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Therapeutics and Pathophysiology of Cognitive Dysfunction

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 November 2025 | Viewed by 573

Special Issue Editor


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Guest Editor
Institute for Regenerative Medicine, Department of Molecular and Cellular Medicine, Texas A&M University College of Medicine, 1114 TAMU, College Station, TX 77842, USA
Interests: neurodegenerative diseases; therapeutic strategies; cognitive function; cellular and transcriptomic alterations

Special Issue Information

Dear Colleagues,

Cognitive dysfunction typified by impaired attention, learning, memory, and problem-solving skills is generally referred to as ‘brain fog’ associated with neuroimmune imbalance in multiple neurodegenerative diseases, malignancies, and associated metabolic conditions. In neuropsychiatric diseases, cognitive impairments are associated with suicidal tendencies, which are predictive of depression relapse and are frequently retained in individuals in remission from depressive episodes. Nonetheless, cognitive dysfunction has a significant effect on quality of life but is clinically underreported, likely due to its limitation in detection at subclinical levels. Therefore, strategies aimed at enhancing the detection threshold of cognitive impairments and attenuating these deficits through modulating the underlying pathologies, such as diminishing neuroinflammation, enhancing neurogenesis, and metabolic fitness have garnered significant attention. The possibility of non-pharmacological methods like music therapy and pharmaceutical methods, particularly those that target the GABAergic system, to alleviate cognitive symptoms has recently been investigated. To increase the quality of life, however, this domain requires more attention.

Dr. Maheedhar Kodali
Guest Editor

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Keywords

  • cognition
  • neurologic diseases
  • neuroinflammation

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Published Papers (1 paper)

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Research

19 pages, 1688 KiB  
Article
Shorter Telomere Length in Individuals with Neurocognitive Disorder and APOE ε4 Genotype
by Paola Mejía-Ortiz, Alma Delia Genis-Mendoza, Ramon Ramírez Villanueva, Susana López Ramírez, Rafael Guzmán Sánchez, Thalia Fernández, Jorge Sigg-Alonso and Humberto Nicolini-Sánchez
Int. J. Mol. Sci. 2025, 26(10), 4577; https://doi.org/10.3390/ijms26104577 - 10 May 2025
Viewed by 153
Abstract
Neurocognitive disorders (NCD) are neurodegenerative diseases characterized by decline or loss of cognitive functions. Aging and the APOE genotype have been identified as major risk factors. Telomere length (TL) has been proposed as a biomarker of aging, with shorter TL associated with cognitive [...] Read more.
Neurocognitive disorders (NCD) are neurodegenerative diseases characterized by decline or loss of cognitive functions. Aging and the APOE genotype have been identified as major risk factors. Telomere length (TL) has been proposed as a biomarker of aging, with shorter TL associated with cognitive decline. This study investigated the relationship between TL and the APOE genotype in individuals with cognitive impairments (CIs). A total of 170 participants aged >55 years were included. Cognitive function was assessed using the MMSE and MoCA tests. Relative telomere quantification and APOE genotype were determined by real-time PCR. A significant association was observed between shorter TL and an increased risk of CI (p < 0.001). Although APOE ε4 is a known genetic risk factor, its association with CI was less clear in this study population, as a considerable proportion of ε4 carriers did not present cognitive impairment (p < 0.05). However, ε4 carriers with CI tended to have shorter TL than those with non-cognitive impairment (NCI-SMC). Furthermore, fewer years of education were strongly correlated with higher CI risk (p < 0.0001). Overall, individuals with both shorter telomeres and lower educational levels exhibited the highest risk of CI. APOE ε4 may contribute to telomere shortening. Full article
(This article belongs to the Special Issue Therapeutics and Pathophysiology of Cognitive Dysfunction)
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