Khairunnuur Fairuz Azman

Introduction/Objective: Alzheimer's disease is a neurodegenerative disorder characterized by progressive cognitive decline and memory loss. In recent years, inflammation has gained recognition as a key contributor to both the onset and progression of Alzheimer's disease, acting through complex pathways that include neuroinflammation and immune system dysregulation. This study aims to systematically review the relationship between Alzheimer's disease and inflammation, focusing on publication trends from 2000 to 2023. Methods: Using the Scopus database, a bibliometric analysis was conducted through Microsoft Excel, Harzing’s Publish or Perish, and VOSviewer, examining publication trends, citation metrics, and co-network visualization. Results: A total of 1,205 relevant publications were identified, revealing a steady increase in research output. The majority of contributions came from the United States (33.1%), China (16.8%), and the United Kingdom (8.8%). Key terms such as "neuroinflammation", "cytokine", "microglia", "amyloid beta", and "oxidative stress" dominated the literature, while emerging keywords included "neuroprotection", "BDNF", "inflammasome", and "mitochondria". Conclusion: These findings underscore the growing focus on the role of inflammatory processes in the etiopathology of Alzheimer's disease, as well as efforts to identify biomarkers and neuroprotective therapeutic targets. This study provides a detailed mapping of the research landscape, offering insights into the evolving knowledge structure and highlighting prominent countries, institutions, authors, journals, and highly cited articles. By identifying key trends, this review advances our understanding of the interplay between inflammation and Alzheimer's disease, paving the way for future research and clinical strategies.

Stress is a multifaceted response involving physiological, psychological, and behavioural processes, with neurotransmitters such as serotonin, dopamine, and norepinephrine playing key modulatory roles. This study aimed to map global research trends on stress and neurotransmitters, identify thematic clusters, and highlight emerging frontiers relevant to health and disease. A bibliometric analysis was conducted on 4,132 publications indexed in Scopus between 2000 and 2023. Data were retrieved and processed using Excel and Harzing’s Publish or Perish, and analyzed with VOSviewer to generate co-authorship, co-occurrence, and citation network visualizations. Publications on stress and neurotransmitters have shown a consistent upward trend over the past two decades. The United States, China, and Japan emerged as the leading contributors. Core keywords included stress, neurotransmitters, serotonin, dopamine, glutamate, depression, anxiety, and oxidative stress. Emerging terms such as antioxidants, neuroprotection, inflammation, BDNF, GABA, acetylcholinesterase, metabolism, and gene expression indicate growing interest in neurochemical pathways and their role in mental and neurodegenerative disorders. The network analysis revealed strong global collaboration and multidisciplinary research across neuroscience, psychology, and molecular biology. This study provides the first comprehensive bibliometric mapping of global research on the links between stress and neurotransmitters. By highlighting established themes and emerging areas such as BDNF-related signaling and metabolic-neurochemical interactions, the findings contribute to a deeper understanding of stress modulation mechanisms. These insights may guide future translational research and inform the development of targeted strategies for managing stress-related physical and mental health disorders.

Diabetes mellitus (DM) is a long-term metabolic condition associated with hyperglycemia, which either insulin resistance, insulin secretion insufficiency, or a combination of both can cause. The antidiabetic treatment options, insulin, metformin, and more recent pharmacological treatments, possess some limitations, such as adverse effects, insufficient efficacy, and poor adherence, which require safer and more thorough treatment strategies. Geniposide is a multitarget antidiabetic agent with β-cell protective and glucose homeostasis-regulatory effects. In preclinical research, geniposide inhibits hepatic gluconeogenesis by AMPK-FoxO1 signaling, raises insulin release, lowers oxidative stress and inflammation, and promotes peripheral glucose absorption through PI3K/Akt-GLUT4. Geniposide also regulates metabolic homeostasis by modulating the composition and activity of gut microbiota. It is synergistic with other bioactives, such as baicalin, berberine, crocin I, and TUDCA, which can improve its therapeutic potential and highlight the possibilities of combination therapy. Although preclinical evidence is promising, clinical trials are still limited, particularly, ideal dosing, long-term safety, and bioavailability. This review presents an overview of the mechanistic understanding, organ-specific actions, pharmacokinetic, and combination therapy prospective of geniposide with special focus on its potential as a multitarget antidiabetic biomolecule. Further studies incorporating modern drug delivery technology and clinical studies are needed to validate preclinical results into effective, safe, and patient-specific treatments against DM.

