Yuliarni Syafrita

Background/Objectives: Alzheimer’s disease (AD) is a leading cause of dementia globally, yet standard diagnostic markers like cerebrospinal fluid (CSF) analysis and molecular imaging are invasive and resource-intensive. While artificial intelligence (AI)-based volumetric magnetic resonance imaging (MRI) offers a scalable and non-invasive alternative, data correlating these structural metrics with fluid biomarkers and cognitive status in Southeast Asian populations are scarce. This study addresses this critical gap by examining the within-cohort relationship between CSF biomarkers and regional brain volumes derived from AI-assisted MRI in Indonesian patients with clinically diagnosed AD, providing novel data for an underrepresented population. Methods: Twenty-one AD patients from three national referral hospitals in Indonesia underwent lumbar puncture for CSF biomarker analysis and 3 Tesla structural brain MRI. Brain volumes were analyzed using United Imaging Intelligence software, focusing on AD-relevant regions (hippocampus, entorhinal cortex, parahippocampus, precuneus, and posterior cingulate cortex [PCC]). Results: Spearman’s correlation revealed significant positive associations between CSF Aβ42 levels and several brain regions. Strong correlations were found with the right entorhinal volume indexed to intracranial volume (VICV) (r = 0.601, p = 0.004), right PCC VICV (r = 0.603, p = 0.004), right entorhinal volume (r = 0.533, p = 0.013), and right hippocampus VICV (r = 0.503, p = 0.020). Furthermore, MoCA-InA scores demonstrated highly significant positive correlations with CSF Aβ42 concentrations (r = 0.720, p < 0.001), right Hippocampus VICV (r = 0.703, p < 0.001), and right PCC VICV (r = 0.695, p < 0.001). No significant correlations were found between CSF pTau or the pTau/Aβ42 ratio and regional volumes. Conclusions: These results highlight the entorhinal cortex and PCC as early affected regions where CSF Aβ42 correlates with preserved volume, supporting their role as structural markers in early AD. The absence of pTau associations may reflect early-stage pathology or limitations of cross-sectional volumetry. In resource-limited settings, AI-assisted volumetric MRI demonstrates potential utility as a non-invasive tool for stratifying amyloid-associated brain atrophy and staging disease severity.

Background: Chemotherapy-induced cognitive impairment (CICI), colloquially termed "chemobrain," represents a significant challenge for cancer survivors, potentially affecting up to 85% of patients undergoing treatment. Diagnosis often relies on neuropsychological testing and imaging, which may lack sensitivity for early detection or reflect chronic changes. Neurofilament light chain (NfL), a neuronal structural protein released into biofluids upon neuroaxonal damage, emerges as a promising biomarker. This study investigated the relationship between serum NfL levels and the degree of cognitive impairment in patients receiving chemotherapy. Methods: An observational, cross-sectional study was conducted involving 50 cancer patients undergoing chemotherapy at Dr. M. Djamil General Hospital Padang between October and December 2024. Cognitive function was assessed using the Montreal Cognitive Assessment Indonesian version (MoCA-Ina), and depression was screened using the Patient Health Questionnaire-9 (PHQ-9). Serum NfL levels were quantified using an Enzyme-Linked Immunosorbent Assay (ELISA) method. The Kruskal-Wallis test was employed to analyze the relationship between serum NfL levels and cognitive function status (normal, mild impairment, moderate-severe impairment). Results: Cognitive impairment (MoCA-Ina assessed) was identified in 41 (82%) of the 50 participants, with 30 (60%) exhibiting mild and 11 (22%) exhibiting moderate to severe impairment. The median serum NfL level across all subjects was 23.44 pg/ml (range: 13.81-68.71 pg/ml). A statistically significant relationship was observed between serum NfL levels and the presence and severity of cognitive impairment (p = 0.02). Median NfL levels progressively increased from the cognitively normal group (18.49 pg/ml) to the mild impairment group (23.5 pg/ml) and the moderate-severe impairment group (24.5 pg/ml). Post-hoc analysis revealed significant differences in NfL levels between the normal group and both the mild (p=0.03) and moderate-severe (p=0.01) impairment groups. Conclusion: This study demonstrated a significant positive association between serum NfL levels and the presence and severity of cognitive impairment in cancer patients undergoing chemotherapy. These findings support the potential utility of serum NfL as an accessible biomarker for detecting chemotherapy-associated neuroaxonal damage and concomitant cognitive decline.

Background : Traumatic brain injury is still the main cause of death and disability in productive age. Assessment the level of consciousness and imaging examinations after a brain injury can not always describe the severity of damage in the brain, this is because the pathological process is still ongoing due to secondary brain injury. Therefore, it is necessary to examine biomarkers that can describe the severity of the pathological process that occurs. The purpose of this study was to assess serum neuron-specific enolase (NSE) levels and their relationship to the severity and outcome of a traumatic brain injury. Methods : A cross sectional design was conducted in the emergency department of DR M Djamil Hospital, Padang. There were 72 patients who met the inclusion criteria. A Glasgow Coma Scale examination was performed to assess the severity of brain injury and examination of NSE serum levels at 48 hours post- injury using ELISA technique and assess the Glasgow outcome scale (GOS) at 6 weeks post-injury. Data analysis using SPSS 22 program, the results are significance if the p value <0.05 Results : The average NSE level was higher in severe brain injuries than moderate and mild brain injuries and this difference was statistically significant (p<0.05). The NSE serum levels were higher in poor outcomes than in good outcomes and this difference was statistically significant (p<0.05). Conclusion : High NSE serum levels in the acute phase were associated with the severity of the brain injury and poor outcome 6 weeks after the brain injury.