• Title/Summary/Keyword: cognitive mechanisms

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Fermented Laminaria japonica improves working memory and antioxidant defense mechanism in healthy adults: a randomized, double-blind, and placebo-controlled clinical study

  • Kim, Young-Sang;Reid, Storm N.S.;Ryu, Jeh-Kwang;Lee, Bae-Jin;Jeon, Byeong Hwan
    • Fisheries and Aquatic Sciences
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    • v.25 no.8
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    • pp.450-461
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    • 2022
  • A randomized, double-blind, and placebo-controlled clinical study was used to determine the cognitive functions related to working memory (WM) and antioxidant properties of fermented Laminaria japonica (FLJ) on healthy volunteers. Eighty participants were divided into a placebo group (n = 40) and FLJ group (n = 40) that received FLJ (1.5 g/day) for 6 weeks. Memory-related blood indices (brain-derived neurotrophic factor, BDNF; angiotensin-converting enzyme; human growth hormone, HGH; insulin-like growth factor-1, IGF-1) and antioxidant function-related indices (catalase, CAT; malondialdehyde, MDA; 8-oxo-2'-deoxyguanosine, 8-oxo-dG; thiobarbituric acid reactive substances, TBARS) were determined before and after the trial. In addition, standardized cognitive tests were conducted using the Cambridge Neuropsychological Test Automated Batteries. Furthermore, the Korean Wechsler Adult Intelligence Scale (K-WAIS)-IV, and the Korean version of the Montreal Cognitive Assessment (MoCA-K) were used to assess the pre and post intake changes on WM-related properties. According to the results, FLJ significantly increased the level of CAT, BDNF, HGH, and IGF-1. FLJ reduced the level of TBARS, MDA, and 8-oxo-dG in serum. Furthermore, FLJ improved physical activities related to cognitive functions such as K-WAIS-IV, MoCA-K, Paired Associates Learning, and Spatial Working Memory compared to the placebo group. Our results suggest that FLJ is a potential candidate to develop functional materials reflecting its capability to induce antioxidant mechanisms together with WM-related indices.

Probiotics that Ameliorate Cognitive Impairment through Anti-Inflammation and Anti-Oxidation in Mice

  • Shinhui Lee;Sanung Eom;Jiwon Lee;Minsu Pyeon;Kieup Kim;Kyu Yeong Choi;Jung Hee Lee;Da Jeong Shin;Kun Ho Lee;Sejong Oh;Junho H Lee
    • Food Science of Animal Resources
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    • v.43 no.4
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    • pp.612-624
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    • 2023
  • The gut-brain axis encompasses a bidirectional communication pathway between the gastrointestinal microbiota and the central nervous system. There is some evidence to suggest that probiotics may have a positive effect on cognitive function, but more research is needed before any definitive conclusions can be drawn. Inflammation-induced by lipopolysaccharide (LPS) may affect cognitive function. To confirm the effect of probiotics on oxidative stress induced by LPS, the relative expression of antioxidant factors was confirmed, and it was revealed that the administration of probiotics had a positive effect on the expression of antioxidant-related factors. After oral administration of probiotics to mice, an intentional inflammatory response was induced through LPS i.p., and the effect on cognition was confirmed by the Morris water maze test, nitric oxide (NO) assay, and interleukin (IL)-1β enzyme-linked immunosorbent assay performed. Experimental results, levels of NO and IL-1β in the blood of LPS i.p. mice were significantly decreased, and cognitive evaluation using the Morris water maze test showed significant values in the latency and target quadrant percentages in the group that received probiotics. This proves that intake of these probiotics improves cognitive impairment and memory loss through anti-inflammatory and antioxidant mechanisms.

