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Creutzfeldt-Jakob disease mimicking Hashimoto’s encephalopathy: steroid response followed by decline

  • Tian-Chen Wu , Feng Zhao , Yan Liang , Zheng-Zheng Wu , Jin-Bin Chen , Zhen-Nian Zhang and Hui Yang EMAIL logo
Published/Copyright: December 30, 2025
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Open Life Sciences
From the journal Open Life Sciences Volume 20 Issue 1

Abstract

The diagnosis of Creutzfeldt–Jakob disease (CJD) is particularly challenging because its heterogeneous clinical presentations mimic other rapidly progressive dementias and neurodegenerative disorders (e.g., Hashimoto’s encephalopathy, autoimmune encephalitis, atypical Alzheimer’s disease). Diffusion-weighted imaging (DWI) is the most sensitive neuroimaging sequence for diagnosing CJD. However, early magnetic resonance imaging (MRI) findings may be subtle or evolving, and autoimmune etiologies often remain in the differential. Therefore, empiric corticosteroids are reserved for cases in which an autoimmune etiology is under consideration while definitive tests are pending. A 67-year-old woman presented with rapidly progressive cognitive decline, ataxia, and visual symptoms. Short-course glucocorticoids produced transient improvement for three days, followed by rapid deterioration within a week. Serial MRI evolved from cortical ribboning to basal ganglia involvement. Electroencephalogram (EEG) showed non-convulsive status epilepticus that responded to diazepam and valproate. Cerebrospinal fluid (CSF) 14-3-3 protein (14-3-3) and RT-QuIC were positive, confirming prion disease. CJD can present with features resembling HE, and brief improvement after a short course of glucocorticoids, even in the presence of markedly elevated thyroid antibodies, does not exclude CJD. To avoid diagnostic delay, obtain CSF RT-QuIC and 14-3-3 at presentation before or in parallel with glucocorticoids, and use serial MRI and EEG to arbitrate.

Keywords: Creutzfeldt-Jakob disease; electroencephalogram; glucocorticoid pulse therapy; Hashimoto’s encephalopathy; magnetic resonance imaging

1 Background

Creutzfeldt–Jakob disease (CJD) is a uniformly fatal prion disease that presents with rapidly progressive dementia accompanied by myoclonus, visual or cerebellar dysfunction, extrapyramidal or pyramidal signs, and akinetic mutism [1], 2]. Diagnosis relies on clinical features supported by diffusion-weighted magnetic resonance imaging (MRI) showing cortical ribboning or basal ganglia hyperintensities, electroencephalogram (EEG) with periodic sharp-wave complexes, and cerebrospinal fluid (CSF) biomarkers such as RT-QuIC, 14-3-3 protein (14-3-3), and total tau [3]. Hashimoto’s encephalopathy (HE), also termed steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT), is an autoimmune encephalopathy with subacute cognitive and psychiatric symptoms, seizures, and tremor or ataxia. MRI is often normal or nonspecific, EEG typically shows generalized slowing, CSF protein may be mildly elevated, and most patients improve with corticosteroids, IVIG, or plasma exchange [4], 5]. Misdiagnosis arises because CJD can mimic autoimmune encephalopathies [6] and antithyroid antibodies are prevalent and nonspecific, particularly in older adults; the diagnostic yield of a single early MRI or EEG may be limited and can improve on serial studies [7], 8]; CSF testing is often delayed due to its invasive nature and consent or logistical constraints; and limited access to RT-QuIC with slow turnaround encourages empiric immunosuppression while definitive results are pending. We report a patient with CJD who had elevated thyroid antibodies, transient cognitive improvement, and rapid deterioration after glucocorticoid pulse therapy, underscoring diagnostic pitfalls and the need to prioritize prion-specific biomarkers.

2 Case report

A 67-year-old woman was admitted to the hospital with a 2-week history of worsening neurological symptoms, including vertigo, blurred vision, diplopia, ataxia, and rapidly declining cognitive function. Four days before admission, she developed irritability and difficulty in expressing herself verbally. Her past medical, surgical, and family history was otherwise unremarkable, with no history of raw meat consumption, substance abuse, familial neurological disorders, neurosurgical procedures, blood transfusion, organ or tissue transplantation, or known exposure to individuals with similar symptoms. Detailed review of her residence history, dietary habits, and vaccination history did not reveal any clear source of prion exposure or infection.

