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Research on Neural and Cognitive Molecular Mechanisms of Memory and Executive Control

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 4278

Special Issue Editor

Dr. Jee Hyang Jeong

E-Mail Website
Guest Editor
School of Medicine, Ewha Womans University, Seoul, Korea
Interests: Alzheimer's disease; neuropsychological tests; mild cognitive impairment

Special Issue Information

Dear Colleagues,

Cognitive, and motivational development entails co-constructive interactions between the environmental and social influences from the developmental context, on the one hand, and the individual's neurobiological inheritance, on the other hand. Key brain networks underlying cognition, emotion, and motivation are innervated by major transmitter systems (e.g., the catecholamines and acetylcholine). Thus, the maturation and senescence of neurotransmitter systems have direct implications for lifespan development.

Although dysexecutive syndromes have been traditionally associated with dorsolateral prefrontal cortex injury, it is now recognized that they can also result from an impaired parietal-temporal-frontal system, which is targeted in a distinct form of atypical Alzheimer disease. Thus the molecular mechanisms of memory and executive control are still poorly understood.

We invite researchers working on the Molecular Mechanisms of Cognitive Impairment to contribute to this Special Issue. Original research articles or reviews on molecular and cellular mechanisms related to the Neural and Cognitive are welcome. Articles with insights on biological and therapeutic perspectives are especially welcome.

Dr. Jee Hyang Jeong
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cognitive impairment
  • memory
  • Alzheimer's disease
  • neuropsychological tests

Published Papers (2 papers)

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Research

19 pages, 7160 KiB  
Article
Korean Red Ginseng Prevents the Deterioration of Lung and Brain Function in Chronic PM2.5-Exposed Mice by Regulating Systemic Inflammation
by Ju Hui Kim, Jong Min Kim, Hyo Lim Lee, Min Ji Go, Tae Yoon Kim, Seung Gyum Joo, Han Su Lee and Ho Jin Heo
Int. J. Mol. Sci. 2023, 24(17), 13266; https://doi.org/10.3390/ijms241713266 - 26 Aug 2023
Viewed by 1839
Abstract
This study was conducted to confirm the effects of Korean red ginseng on lung and brain dysfunction in a BALB/c mice model exposed to particulate matter (PM)2.5 for 12 weeks. Learning and cognitive abilities were assessed with Y-maze, passive avoidance, and Morris [...] Read more.
This study was conducted to confirm the effects of Korean red ginseng on lung and brain dysfunction in a BALB/c mice model exposed to particulate matter (PM)2.5 for 12 weeks. Learning and cognitive abilities were assessed with Y-maze, passive avoidance, and Morris water maze tests. To evaluate the ameliorating effect of red ginseng extract (RGE), the antioxidant system and mitochondrial function were investigated. The administration of RGE protected lung and brain impairment by regulating the antioxidant system and mitochondrial functions damaged by PM2.5-induced toxicity. Moreover, RGE prevented pulmonary fibrosis by regulating the transforming growth factor beta 1 (TGF-β1) pathway. RGE attenuated PM2.5-induced pulmonary and cognitive dysfunction by regulating systemic inflammation and apoptosis via the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)/c-Jun N-terminal kinases (JNK) pathway. In conclusion, RGE might be a potential material that can regulate chronic PM2.5-induced lung and brain cognitive dysfunction. Full article
(This article belongs to the Special Issue Research on Neural and Cognitive Molecular Mechanisms of Memory and Executive Control)
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15 pages, 2243 KiB  
Article
Metabolic Disturbance of High-Saturated Fatty Acid Diet in Cognitive Preservation
by Antonio Rivas-Domínguez, Himan Mohamed-Mohamed, Margarita Jimenez-Palomares, Victoria García-Morales, Laura Martinez-Lopez, Manuel Luis Orta, Juan José Ramos-Rodriguez and Beatriz Bermudez-Pulgarin
Int. J. Mol. Sci. 2023, 24(9), 8042; https://doi.org/10.3390/ijms24098042 - 28 Apr 2023
Cited by 1 | Viewed by 2037
Abstract
Aging continues to be the main cause of the development of Alzheimer’s, although it has been described that certain chronic inflammatory pathologies can negatively influence the progress of dementia, including obesity and hyperlipidemia. In this sense, previous studies have shown a relationship between [...] Read more.
Aging continues to be the main cause of the development of Alzheimer’s, although it has been described that certain chronic inflammatory pathologies can negatively influence the progress of dementia, including obesity and hyperlipidemia. In this sense, previous studies have shown a relationship between low-density lipoprotein receptor (LDLR) and the amyloid-beta (Aβ) binding activity, one of the main neuropathological features of Alzheimer’s disease (AD). LDLR is involved in several processes, including lipid transport, regulation of inflammatory response and lipid metabolism. From this perspective, LDLR−/− mice are a widely accepted animal model for the study of pathologies associated with alterations in lipid metabolism, such as familial hypercholesterolemia, cardiovascular diseases, metabolic syndrome, or early cognitive decline. In this context, we induced hyperlipidemia in LDLR−/− mice after feeding with a high-saturated fatty acid diet (HFD) for 44 weeks. LDLR−/−-HFD mice exhibited obesity, hypertriglyceridemia, higher glucose levels, and early hepatic steatosis. In addition, HFD increased plasmatic APOE and ubiquitin 60S levels. These proteins are related to neuronal integrity and health maintenance. In agreement, we detected mild cognitive dysfunctions in mice fed with HFD, whereas LDLR−/−-HFD mice showed a more severe and evident affectation. Our data suggest central nervous system dysfunction is associated with a well-established metabolic syndrome. As a late consequence, metabolic syndrome boots many behavioral and pathological alterations recognized in dementia, supporting that the control of metabolic parameters could improve cognitive preservation and prognosis. Full article
(This article belongs to the Special Issue Research on Neural and Cognitive Molecular Mechanisms of Memory and Executive Control)
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