An Analysis of the Discovery of Chaos Based on Socio-Cognitive Perspectives (카오스의 발견과 이해에 대한 분석적 검토: 사회적, 인지적 측면을 중심으로)

  • Kim, Jong-Baeg
    • Journal of The Korean Association For Science Education
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    • v.25 no.7
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    • pp.711-720
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    • 2005
  • The purpose of this study was to understand mechanisms of scientific discovery and how this can help students, as young scientists, to understand scientific ideas in the science classroom. To unravel this mechanism, this study employed the notion of chaos. This phenomena was rediscovered by Edward Lorenz. In this paper, the general concept of chaos was briefly discussed in relation with previous scientific theories such as Newtonian physics and quantum mechanics. Following this, discovery constraints in terms of available technology at the time was described. In addition, Lorenz's psychological processes during the discovery was also discussed. Based on analysis, major implications for the field of science education were the provision of relevant schemata, the use of cognitive tools, the presentation of problems with various representational forms, and the sharing of ideas with others.

Naturalizing Intentionality (지향성-문제와접근)

  • 민찬홍
    • Korean Journal of Cognitive Science
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    • v.8 no.1
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    • pp.7-36
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    • 1997
  • Beginning with the historical background under the light of which the program of naturalization proves to presuppose the mechanistic mechanistic materilalism, this paper first exposes what is the problem about intentionality, and then explains and examines the approaches to the program of naturalization of intentionality. Churchland's eliminativism and Dennett's instrumentalism are examined critically. Intentional realism is argued for;however, Dretaske's theory is preferred to than Foder's because the former but not the latter reveals least one of the various possible mechanisms of misrepresentations.

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Insulin resistance and Alzheimer's disease

  • De La Monte, Suzanne M.
    • BMB Reports
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    • v.42 no.8
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    • pp.475-481
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    • 2009
  • Emerging data demonstrate pivotal roles for brain insulin resistance and insulin deficiency as mediators of cognitive impairment and neurodegeneration, particularly Alzheimer's disease (AD). Insulin and insulin-like growth factors (IGFs) regulate neuronal survival, energy metabolism, and plasticity, which are required for learning and memory. Hence, endogenous brain-specific impairments in insulin and IGF signaling account for the majority of AD-associated abnormalities. However, a second major mechanism of cognitive impairment has been linked to obesity and Type 2 diabetes (T2DM). Human and experimental animal studies revealed that neurodegeneration associated with peripheral insulin resistance is likely effectuated via a liver-brain axis whereby toxic lipids, including ceramides, cross the blood brain barrier and cause brain insulin resistance, oxidative stress, neuro-inflammation, and cell death. In essence, there are dual mechanisms of brain insulin resistance leading to AD-type neurodegeneration: one mediated by endogenous, CNS factors; and the other, peripheral insulin resistance with excess cytotoxic ceramide production.

Exploring the Psychological Mechanism Underlying the Effect of COVID-19 Information Exposure via Digital Media on COVID-19 Preventive Behavioral Intention

  • Choi, Ji Hye;Noh, Ghee-Young
    • Asian Journal for Public Opinion Research
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    • v.10 no.2
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    • pp.76-101
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    • 2022
  • Despite the increasing use of digital media and their powerful impact on risk management during recent outbreaks of emerging infectious diseases, the question of how digital media exposure influences preventive behaviors has not been fully explained. Using the appraisal tendency framework and protection motivation theory as theoretical frameworks, we theorized the affective and cognitive mechanisms under which the differential roles of three negative emotions (fear, anger, worry) on two cognitive appraisals (perceived threat and perceived efficacy) were examined. Based on data collected from a survey of 1,500 South Koreans during the COVID-19 pandemic, we found that while worry and anger increased perceived efficacy, fear reduced perceived efficacy. The results also showed that although exposure to COVID-19 information via digital formats increased preventive behavioral intention in general, digital media use for COVID-19 information had a negative influence on preventive behavioral intention through the sequential mediation of fear and perceived efficacy.

Treatment for Burning Mouth Syndrome: A Clinical Review

  • YoungJoo Shim
    • Journal of Oral Medicine and Pain
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    • v.48 no.1
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    • pp.11-15
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    • 2023
  • Burning mouth syndrome (BMS) is a chronic idiopathic orofacial pain. BMS is currently classified as a neuropathic pain condition, but it is difficult to pinpoint the precise neuropathic mechanisms involved in each patient. It is challenging to complete the cure for BMS. Clinicians should treat BMS patients based on evidence. There is pharmacological and non-pharmacological therapy in the treatment modalities of BMS. The provision of objective information and reassurance as part of cognitive behavioral therapy is critical in the treatment of BMS. This paper will review the evidence-based treatment of BMS and discuss what we need to do.