On admission, her vital signs were stable, and general physical examination showed no abnormalities outside the nervous system. Routine laboratory tests, including complete blood count, serum electrolytes, liver and renal function tests, coagulation profile, and fasting glucose, were within normal limits. Screening for common infectious diseases (including hepatitis B and C, human immunodeficiency virus, and syphilis) was negative, and tumor markers were not elevated.

Gait impairment with rightward drift, recent memory loss, and tremors in the distal upper extremities was identified through a neurological examination upon admission. Muscle tone was normal, Romberg’s sign was positive, and bilateral Babinski and Hoffman signs were absent. Cognitive assessment revealed mild impairment, with a MoCA-BJ score of 17 [9]. Initial brain MRI demonstrated abnormal signals in the bilateral temporal, parietal, and occipital cortices, as well as the left frontal cortex and left semioval center (Figure 1). EEG indicated frontal slow waves (Figure 2A).

Figure 1: Serial brain MRI progression in prion disease. Images acquired on admission day 1 (top row), day 3 (middle row), and day 7 post-glucocorticoid (bottom row), across T2-weighted, MRA, ADC, and DWI sequences (left to right). Key DWI findings: day 1 – cortical ribbon sign with hyperintensity in bilateral temporoparietal and occipital cortices; day 3 – development of hockey stick sign in bilateral caudate heads and medial thalami (arrows); day 7 – new hyperintensity in the right globus pallidus (arrow) and more extensive cortical and deep gray matter involvement.
Figure 1:

Serial brain MRI progression in prion disease. Images acquired on admission day 1 (top row), day 3 (middle row), and day 7 post-glucocorticoid (bottom row), across T2-weighted, MRA, ADC, and DWI sequences (left to right). Key DWI findings: day 1 – cortical ribbon sign with hyperintensity in bilateral temporoparietal and occipital cortices; day 3 – development of hockey stick sign in bilateral caudate heads and medial thalami (arrows); day 7 – new hyperintensity in the right globus pallidus (arrow) and more extensive cortical and deep gray matter involvement.

Figure 2: Serial EEG changes during hospitalization. (A) Day 1: slowed α background with mildly increased δ activity in all leads (arrows). (B) Day 3: after diazepam, normal α background with mildly increased medium-amplitude δ activity, most prominent over the right frontal and temporal regions (arrows). (C) Day 7: θ background after glucocorticoid therapy. EEG was recorded using an average reference (AV).
Figure 2:

Serial EEG changes during hospitalization. (A) Day 1: slowed α background with mildly increased δ activity in all leads (arrows). (B) Day 3: after diazepam, normal α background with mildly increased medium-amplitude δ activity, most prominent over the right frontal and temporal regions (arrows). (C) Day 7: θ background after glucocorticoid therapy. EEG was recorded using an average reference (AV).

The patient exhibited an unsteady gait, perseverative behaviors, and thalamic aphasia, along with increased upper limb tremors and worsening cognitive function by the third day of hospitalization. Follow-up MRI revealed new abnormalities in the caudate nuclei and putamen (Figure 1: D2-3). Suspected non-convulsive status epilepticus (NCSE) was managed with intravenous diazepam and oral sodium valproate, resulting in temporary improvement (Figure 2).

