Applications of Biomedical Technology and Molecular Biological Approach in Brain Diseases, 2nd Edition

Topic Information

Dear Colleagues,

This topic issue is a continuation of the previous successful topic “Applications of Biomedical Technology and Molecular Biological Approach in Brain Diseases”.

This topic includes the assessment of brain diseases and their mechanisms using various biomedical technologies and molecular biological approaches and also includes developments in novel treatments and interventions. In this topic issue, the range of brain diseases comprise neurological diseases and psychiatric disorders. Neurological diseases (e.g., Alzheimer’s disease and Parkinson’s disease) are hot topics for aging societies across many counties, and their treatments and interventions remain unsolved questions. By contrast, patients with psychiatric disorders suffer from chronic symptoms and relapse. Moreover, many psychiatric diseases such as schizophrenia, post-traumatic stress disorder, bipolar disorders, and anxiety disorders cannot be treated using long-term medicinal treatments or psychological interventions.

This topic issue encourages researchers to submit any manuscripts that examine the mechanisms of and/or treatments for any brain diseases, including neurological diseases and psychiatric disorders. The scope of this topic issue includes, but is not limited to, the following technologies and approaches to investigating brain diseases:

1. Brain mapping: fMRI, MRI, PET, and CT;
2. Molecular and protein labeling: IHC, IF, WB, ELISA, IP, and ICC;
3. mRNA labeling: PCR, qRT-PCR, and Fish;
4. Others: optogenetics, chemogenetics, and HPLC.

Prof. Dr. Andrew Chih Wei Huang
Dr. Muh-Shi Lin
Dr. Anna Kozłowska
Dr. Bai Chuang Shyu
Prof. Dr. Seong Soo A. An
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Biomedicines biomedicines	3.9	6.8	2013	17 Days	CHF 2600	Submit
Brain Sciences brainsci	2.8	5.6	2011	16.2 Days	CHF 2200	Submit
Cells cells	5.2	10.5	2012	16 Days	CHF 2700	Submit
International Journal of Molecular Sciences ijms	4.9	9.0	2000	20.5 Days	CHF 2900	Submit
Journal of Clinical Medicine jcm	2.9	5.2	2012	17.7 Days	CHF 2600	Submit
Neurology International neurolint	3.0	4.8	2009	21.4 Days	CHF 1800	Submit

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Published Papers (2 papers)

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All Biomedicines Brain Sciences Cells IJMS JCM Neurology International

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28 pages, 2056 KB  

Open AccessReview

From Aberrant Brainwaves to Altered Plasticity: A Review of QEEG Biomarkers and Neurofeedback in the Neurobiological Landscape of ADHD

by Marta Kopańska and Julia Trojniak

Cells 2025, 14(17), 1339; https://doi.org/10.3390/cells14171339 - 29 Aug 2025

Viewed by 693

Abstract

This critical review synthesizes findings from quantitative electroencephalography (QEEG) to bridge the gap between systems-level neurophysiology and the underlying cellular pathology of Attention-Deficit/Hyperactivity Disorder (ADHD). As a prevalent neurodevelopmental disorder, ADHD diagnosis is challenged by symptomatic heterogeneity, creating an urgent need for objective [...] Read more.

This critical review synthesizes findings from quantitative electroencephalography (QEEG) to bridge the gap between systems-level neurophysiology and the underlying cellular pathology of Attention-Deficit/Hyperactivity Disorder (ADHD). As a prevalent neurodevelopmental disorder, ADHD diagnosis is challenged by symptomatic heterogeneity, creating an urgent need for objective biological indicators. Analysis of QEEG data reveals consistent neurophysiological patterns in ADHD, primarily an excess of Theta-band activity and a deficit in Beta-band activity. These findings have led to the proposal of specific biomarkers, such as the Theta/Beta Ratio (TBR), and serve as the basis for neurofeedback interventions aimed at modulating brainwave activity. While not a standalone diagnostic tool, this review posits that QEEG-based biomarkers and Neurofeedback responses are systems-level manifestations of putative cellular and synaptic dysfunctions. By outlining these robust macro-scale patterns, this work provides a conceptual framework intended to guide future molecular and cellular research into the fundamental biology of ADHD. Full article

(This article belongs to the Topic Applications of Biomedical Technology and Molecular Biological Approach in Brain Diseases, 2nd Edition)

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19 pages, 3496 KB  

Open AccessArticle

Sulbactam: A β–Lactam Compound with Neuroprotective Effects in Epilepsy

by Fang-Chia Chang, Chiung-Hui Liu, Wen-Chieh Liao, Yu-Shiuan Tzeng, Ru-Yin Tsai, Li-Ho Tseng, Ching-Sui Hung, Shey-Lin Wu and Ying-Jui Ho

Neurol. Int. 2025, 17(9), 135; https://doi.org/10.3390/neurolint17090135 - 27 Aug 2025

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Abstract

Background: The pathophysiology of epilepsy is characterized by increased neuronal activity due to an excess of the excitatory neurotransmitter glutamate and a deficiency in the inhibitory neurotransmitter gamma–aminobutyric acid (GABA). Epilepsy presents with seizures, neuronal loss, and hyperactivity in the subthalamic nucleus (STN). [...] Read more.

Background: The pathophysiology of epilepsy is characterized by increased neuronal activity due to an excess of the excitatory neurotransmitter glutamate and a deficiency in the inhibitory neurotransmitter gamma–aminobutyric acid (GABA). Epilepsy presents with seizures, neuronal loss, and hyperactivity in the subthalamic nucleus (STN). Astrocytes play a crucial role by absorbing extracellular glutamate through glutamate transporter–1 (GLT–1), thereby reducing neuronal excitation. Upregulating the expression of astrocytic GLT–1 is a promising therapeutic strategy for epilepsy. Sulbactam (SUL), a β–lactam antibiotic, has been demonstrated to exert neuroprotective effects by upregulating GLT–1 expression. Objectives: This study investigated the impact of SUL on neuronal and behavioral changes in epilepsy by using a pentylenetetrazol (PTZ)-induced rat model of epilepsy. Methods: Rats were treated with saline, SUL (50 and 150 mg/kg), or a combination of SUL and the GLT–1 blocker dihydrokainate (DHK) for 20 days. Subsequently, behavioral tasks were conducted to assess recognition, anxiety, and memory. Results: Histological analyses revealed that SUL ameliorated neuronal deficits, increased astrocytic GLT–1 expression, and reduced hyperactivity in the STN. Additionally, SUL promoted astrocyte proliferation, indicating a new dimension of its neuroprotective properties. However, the beneficial effects of SUL were prevented by DHK. Conclusions: This pioneering study highlights multiple benefits of SUL, including seizure suppression, increased GLT–1 expression, and astrocyte proliferation, underscoring its high potential as a treatment for epilepsy. Full article

(This article belongs to the Topic Applications of Biomedical Technology and Molecular Biological Approach in Brain Diseases, 2nd Edition)

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