Molecular and Cellular Basis of Neurodegeneration in Alzheimer's Disease

  • Jeong, Sangyun
    • Molecules and Cells
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    • v.40 no.9
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    • pp.613-620
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    • 2017
  • The most common form of senile dementia is Alzheimer's disease (AD), which is characterized by the extracellular deposition of amyloid ${\beta}-peptide$ ($A{\beta}$) plaques and the intracellular formation of neurofibrillary tangles (NFTs) in the cerebral cortex. Tau abnormalities are commonly observed in many neurodegenerative diseases including AD, Parkinson's disease, and Pick's disease. Interestingly, tau-mediated formation of NFTs in AD brains shows better correlation with cognitive impairment than $A{\beta}$ plaque accumulation; pathological tau alone is sufficient to elicit frontotemporal dementia, but it does not cause AD. A growing amount of evidence suggests that soluble $A{\beta}$ oligomers in concert with hyperphosphorylated tau (pTau) serve as the major pathogenic drivers of neurodegeneration in AD. Increased $A{\beta}$ oligomers trigger neuronal dysfunction and network alternations in learning and memory circuitry prior to clinical onset of AD, leading to cognitive decline. Furthermore, accumulated damage to mitochondria in the course of aging, which is the best-known nongenetic risk factor for AD, may collaborate with soluble $A{\beta}$ and pTau to induce synapse loss and cognitive impairment in AD. In this review, I summarize and discuss the current knowledge of the molecular and cellular biology of AD and also the mechanisms that underlie $A{\beta}-mediated$ neurodegeneration.

A Korean Normative Study of 213 Pictures (한국판 그림자극의 규준연구)

  • 박미자;박태진
    • Korean Journal of Cognitive Science
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    • v.11 no.3_4
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    • pp.57-72
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    • 2000
  • A Korean standardized set of pictures has been called for as more and more studies utilized picture stimuli among memory and representation research. This article presents a Korean standardized set of pictures for studies probing the cognitive mechanisms that underlie picture and word processing or studies that simply utilize pictures stimuli. This norm provides 213 pictures, data on several variables such as name agreement, appropriateness of pictures. and familiarity. Previous data on such variables as frequency. category. and frequency within a category have been integrated 1 into this norm. Limitation, usage. and application of this set are discussed in terms of 1 implicit and explicit memory, and those variables mentioned previously.

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Inflammasomes: Molecular Regulation and Implications for Metabolic and Cognitive Diseases

  • Choi, Alexander J.S.;Ryter, Stefan W.
    • Molecules and Cells
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    • v.37 no.6
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    • pp.441-448
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    • 2014
  • Inflammasomes are specialized signaling platforms critical for the regulation of innate immune and inflammatory responses. Various NLR family members (i.e., NLRP1, NLRP3, and IPAF) as well as the PYHIN family member AIM2 can form inflammasome complexes. These multiprotein complexes activate inflammatory caspases (i.e., caspase-1) which in turn catalyze the maturation of select pro-inflammatory cytokines, including interleukin (IL)-$1{\beta}$ and IL-18. Activation of the NLRP3 inflammasome typically requires two initiating signals. Toll-like receptor (TLR) and NOD-like receptor (NLR) agonists activate the transcription of pro-inflammatory cytokine genes through an NF-${\kappa}B$-dependent priming signal. Following exposure to extracellular ATP, stimulation of the P2X purinoreceptor-7 ($P2X_7R$), which results in $K^+$ efflux, is required as a second signal for NLRP3 inflammasome formation. Alternative models for NLRP3 activation involve lysosomal destabilization and phagocytic NADPH oxidase and /or mitochondria-dependent reactive oxygen species (ROS) production. In this review we examine regulatory mechanisms that activate the NLRP3 inflammasome pathway. Furthermore, we discuss the potential roles of NLRP3 in metabolic and cognitive diseases, including obesity, type 2 diabetes mellitus, Alzheimer's disease, and major depressive disorder. Novel therapeutics involving inflammasome activation may result in possible clinical applications in the near future.