The patient’s cognitive function declined significantly one week after admission. CSF analysis revealed normal cell counts, protein, and glucose levels, with no abnormalities. CSF findings are summarized in Supplementary Table S1. Thyroid ultrasonography showed diffuse thyroid enlargement, and serum anti-TPO and anti-TG antibodies were elevated. After endocrinology consultation, HE remained a leading consideration; therefore, a brief empiric course of high-dose glucocorticoids plus selenium yeast tablets was initiated while CSF prion studies were arranged, as CJD remained in the differential given diffusion-weighted imaging (DWI) cortical ribboning and concurrent NCSE. Despite initial improvement, the patient’s condition rapidly worsened seven days after starting glucocorticoid therapy. A comprehensive autoimmune panel, including serum and CSF autoantibodies (anti-NMDAR, anti-AMPAR, anti-GABAR, anti-LGI1, anti-CASPR2, and anti-aquaporin 4), returned negative results. Follow-up MRI showed progressive abnormalities (Figure 1: D3-3). CSF analysis by the Chinese CDC detected positive 14-3-3 protein, and RT-QuIC confirmed the presence of abnormal prion protein (PrP). Based on the clinical presentation, neuroimaging findings, and positive CSF biomarkers (14-3-3 protein and RT-QuIC), a definitive diagnosis of sporadic CJD was made. The patient succumbed 8 months after symptom onset. Postmortem neuropathological examination confirmed pathological prion protein (PrPSc), confirming the diagnosis of CJD.

3 Discussion

A patient diagnosed with sporadic Creutzfeldt-Jakob disease (sCJD) is presented in this case, characterized by rapid cognitive decline, cerebellar ataxia, visual impairment, and transient improvement of symptoms following glucocorticoid therapy. The presence of the ribbon sign on MRI, indicating cortical necrosis, contributed to the diagnosis.

Rapidly progressive cognitive decline requires a broad differential diagnosis including prion disease, rapidly progressive neurodegenerative dementia, autoimmune or infectious encephalitis, metabolic or toxic encephalopathy, vascular or inflammatory disease, and neoplastic involvement of the central nervous system. Huntington’s disease can also cause cognitive decline with psychiatric and behavioral symptoms [10], but usually follows a slow and insidious course rather than the subacute deterioration seen in our patient.

From a pathophysiological perspective, neurobehavioral manifestations in CJD are thought to result from dysfunction of large scale networks that include the frontal lobes, basal ganglia, and limbic system. Synaptic and mitochondrial impairment related to prion pathology in these regions may disturb cortical and subcortical connectivity as well as redox balance [11], and may underlie the rapid cognitive and behavioral decline in our patient.

The serial MRI findings in this case demonstrated the characteristic progression pattern of sCJD, offering crucial diagnostic evidence. The initial DWI sequences revealed cortical ribboning in the bilateral temporal, parietal, and occipital regions, which rapidly progressed to involve the basal ganglia within three days. This imaging evolution is consistent with recent studies, which demonstrates that DWI is the most sensitive neuroimaging sequence for diagnosing CJD, with cortical signal abnormalities detected in approximately 80–90 % of cases [8], 12]. The “cortical ribbon sign” observed represents restricted diffusion in the cerebral cortex, which has been established as an early and specific marker of CJD [8]. MRI revealed early, symmetrical hyperintensities in the basal ganglia, a pattern suggestive of prion-related pathology. Recent findings have demonstrated that basal ganglia involvement is present in approximately 73.4 % of CJD cases on DWI, compared to 37.8 % on FLAIR sequences [3]. The combination of cortical and basal ganglia involvement has demonstrated a sensitivity of 92 % and specificity of 80 % for diagnosing sCJD [8]. The imaging findings in this patient progressed from cortical ribboning to symmetrical basal ganglia hyperintensities, a pattern consistent with the temporal evolution reported in prion disease literature. The progressive nature of these changes, despite immunotherapy, further reinforced the diagnosis of CJD over other rapidly progressive dementias. Recent large cohorts and systematic reviews have shown that characteristic MRI abnormalities are present in roughly 80–90 % of patients with CJD, with a specificity in a similar 80–90 % range when distinguishing CJD from non-prion causes of rapidly progressive dementia [3], 8], 12].

