion (CCAO). Male rats were grouped as follows: (1) Zn96h, rats injected with ZnCl2(one dose every 24 h during four days); (2) Zn96h + CCAO, rats treated with ZnCl2before CCAO; (3) CCAO, rats with CCAO only; (4) Sham group, rats with mock CCAO; and (5) untreated rats. The cerebral cortex-hippocampus was dissected at different times before and after CCAO. CCL2/CCR2, FGF2, and IGF-1 expression was assessed by RT-PCR and ELISA. Learning in Morris Water Maze was achieved by daily training during 5 days. Long-term memory was evaluated on day 7 after learning. Subacute administration of zinc increased expression of CCL2, CCR2, FGF2, and IGF-1 in the early and late phases of postreperfusion and prevented the CCAO-induced memory loss in the rat. These results might be explained by the induction of neural plasticity because of the expression of CCL2 and growth factors.

Maternal Food Memories in Lin Cheng-sheng's 27°C: Loaf Rock and Eric Khoo's Recipe: A Film on Dementia

2018 ◽  
Vol 18 (4) ◽  
pp. 26-40 ◽  
Author(s):  
Michelle E. Bloom
Keyword(s):  
Cultural Memory ◽  
Short Term Memory ◽  
Chinese Language ◽  
Memory Loss ◽  
Long Term Memory ◽  
Culinary Arts ◽  
Short Term ◽  
Term Memory ◽  
Individual Memory

Elderly mothers pick pineapple in Taiwanese fields and cook curry rice in a Singaporean hawker stand in Lin Cheng-sheng's biopic, 27°C: Loaf Rock, and Eric Khoo's telefilm, Recipe: A Film on Dementia, respectively. Both 2013 Chinese language films employ flashbacks to portray maternal food memories. Lin and Khoo depict food as comforting and possessing a unique ability to stimulate long-term memory to counter the short-term memory loss symptomatic of this form of dementia. The gustatory and the olfactory act directly upon the limbic brain, which houses emotions. In depicting Alzheimer's sufferers and their responses to food, 27°C and Recipe fight for causes. Lin calls attention to the marginalized in his portrayal of the mother succumbing to the disease from the perspective of her son—a character based on contemporary Taiwanese baker Wu Pao-chun, who overcame the adversity of impoverishment to win the world famous Master's de la Boulangerie and found prestigious eponymous bakeries. Parallel to its role in individual memory, food preserves cultural memory. Analogous to culinary arts, cinema, which is made for consumption, combines art and science, embodies culture, and incorporates tradition and innovation, as I show in this comparative study.

Long-term memory loss and the effects of tianeptine in young and aged mice

1993 ◽  
Vol 8 (S2) ◽  
pp. 81s-88s
Author(s):  
C Lebrun ◽  
R Jaffard
Keyword(s):  
Hippocampal Formation ◽  
Alcohol Intoxication ◽  
Memory Loss ◽  
Memory Deficits ◽  
Long Term Memory ◽  
Term Memory ◽  
Long Term Retention ◽  
Brain Target ◽  
Different Levels

SummaryPrevious experiments have shown that tianeptine, a new psychotropic agent with antidepressant properties, improves performance in several learning and memory tasks in mice. In more recent investigations, tianeptine was found to completely alleviate working memory deficits produced by long-term alcohol intoxication and to prevent abnormal memory loss in aged animals (Jaffard et al, 1991b, 1991c). The aim of this paper was to examine how this last finding may be integrated in our understanding of brain mechanisms involved in memory loss. For this purpose, we present a brief review of experimental data and theories which, at different levels of analysis, seems to be relevant to this issue. Together with the subsequent examination of the conditions in which tianeptine was found to improve long-term retention, we suggest that: i) long-term memory loss would be largely determined by the initial encoding of information, so that ii) tianeptine would help aged animals to use spatial mapping or configural associations more efficiently at the time of initial acquisition. This, in turn, suggests that one of the main brain target sites for tianeptine in enhancing memory is the hippocampal formation.

scholarly journals Antibody Protection against Long-Term Memory Loss Induced by Monomeric C-Reactive Protein in a Mouse Model of Dementia

