Hongjun Zhen’s scientific contributions

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Publications (2)


FIGURE E
FIGURE Association between Aβ and age in AD and non-AD groups. The cyan dots and lines represent the samples and fitted lines for the non-AD group, respectively. Red dots and lines represent samples and fitted lines for the AD group, respectively. Scatterplot of the association between Aβ and age (A) and Fitted curves for all participants (B). Association between Aβ and age in the AD and non-AD groups (C) and the p-value and R-value for each of the two groups (D).
Association between Alzheimer's disease pathologic products and age and a pathologic product-based diagnostic model for Alzheimer's disease
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December 2024

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18 Reads

Frontiers in Aging Neuroscience

Weizhe Zhen

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Yu Wang

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Hongjun Zhen

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Background Alzheimer's disease (AD) has a major negative impact on people's quality of life, life, and health. More research is needed to determine the relationship between age and the pathologic products associated with AD. Meanwhile, the construction of an early diagnostic model of AD, which is mainly characterized by pathological products, is very important for the diagnosis and treatment of AD. Method We collected clinical study data from September 2005 to August 2024 from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database. Using correlation analysis method like cor function, we analyzed the pathology products (t-Tau, p-Tau, and Aβ proteins), age, gender, and Minimum Mental State Examination (MMSE) scores in the ADNI data. Next, we investigated the relationship between pathologic products and age in the AD and non-AD groups using linear regression. Ultimately, we used these features to build a diagnostic model for AD. Results A total of 1,255 individuals were included in the study (mean [SD] age, 73.27 [7.26] years; 691male [55.1%]; 564 female [44.9%]). The results of the correlation analysis showed that the correlations between pathologic products and age were, in descending order, Tau (Corr=0.75), p-Tau (Corr=0.71), and Aβ (Corr=0.54). In the AD group, t-Tau protein showed a tendency to decrease with age, but it was not statistically significant. p-Tau protein levels similarly decreased with age and its decrease was statistically significant. In contrast to Tau protein, in the AD group, Aβ levels increased progressively with age. In the non-AD group, the trend of pathologic product levels with age was consistently opposite to that of the AD group. We finally screened the optimal AD diagnostic model (AUC=0.959) based on the results of correlation analysis and by using the Xgboost algorithm and SVM algorithm. Conclusion In a novel finding, we observed that Tau protein and Aβ had opposite trends with age in both the AD and non-AD groups. The linear regression curves of the AD and non-AD groups had completely opposite trends. Through a machine learning approach, we constructed an AD diagnostic model with excellent performance based on the selected features.

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FIGURE 1
Herbal drugs that promote nerve regeneration through other ways.
Mechanism of ERK/CREB pathway in pain and analgesia

March 2023

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46 Reads

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13 Citations

Frontiers in Molecular Neuroscience

Research has long centered on the pathophysiology of pain. The Transient Receiver Potential (TRP) protein family is well known for its function in the pathophysiology of pain, and extensive study has been done in this area. One of the significant mechanisms of pain etiology and analgesia that lacks a systematic synthesis and review is the ERK/CREB (Extracellular Signal-Regulated Kinase/CAMP Response Element Binding Protein) pathway. The ERK/CREB pathway-targeting analgesics may also cause a variety of adverse effects that call for specialized medical care. In this review, we systematically compiled the mechanism of the ERK/CREB pathway in the process of pain and analgesia, as well as the potential adverse effects on the nervous system brought on by the inhibition of the ERK/CREB pathway in analgesic drugs, and we suggested the corresponding solutions.

Citations (1)


... In a neuropathic pain model, ERK activation in spinal neurons and microglia leads to spontaneous firing and sustained ERK activation, contributing to pain transmission 38 . Peripheral noxious stimuli trigger ERK phosphorylation in neurons, influencing neurotransmitter receptors, glycine receptors, potassium channels, and gene transcription, which together promote pain and negative emotions 39 . ERK also mediates central sensitization through various pathways 40 and is activated in brain regions like the amygdala and hippocampus in response to peripheral nociception, influencing pain-related emotions [41][42][43][44] . ...

Reference:

Astragalin relieves inflammatory pain and negative mood in CFA mice by down-regulating mGluR5 signaling pathway
Mechanism of ERK/CREB pathway in pain and analgesia

Frontiers in Molecular Neuroscience