The serial EEG recordings in this case revealed valuable diagnostic and monitoring features throughout the disease course. Initially, the EEG displayed nonspecific frontal slow waves, consistent with early-stage CJD, as reported by Hermann et al. [8]. Importantly, characteristic periodic sharp wave complexes (PSWCs) were not observed at any stage, even though such discharges are reported in roughly one-half to two-thirds of patients with sporadic CJD, particularly in more advanced phases of the disease [12], 13]. During the period of rapid neurological deterioration, the EEG instead showed patterns compatible with non-convulsive status epilepticus, with transient improvement after diazepam and sodium valproate, consistent with recent data indicating that seizures or seizure-like activity occur in a minority (approximately 15–20 %) of patients with CJD [12]. The absence of classic PSWCs in this case, despite a confirmed CJD diagnosis, supports the growing understanding that EEG patterns in CJD can be heterogeneous [14]. While EEG is a crucial diagnostic tool for CJD, this case highlights the need for careful interpretation taking into account the clinical context, disease stage, and potential confounding factors. It should also be integrated with other diagnostic methods for accurate diagnosis and management [15], 16]. Notably, peri-ictal cortical diffusion restriction associated with NCSE can mimic the cortical “ribbon sign” on DWI, which complicated early differentiation from autoimmune encephalopathy at presentation.

Interestingly, despite the progressive spread of abnormal MRI signals in the basal ganglia and cortex, a gradual resolution of sharp slow waves on the EEG was observed following the initiation of sodium valproate therapy, with no subsequent seizure manifestations. This therapeutic response indicates that the early recognition and prompt administration of antiepileptic medications in patients with probable CJD exhibiting seizure-like activities may be beneficial for symptom management. This observation aligns with recent studies, which indicate that timely anticonvulsant intervention may reduce seizure burden and improve the quality of life in patients with CJD, even as the underlying disease continues to progress [17]. This case underscores the significance of considering early antiepileptic treatment as part of the management strategy for probable patients with CJD presenting with seizure-like symptoms.

The definitive diagnosis of CJD in the case was supported by positive CSF 14-3-3 protein and RT-QuIC assay results. While 14-3-3 protein has traditionally served as a biomarker for CJD, with a sensitivity ranging from 85 % to 95 %, its specificity is relatively limited (60–75 %) due to its elevation in other neurological conditions [8]. In contrast, RT-QuIC has emerged as a groundbreaking diagnostic tool, demonstrating remarkable specificity (> 99 %) and sensitivity (92–96 %) for CJD diagnosis [18]. The combination of these biomarkers, especially the high specificity of RT-QuIC, facilitated rapid and accurate diagnosis of the patient. This is consistent with current diagnostic criteria, which highlight the importance of RT-QuIC as a dependable biomarker for ante-mortem CJD diagnosis [8], 12], 19]. In our setting, however, CSF 14-3-3 and RT-QuIC were available only as send-out tests (approximately 1-week turnaround), which delayed definitive confirmation at presentation.

CJD and HE can present with overlapping clinical features such as rapid cognitive decline, neuropsychiatric symptoms, and abnormal EEG findings - making misdiagnosis a critical concern. CJD, a fatal prion disease, along with positive CSF biomarkers like 14-3-3 protein and RT-QuIC [12]. In contrast, HE is an autoimmune encephalopathy associated with elevated anti-thyroid antibodies and often responds dramatically to corticosteroids [5]. Misdiagnosis arises when HE mimics CJD’s clinical trajectory but lacks definitive prion markers, leading to missed therapeutic windows. To prevent this, thyroid antibody testing, and CSF 14-3-3, RT-QuIC assays need to be included in the workup of rapidly progressive dementia, especially in middle-aged women, while consider a trial of high-dose glucocorticoid pulse therapy when autoimmune encephalopathy is suspected.

Due to abnormal thyroid-related antibody tests, HE was suspected, and glucocorticoid pulse therapy was administered. This decision balanced the differential while send-out prion testing was pending, with close MRI, EEG follow-up. While the patient exhibited initial improvement within 7 days of treatment, likely due to a reduction in neuroinflammation, the subsequent clinical course was characterized by dramatic deterioration, accompanied by newly developed abnormal signals in the right lentiform nucleus on the third MRI. This pattern, though differing, shares key similarities with the case reported by Jang et al., where a patient with CJD presenting with features mimicking HE demonstrated immediate deterioration following glucocorticoid pulse therapy [20]. The eventual rapid decline in the patient, despite the initial response, raises concerns about the potential role of glucocorticoids in accelerating CJD progression. This observation underscores the importance of excluding CJD through CSF 14-3-3 protein and RT-QuIC testing before initiating steroid therapy in suspected HE cases, particularly those presenting with rapid progressive dementia [3], 21].

