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Neurological Diseases: From Molecular Basis to Therapy

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: 30 November 2024 | Viewed by 1246

Special Issue Editor

Special Issue Information

Dear Colleagues,

Neurological diseases represent a complex and challenging spectrum of disorders that affect the central and peripheral nervous systems, including the brain, spinal cord, and peripheral nerves. They include a variety of conditions such as neurodegenerative, neurovascular, neuro-oncological, neuroinflammatory, and infectious diseases, as well as traumatic brain and spinal cord injuries.

Neurological disorders can severely affect a person's quality of life, causing physical, emotional, and cognitive impairment. Managing neurological conditions often requires specialized care and complicated treatment options. In addition, the complexity of these conditions makes diagnosis and treatment difficult. This can lead to misdiagnosis and delayed treatment, which can worsen symptoms and increase the burden on patients and caregivers. The World Health Organization (WHO) has reported an increase in neurological diseases, due in part to an ageing population and the lack of definitive therapies, with a major impact on the sustainability of health and social systems, and a large number of people with disabilities, with serious economic and social consequences for their families. Developing effective treatments for neurological disorders is critical to alleviating symptoms, improving patient outcomes, and enhancing overall quality of life. Despite advances in medical science, many neurological disorders remain incurable or inadequately treated. Therefore, new scientific and epidemiological evidence is needed to develop innovative therapies and interventions.

The aim of this Special Issue is to focus on advances in research into neurological disorders, from understanding the causes and mechanisms of disease, to identifying new therapeutic targets, developing methods for early diagnosis and screening of individuals at risk, and developing new therapies and preventive strategies to improve the management and quality of life of neurological patients. Various disciplines including biology, genetics, pharmacology, neurology, neurosurgery, and related fields are involved in this research.

We encourage the submission of research articles, reviews, and perspectives on all relevant topics.

Dr. Claudia Ricci
Guest Editor

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Keywords

  • neurological diseases
  • pathogenesis
  • therapy
  • personalized medicine
  • early diagnosis
  • genetics
  • neurology
  • pharmacology

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Published Papers (1 paper)

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Research

16 pages, 5765 KiB  
Article
Gene Expression of Neurogenesis Related to Exercise Intensity in a Cerebral Infarction Rat Model
by Min-Keun Song, Hyun-Seok Jo, Eun-Jong Kim, Jung-Kook Kim and Sam-Gyu Lee
Int. J. Mol. Sci. 2024, 25(16), 8997; https://doi.org/10.3390/ijms25168997 - 19 Aug 2024
Viewed by 861
Abstract
Regular exercise improves several functions, including cognition, in patients with stroke. However, the effect of regular exercise on neurogenesis related to cognition remains doubtful. We investigated the most effective exercise intensity for functional recovery after stroke using RNA sequencing following regular treadmill exercise. [...] Read more.
Regular exercise improves several functions, including cognition, in patients with stroke. However, the effect of regular exercise on neurogenesis related to cognition remains doubtful. We investigated the most effective exercise intensity for functional recovery after stroke using RNA sequencing following regular treadmill exercise. Photothrombotic cerebral infarction was conducted for 10-week-old male Sprague-Dawley rats (n = 36). A Morris water maze (MWM) test was performed before a regular treadmill exercise program (5 days/week, 4 weeks). Rats were randomly divided into four groups: group A (no exercise); group B (low intensity, maximal velocity 18 m/min); group C (moderate intensity, maximal velocity 24 m/min) and group D (high intensity, maximal velocity 30 m/min). After 4 weeks, another MWM test was performed, and all rats were sacrificed. RNA sequencing was performed with ipsilesional hippocampal tissue. On the day after cerebral infarction, no differences in escape latency and velocity were observed among the groups. At 4 weeks after cerebral infarction, the escape latencies in groups B, C, and D were shorter than in group A. The escape latencies in groups B and C were shorter than in group D. The velocity in groups A, B, and C was faster than in group D. Thirty gene symbols related to neurogenesis were detected (p < 0.05, fold change > 1.0, average normalized read count > four times). In the neurotrophin-signaling pathway, the CHK gene was upregulated, and the NF-κB gene was downregulated in the low-intensity group. The CHK and NF-κB genes were both downregulated in the moderate-intensity group. The Raf and IRAK genes were downregulated in the high-intensity group. Western blot analysis showed that NF-κB expression was lowest in the moderate-intensity group, whereas CHK and Raf were elevated, and IRAK was decreased in the high-intensity group. Moderate-intensity exercise may contribute to neuroplasticity. Variation in the expression of neurotrophins in neurogenesis according to exercise intensity may reveal the mechanism of neuroplasticity. Thus, NF-κB is the key neurotrophin for neurogenesis related to exercise intensity. Full article
(This article belongs to the Special Issue Neurological Diseases: From Molecular Basis to Therapy)
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