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 828
Author(s):  
Elisa García-Lara ◽  
Samuel Aguirre ◽  
Núria Clotet ◽  
Xenia Sawkulycz ◽  
Clara Bartra ◽  
...  
Keyword(s):  
Memory Loss ◽  
Long Term Memory ◽  
C Reactive Protein ◽  
Human Brain Tissue ◽  
Term Memory ◽  
Reactive Protein ◽  
Microglial Cell Line

Monomeric C-reactive protein (mCRP), the activated isoform of CRP, induces tissue damage in a range of inflammatory pathologies. Its detection in infarcted human brain tissue and its experimentally proven ability to promote dementia with Alzheimer’s disease (AD) traits at 4 weeks after intrahippocampal injection in mice have suggested that it may contribute to the development of AD after cerebrovascular injury. Here, we showed that a single hippocampal administration of mCRP in mice induced memory loss, lasting at least 6 months, along with neurodegenerative changes detected by increased levels of hyperphosphorylated tau protein and a decrease of the neuroplasticity marker Egr1. Furthermore, co-treatment with the monoclonal antibody 8C10 specific for mCRP showed that long-term memory loss and tau pathology were entirely avoided by early blockade of mCRP. Notably, 8C10 mitigated Egr1 decrease in the mouse hippocampus. 8C10 also protected against mCRP-induced inflammatory pathways in a microglial cell line, as shown by the prevention of increased generation of nitric oxide. Additional in vivo and in vitro neuroprotective testing with the anti-inflammatory agent TPPU, an inhibitor of the soluble epoxide hydrolase enzyme, confirmed the predominant involvement of neuroinflammatory processes in the dementia induced by mCRP. Therefore, locally deposited mCRP in the infarcted brain may be a novel biomarker for AD prognosis, and its antibody blockade opens up therapeutic opportunities for reducing post-stroke AD risk.

scholarly journals Bioactive Peptide VHVV Upregulates the Long-Term Memory-Related Biomarkers in Adult Spontaneously Hypertensive Rats

2019 ◽  
Vol 20 (12) ◽  
pp. 3069 ◽  
Author(s):  
Da-Tong Ju ◽  
Ashok Kumar K. ◽  
Wei-Wen Kuo ◽  
Tsung-Jung Ho ◽  
Ruey-Lin Chang ◽  
...  
Keyword(s):  
Oral Administration ◽  
Spontaneously Hypertensive Rats ◽  
Neuronal Degeneration ◽  
Memory Loss ◽  
Bioactive Peptide ◽  
Long Term Memory ◽  
Hypertensive Rats ◽  
Term Memory ◽  
Spontaneously Hypertensive

Hypertension is one of the growing risk factors for the progression of long-term memory loss. Hypertension-mediated memory loss and treatment remain not thoroughly elucidated to date. Plant-based natural compounds are an alternative solution to treating human diseases without side effects associated with commercial drugs. This study reveals that bioactive peptides extracted from soy hydrolysates mimic hypertension-mediated memory loss and neuronal degeneration and alters the memory molecular pathway in spontaneously hypertensive rats (SHR). The SHR animal model was treated with bioactive peptide VHVV (10 mg/kg/oral administration) and angiotensin-converting-enzyme (ACE) inhibitors (5 mg/kg/oral administration) for 24 weeks. We evaluated molecular level expression of brain-derived neurotrophic factor (BDNF), cAMP response element binding protein (CREB), and survival markers phospho-protein kinase B (P-AKT) and phosphoinositide 3-kinase (PI3K) after 24 weeks of treatment for SHR in this study. Western blotting, hematoxylin and eosin (H&E) staining, and immunohistochemistry showed long-term memory loss and neuronal degeneration in SHR animals. Bioactive peptide VHVV-treated animals upregulated the expression of long-term memory-relate proteins and neuronal survival. Spontaneously hypertensive rats treated with oral administration of bioactive peptide VHVV had activated CREB-mediated downstream proteins which may reduce hypertension-mediated long-term memory loss and maintain neuronal survival.

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