Additionally, our investigation of the patient’s residence history, dietary habits, and vaccination history revealed no clear source of infection, and our patient had no documented SARS-CoV-2 infection. Recent reports suggest that long COVID may present with neurological symptoms and MRI findings overlapping with prion diseases [22], 23]. Therefore, asymptomatic prior infection cannot be entirely excluded.

4 Conclusions

CJD can present with features resembling HE, and brief improvement after a short course of glucocorticoids, even in the presence of markedly elevated thyroid antibodies, does not exclude CJD; the rapid deterioration after steroids observed in this case and in a prior Korean report raises concern for possible acceleration, although causality cannot be established. To avoid diagnostic delay, obtain CSF RT-QuIC and 14-3-3 at presentation before or in parallel with glucocorticoids, and use serial MRI and EEG to arbitrate.

Corresponding author: Hui Yang, School of Nursing, Nanjing University of Chinese Medicine, No. 138 of Xianlin Road, Qixia District, Nanjing 210000, China, E-mail:
Tian-Chen Wu and Feng Zhao contributed equally to this study.

Acknowledgments

The authors are grateful for the reviewers’ valuable comments that improved the manuscript.

  1. Funding information: This study was funded by the Natural Science Foundation of the Jiangsu Higher Education Institutions of China (No.24KJB360012), the Priority Academic Program Development of Jiangsu Higher Education Institutions (YSHL202517), National Natural Science Foundation of China (No. 81904112), and the Natural Science Foundation of Jiangsu Province (No. BK20190136). The funding bodies had no role in the design of the study and collection, analysis, and interpretation of data and in writing the manuscript.

  2. Author contribution: Tian-Chen Wu: Data curation, Funding acquisition, Writing – original draft, Writing – review & editing. Feng Zhao: Data curation, Formal Analysis, Writing – original draft, Writing – review & editing. Yan Liang: Data curation, Formal Analysis, Writing – original draft. Zheng-Zheng Wu: Software, Visualization. Jin-Bin Chen: Data curation, Formal Analysis, Software, Visualization. Zhen-Nian Zhang: Data curation, Formal Analysis, Visualization. Hui Yang: Conceptualization, Data curation, Formal Analysis, Funding acquisition, Writing – original draft, Writing – review & editing. All authors read and approved the final draft.

  3. Conflict of interest: Authors state no conflict of interest.

  4. Data availability statement: The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.

  5. Informed consent: Informed consent has been obtained from all individuals included in this study.

  6. Ethical approval: The research related to human use has been complied with all the relevant national regulations, institutional policies and in accordance with the tenets of the Helsinki Declaration, and has been approved by the Ethics Committee of Nanjing Hospital of Chinese Medicine (Approval No. KY2025071).

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Supplementary Material

This article contains supplementary material (https://doi.org/10.1515/biol-2025-1245).

Received: 2025-05-26
Accepted: 2025-12-01
Published Online: 2025-12-30

© 2025 the author(s), published by De Gruyter, Berlin/Boston

This work is licensed under the Creative Commons Attribution 4.0 International License.

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  231. Corrigendum
  232. Corrigendum to “Utilization of convolutional neural networks to analyze microscopic images for high-throughput screening of mesenchymal stem cells”
  233. Corrigendum to “Effects of Ire1 gene on virulence and pathogenicity of Candida albicans”
  234. Retraction
  235. Retraction of “Down-regulation of miR-539 indicates poor prognosis in patients with pancreatic cancer”
https://doi.org/10.1515/biol-2025-1245
Keywords for this article
Creutzfeldt-Jakob disease; electroencephalogram; glucocorticoid pulse therapy; Hashimoto’s encephalopathy; magnetic resonance imaging
Creative Commons
BY 4.0