Chronic pain is a significant and global healthcare issue that hugely implies the quality of life and productivity of the affected individuals. It is challenging to treat and thus necessitates a deeper understanding of its underlying pathomechanisms to develop targeted interventions. Serotonin is one of the essential neurotransmitters involved in the propagation of pain signals through both ascending and descending pathways, acting via various receptor subtypes, including the 5-hydroxytryptamine receptor-6 (5-HT6R). Recent studies have shed light on the involvement of 5-HT6R in the pathophysiology of chronic pain. This review aimed to uncover the emerging roles of 5-HT6R in chronic pain research by focusing on its functions in pain modulation, neuronal excitability, and pain processing. Although 5-HT6R has been recently discovered, previous studies have revealed its therapeutic effects in modulating chronic pain. Understanding the precise mechanism underlying the 5-HT6R may offer new avenues for future strategies of chronic pain management and indirectly improve the individual’s quality of life. However, further research is warranted to elucidate the intricate interplay between 5-HT6R and other pain modulatory pathways, paving the way for more effective and tailored therapeutic strategies for chronic pain.

Huntington's disease is a hereditary neurodegenerative disorder marked by severe neurodegeneration in the striatum and cortex. Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family of growth factors. It plays a crucial role in maintaining the survival and proper function of striatal neurons. Depletion of BDNF has been linked to impairment and death of striatal neurons, leading to the manifestation of motor, cognitive, and behavioral dysfunctions characteristic of Huntington's disease. This review highlights the current update on the neurobiology of BDNF in the pathogenesis of Huntington's disease. The molecular evidence and the affected signaling pathways are also discussed. In addition, the impact of experimental manipulation of BDNF levels and its pharmaceutical potential for Huntington's disease treatment are explicitly reviewed.

Neurotrophins, such as brain-derived neurotrophic factor (BDNF), are essential for neuronal survival and growth. The signaling cascades initiated by BDNF and its receptor are the key regulators of synaptic plasticity, which plays important role in learning and memory formation. Changes in BDNF levels and signaling pathways have been identified in several neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease, and have been linked with the symptoms and course of these diseases. This review summarizes the current understanding of the role of BDNF in several neurodegenerative diseases, as well as the underlying molecular mechanism. The therapeutic potential of BDNF treatment is also discussed, in the hope of discovering new avenues for the treatment of neurodegenerative diseases.

Objectives: This study aimed to profile the cognitive aging research landscape from 1956 to 2021. Methods: A total of 3,779 documents were retrieved from the Scopus database for the bibliometric analysis and network visualization. By comparing each keyword’s overall connection strength (centrality), frequency (density), and average year of publication (novelty) to the calculated median values acquired from the overlay view of the VOSviewer map, the enhanced strategic diagrams (ESDs) were constructed. Results: The findings showed an increasing trend in the number of publications. The United States leads the contributing countries in cognitive aging research. The scientific productivity pattern obeyed Lotka’s law. The most productive researcher was Deary, I. J., with the highest number of publications. The collaborative index showed an increasing trend from 1980 onwards. Frontiers in Aging Neuroscience is the most prestigious journal in the field of cognitive aging research. In Bradford core journals zone 1, the top 10 core journals of cognitive aging research provided more than half of the total articles (697, or 55.36 percent). Conclusions: For the next decades, the trending topics in cognitive aging research include neuropsychological assessment, functional connectivity, human immunodeficiency virus (HIV), decision-making, gender, compensation, default mode network, learning and memory, brain-derived neurotrophic factor (BDNF), obesity, D-galactose, epigenetics, frailty, mortality, mini-mental state examination (MMSE), anxiety, and gait speed.

While the pathological mechanism of Alzheimer’s Disease (AD) is unclear, oxidative stress has been proposed to be one of its related theories, which can help to uncover the disease’s pathological factors. This review aims to provide a quantitative description and data visualisation of oxidative stress and AD research from the literature obtained from the Scopus database. Based on the keywords used, which are related to oxidative stress and AD in the article title, 996 documents were retrieved for further analysis. Microsoft Excel, VOSviewer, and Harzing’s Publish or Perish were used to conduct the frequency analysis, data visualization, and citation analysis. There is a continuous growth in the number of publications on research in oxidative stress and AD, starting from 1986 and spanning 35 years. The most cited article was “Oxidative stress hypothesis in Alzheimer's disease”. The Journal of Alzheimer's Disease published the most number of publications related to oxidative stress and AD, while the United States and its institutions were the main contributors. Our findings suggest that research on aetiopathology, biomarkers, and neuroprotective agents for AD dominated this research field. Our bibliometric analysis provides distinct trends in oxidative stress and AD research in the last 35 years. Our findings highlight current hot topics related to biomarkers for screening and diagnosis of AD as well as neuroprotective agents used as disease-modifying therapies of AD.