Role of Inflammation, Oxidative Stress, and Metabolic Dysfunction in Neurodevelopmental and Neurodegenerative Diseases: Pharmacological Targets and Therapeutic Interventions

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neurodegenerative Diseases".

Deadline for manuscript submissions: 16 November 2024 | Viewed by 1375

Special Issue Editor


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Guest Editor
LSUHSC Neuroscience Center, New Orleans, LA, USA
Interests: pharmacology; neuroscience; preclinical research; Alzheimer’s disease; rodent models

Special Issue Information

Dear Colleagues,

Neurodegeneration is a multifactorial progressive phenomenon that primarily arises from neuronal loss in specific brain regions, which leads to various pathological manifestations including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis. Additionally, neurodevelopmental disorders such as autism, cerebral palsy, ADHD mainly occur in infants and children either due to brain damage or altered gene levels. Many of the genes and molecular pathways to be targeted require further exploration.

The etiological factors associated with neurodegenerative and neurodevelopmental disorders also include neuroinflammation, oxidative stress, mitochondrial dysfunction, brain insulin resistance and impairments of the energy metabolism. These cascades might further comprise several molecular bases that result in neurodegeneration or skewed neurodevelopment. Moreover, there are inconclusive findings regarding the pathogenesis of these diseases. Currently, it is only the symptoms of these diseases that are treated, without completely halting the progression of the disease.

This Special Issue will be focused on novel targets that influence the interconnected pathways of inflammation, oxidative stress, and metabolism directly or indirectly. Various potential pharmacological approaches and their mechanistic insights will be explored in order to reverse these detrimental features. Hence, we are soliciting papers that present cutting-edge research and review articles addressing molecular and cellular mechanisms that have not been explored in great detail previously. It is hoped that these can enhance our understanding of innovative therapeutic strategies and open avenues for future clinical research.

Dr. Ansab Akhtar
Guest Editor

Manuscript Submission Information

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Keywords

  • neuroinflammation
  • oxidative stress
  • mitochondrial dysfunction
  • metabolism
  • metabolomics
  • neurodegenerative diseases
  • neurodevelopmental diseases
  • pharmacological targets
  • potential drugs

Published Papers (1 paper)

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Review

23 pages, 2058 KiB  
Review
Indole-3-Carbinol and Its Derivatives as Neuroprotective Modulators
by Alka Ashok Singh, Dhananjay Yadav, Fazlurrahman Khan and Minseok Song
Brain Sci. 2024, 14(7), 674; https://doi.org/10.3390/brainsci14070674 - 2 Jul 2024
Viewed by 846
Abstract
Brain-derived neurotrophic factor (BDNF) and its downstream tropomyosin receptor kinase B (TrkB) signaling pathway play pivotal roles in the resilience and action of antidepressant drugs, making them prominent targets in psychiatric research. Oxidative stress (OS) contributes to various neurological disorders, including neurodegenerative diseases, [...] Read more.
Brain-derived neurotrophic factor (BDNF) and its downstream tropomyosin receptor kinase B (TrkB) signaling pathway play pivotal roles in the resilience and action of antidepressant drugs, making them prominent targets in psychiatric research. Oxidative stress (OS) contributes to various neurological disorders, including neurodegenerative diseases, stroke, and mental illnesses, and exacerbates the aging process. The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant responsive element (ARE) serves as the primary cellular defense mechanism against OS-induced brain damage. Thus, Nrf2 activation may confer endogenous neuroprotection against OS-related cellular damage; notably, the TrkB/phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) pathway, stimulated by BDNF-dependent TrkB signaling, activates Nrf2 and promotes its nuclear translocation. However, insufficient neurotrophin support often leads to the downregulation of the TrkB signaling pathway in brain diseases. Thus, targeting TrkB activation and the Nrf2-ARE system is a promising therapeutic strategy for treating neurodegenerative diseases. Phytochemicals, including indole-3-carbinol (I3C) and its metabolite, diindolylmethane (DIM), exhibit neuroprotective effects through BDNF’s mimetic activity; Akt phosphorylation is induced, and the antioxidant defense mechanism is activated by blocking the Nrf2-kelch-like ECH-associated protein 1 (Keap1) complex. This review emphasizes the therapeutic potential of I3C and its derivatives for concurrently activating neuronal defense mechanisms in the treatment of neurodegenerative diseases. Full article
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