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  124. Treatment of pure red cell aplasia in a chronic kidney disease patient with roxadustat: A case report
  125. Comparative bioinformatics analysis of the Wnt pathway in breast cancer: Selection of novel biomarker panels associated with ER status
  126. Kynurenine facilitates renal cell carcinoma progression by suppressing M2 macrophage pyroptosis through inhibition of CASP1 cleavage
  127. RFX5 promotes the growth, motility, and inhibits apoptosis of gastric adenocarcinoma cells through the SIRT1/AMPK axis
  128. ALKBH5 exacerbates early cardiac damage after radiotherapy for breast cancer via m6A demethylation of TLR4
  129. Phytochemicals of Roman chamomile: Antioxidant, anti-aging, and whitening activities of distillation residues
  130. Circadian gene Cry1 inhibits the tumorigenicity of hepatocellular carcinoma by the BAX/BCL2-mediated apoptosis pathway
  131. The TNFR-RIPK1/RIPK3 signalling pathway mediates the effect of lanthanum on necroptosis of nerve cells
  132. Longitudinal monitoring of autoantibody dynamics in patients with early-stage non-small-cell lung cancer undergoing surgery
  133. The potential role of rutin, a flavonoid, in the management of cancer through modulation of cell signaling pathways
  134. Construction of pectinase gene engineering microbe and its application in tobacco sheets
  135. Construction of a microbial abundance prognostic scoring model based on intratumoral microbial data for predicting the prognosis of lung squamous cell carcinoma
  136. Sepsis complicated by haemophagocytic lymphohistiocytosis triggered by methicillin-resistant Staphylococcus aureus and human herpesvirus 8 in an immunocompromised elderly patient: A case report
  137. Sarcopenia in liver transplantation: A comprehensive bibliometric study of current research trends and future directions
  138. Advances in cancer immunotherapy and future directions in personalized medicine
  139. Can coronavirus disease 2019 affect male fertility or cause spontaneous abortion? A two-sample Mendelian randomization analysis
  140. Heat stroke associated with novel leukaemia inhibitory factor receptor gene variant in a Chinese infant
  141. PSME2 exacerbates ulcerative colitis by disrupting intestinal barrier function and promoting autophagy-dependent inflammation
  142. Hyperosmolar hyperglycemic state with severe hypernatremia coexisting with central diabetes insipidus: A case report and literature review
  143. Efficacy and mechanism of escin in improving the tissue microenvironment of blood vessel walls via anti-inflammatory and anticoagulant effects: Implications for clinical practice
  144. Merkel cell carcinoma: Clinicopathological analysis of three patients and literature review
  145. Genetic variants in VWF exon 26 and their implications for type 1 Von Willebrand disease in a Saudi Arabian population
  146. Lipoxin A4 improves myocardial ischemia/reperfusion injury through the Notch1-Nrf2 signaling pathway
  147. High levels of EPHB2 expression predict a poor prognosis and promote tumor progression in endometrial cancer
  148. Knockdown of SHP-2 delays renal tubular epithelial cell injury in diabetic nephropathy by inhibiting NLRP3 inflammasome-mediated pyroptosis
  149. Exploring the toxicity mechanisms and detoxification methods of Rhizoma Paridis
  150. Concomitant gastric carcinoma and primary hepatic angiosarcoma in a patient: A case report
  151. YAP1 inhibition protects retinal vascular endothelial cells under high glucose by inhibiting autophagy
  152. Identification of secretory protein related biomarkers for primary biliary cholangitis based on machine learning and experimental validation
  153. Integrated genomic and clinical modeling for prognostic assessment of radiotherapy response in rectal neoplasms
  154. Stem cell-based approaches for glaucoma treatment: a mini review
  155. Bacteriophage titering by optical density means: KOTE assays
  156. Neutrophil-related signature characterizes immune landscape and predicts prognosis of esophageal squamous cell carcinoma
  157. Integrated bioinformatic analysis and machine learning strategies to identify new potential immune biomarkers for Alzheimer’s disease and their targeting prediction with geniposide
  158. TRIM21 accelerates ferroptosis in intervertebral disc degeneration by promoting SLC7A11 ubiquitination and degradation
  159. TRIM21 accelerates ferroptosis in intervertebral disc degeneration by promoting SLC7A11 ubiquitination and degradation
  160. Histone modification and non-coding RNAs in skin aging: emerging therapeutic avenues
  161. A multiplicative behavioral model of DNA replication initiation in cells
  162. Biogenic gold nanoparticles synthesized from Pergularia daemia leaves: a novel approach for nasopharyngeal carcinoma therapy
  163. Creutzfeldt-Jakob disease mimicking Hashimoto’s encephalopathy: steroid response followed by decline
  164. Impact of semaphorin, Sema3F, on the gene transcription and protein expression of CREB and its binding protein CREBBP in primary hippocampal neurons of rats
  165. Iron overloaded M0 macrophages regulate hematopoietic stem cell proliferation and senescence via the Nrf2/Keap1/HO-1 pathway
  166. Revisiting the link between NADPH oxidase p22phox C242T polymorphism and ischemic stroke risk: an updated meta-analysis
  167. Exercise training preferentially modulates α1D-adrenergic receptor expression in peripheral arteries of hypertensive rats
  168. Overexpression of HE4/WFDC2 gene in mice leads to keratitis and corneal opacity
  169. Tumoral calcinosis complicating CKD-MBD in hemodialysis: a case report
  170. Mechanism of KLF4 Inhibition of epithelial-mesenchymal transition in gastric cancer cells
  171. Dissecting the molecular mechanisms of T cell infiltration in psoriatic lesions via cell-cell communication and regulatory network analysis
  172. Circadian rhythm-based prognostic features predict immune infiltration and tumor microenvironment in molecular subtypes of hepatocellular carcinoma
  173. Ecology and Environmental Science
  174. Optimization and comparative study of Bacillus consortia for cellulolytic potential and cellulase enzyme activity
  175. The complete mitochondrial genome analysis of Haemaphysalis hystricis Supino, 1897 (Ixodida: Ixodidae) and its phylogenetic implications
  176. Epidemiological characteristics and risk factors analysis of multidrug-resistant tuberculosis among tuberculosis population in Huzhou City, Eastern China
  177. Indices of human impacts on landscapes: How do they reflect the proportions of natural habitats?
  178. Genetic analysis of the Siberian flying squirrel population in the northern Changbai Mountains, Northeast China: Insights into population status and conservation
  179. Diversity and environmental drivers of Suillus communities in Pinus sylvestris var. mongolica forests of Inner Mongolia
  180. Global assessment of the fate of nitrogen deposition in forest ecosystems: Insights from 15N tracer studies
  181. Fungal and bacterial pathogenic co-infections mainly lead to the assembly of microbial community in tobacco stems
  182. Influencing of coal industry related airborne particulate matter on ocular surface tear film injury and inflammatory factor expression in Sprague-Dawley rats
  183. Temperature-dependent development, predation, and life table of Sphaerophoria macrogaster (Thomson) (Diptera: Syrphidae) feeding on Myzus persicae (Sulzer) (Homoptera: Aphididae)
  184. Eleonora’s falcon trophic interactions with insects within its breeding range: A systematic review
  185. Agriculture
  186. Integrated analysis of transcriptome, sRNAome, and degradome involved in the drought-response of maize Zhengdan958
  187. Variation in flower frost tolerance among seven apple cultivars and transcriptome response patterns in two contrastingly frost-tolerant selected cultivars
  188. Heritability of durable resistance to stripe rust in bread wheat (Triticum aestivum L.)
  189. Molecular mechanism of follicular development in laying hens based on the regulation of water metabolism
  190. Molecular identification and control studies on Coridius sp. (Hemiptera: Dinidoridae) in Al-Khamra, south of Jeddah, Saudi Arabia
  191. 10.1515/biol-2025-1218
  192. Animal Science
  193. Effect of sex ratio on the life history traits of an important invasive species, Spodoptera frugiperda
  194. Plant Sciences
  195. Hairpin in a haystack: In silico identification and characterization of plant-conserved microRNA in Rafflesiaceae
  196. Widely targeted metabolomics of different tissues in Rubus corchorifolius
  197. The complete chloroplast genome of Gerbera piloselloides (L.) Cass., 1820 (Carduoideae, Asteraceae) and its phylogenetic analysis
  198. Field trial to correlate mineral solubilization activity of Pseudomonas aeruginosa and biochemical content of groundnut plants
  199. Correlation analysis between semen routine parameters and sperm DNA fragmentation index in patients with semen non-liquefaction: A retrospective study
  200. Plasticity of the anatomical traits of Rhododendron L. (Ericaceae) leaves and its implications in adaptation to the plateau environment
  201. Effects of Piriformospora indica and arbuscular mycorrhizal fungus on growth and physiology of Moringa oleifera under low-temperature stress
  202. Effects of different sources of potassium fertiliser on yield, fruit quality and nutrient absorption in “Harward” kiwifruit (Actinidia deliciosa)
  203. Comparative efficiency and residue levels of spraying programs against powdery mildew in grape varieties
  204. The DREB7 transcription factor enhances salt tolerance in soybean plants under salt stress
  205. Using plant electrical signals of water hyacinth (Eichhornia crassipes) for water pollution monitoring
  206. Response of hybrid grapes (Vitis spp.) to two biotic stress factors and their seedlessness status
  207. Metabolomic profiling reveals systemic metabolic reprogramming in Alternaria alternata under salt stress
  208. Effects of mixed salinity and alkali stress on photosynthetic characteristics and PEPC gene expression of vegetable soybean seedlings
  209. Food Science
  210. Phytochemical analysis of Stachys iva: Discovering the optimal extract conditions and its bioactive compounds
  211. Review on role of honey in disease prevention and treatment through modulation of biological activities
  212. Computational analysis of polymorphic residues in maltose and maltotriose transporters of a wild Saccharomyces cerevisiae strain
  213. Optimization of phenolic compound extraction from Tunisian squash by-products: A sustainable approach for antioxidant and antibacterial applications
  214. Liupao tea aqueous extract alleviates dextran sulfate sodium-induced ulcerative colitis in rats by modulating the gut microbiota
  215. Toxicological qualities and detoxification trends of fruit by-products for valorization: A review
  216. Polyphenolic spectrum of cornelian cherry fruits and their health-promoting effect
  217. Optimizing the encapsulation of the refined extract of squash peels for functional food applications: A sustainable approach to reduce food waste
  218. Advancements in curcuminoid formulations: An update on bioavailability enhancement strategies curcuminoid bioavailability and formulations
  219. Impact of saline sprouting on antioxidant properties and bioactive compounds in chia seeds
  220. The dilemma of food genetics and improvement
  221. Causal effects of trace elements on congenital foot deformities and their subtypes: a Mendelian randomization study with gut microbiota mediation
  222. Honey meets acidity: a novel biopreservative approach against foodborne pathogens
  223. Bioengineering and Biotechnology
  224. Impact of hyaluronic acid-modified hafnium metalorganic frameworks containing rhynchophylline on Alzheimer’s disease
  225. Emerging patterns in nanoparticle-based therapeutic approaches for rheumatoid arthritis: A comprehensive bibliometric and visual analysis spanning two decades
  226. Application of CRISPR/Cas gene editing for infectious disease control in poultry
  227. Preparation of hafnium nitride-coated titanium implants by magnetron sputtering technology and evaluation of their antibacterial properties and biocompatibility
  228. Preparation and characterization of lemongrass oil nanoemulsion: Antimicrobial, antibiofilm, antioxidant, and anticancer activities
  229. Fluorescent detection of sialic acid–binding lectins using functionalized quantum dots in ELISA format
  230. Smart tectorigenin-loaded ZnO hydrogel nanocomposites for targeted wound healing: synthesis, characterization, and biological evaluation
  231. Corrigendum
  232. Corrigendum to “Utilization of convolutional neural networks to analyze microscopic images for high-throughput screening of mesenchymal stem cells”
  233. Corrigendum to “Effects of Ire1 gene on virulence and pathogenicity of Candida albicans”
  234. Retraction
  235. Retraction of “Down-regulation of miR-539 indicates poor prognosis in patients with pancreatic cancer”
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