Paulus Anam Ong

Introduction: The aging process in elderly individuals triggers changes in the brain that can lead to a decline in cognitive function, impacting quality of life. Age-related physiological changes affect the muscles around the oral cavity and the musculoskeletal system. These changes manifest as a decrease in the mass and strength of the chewing muscles. Tooth loss further exacerbates the ability to chew. This study aims to analyze differences in handgrip strength and tooth loss between cognitively normal and impaired elderly. Methods: Observational analytic with cross-sectional design using the Mann-Whitney comparative significance test and independent sample t-test with a significance level of p<0.05 was conducted. A purposive sampling technique was applied to a population residing in Dago Village, Bandung. The inclusion criteria included elderly individuals aged ≥60 years, both male and female, able to communicate effectively, and willing to participate in the study by signing an informed consent form. Cognitive function was assessed through interviews using the Mini Mental State Examination (MMSE), along with an examination of the number of missing teeth and hand grip strength measured with the Electronic Hand Dynamometer (Camry EH101). Analyzed data used the Mann–Whitney test. Results: A total of 34 subjects met the inclusion criteria from the total population of 71 older adults examined. The independent sample t-test for handgrip strength showed that elderly individuals with cognitive impairment had weaker handgrip strength (mean=14.250, SD=5.0285) compared to cognitively normal individuals (mean=22.281, SD=6.0204), with a p-value of 0.0001 (p<0.05). The Mann–Whitney test results for tooth loss indicated that elderly individuals with cognitive impairment experienced greater tooth loss (range=11–32 teeth, mean=20.78) compared to cognitively normal individuals (range=0–10 teeth, mean=13.81), with a p-value of 0.041 (p<0.05). Conclusion: There are differences in hand grip strength and tooth loss were found between cognitively normal and impaired elderly.

Introduction: Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease that often manifests during productive years and frequently involves the central nervous system (CNS), including cognitive dysfunction, which occurs at twice the prevalence of the general population. While the Montreal Cognitive Assessment (MoCA) is effective for detecting mild cognitive impairment, no reliable biomarkers that indicate SLE patients at risk of cognitive dysfunction exist. Neuron-specific enolase (NSE), a specific marker of neuronal cell damage, has been shown in several studies to be highly expressed in cognitive dysfunction. This study serves as a preliminary investigation to examine the relationship between serum NSE levels and cognitive function in SLE patients. Methods: A cross-sectional study was conducted from January to August 2024 at Hasan Sadikin General Hospital, including SLE patients aged 18–55 years meeting the EULAR/ACR 2019 criteria. Exclusion criteria included pregnancy, neurological disorders (e.g., CNS infections, neurodegenerative diseases, stroke, epilepsy, head trauma), psychiatric conditions, substance abuse, systemic metabolic disorders, malignancy, other autoimmune diseases, or HIV. Cognitive function was assessed using MoCA-Indonesian version (MoCA-Ina) and serum NSE levels were measured. Associations between serum NSE and MoCA-Ina scores were analyzed using Spearman’s correlation ( p < .05). Results: Eighty-one participants (median age 32 years; 93.8% female) were included. Cognitive dysfunction (MoCA-Ina p = .022) and executive function (r = −0.204, p = .034). Cognitive dysfunction was also associated with longer disease duration and a history of seizures. Conclusion: This study demonstrates a significant association between neuronal injury, as indicated by elevated serum neuron-specific enolase (NSE) levels, and cognitive impairment in SLE patients, with a particular impact on executive function. Longitudinal studies incorporating neuronal biomarkers are essential to provide deeper insights into the progression of cognitive dysfunction in SLE patients.

Background: Systemic Lupus Erythematosus (SLE) patients tend to have accelerated atherosclerosis. It mayhave a role in the impairment of cognitive function related to a decrease in cerebrovascular blood flow. Methods: Sixty SLE patients and 61 healthy subjects as participants underwent: history taking, physicalexamination, blood examination, medication, carotid Doppler ultrasound test, and cognitive function test.We compared Carotid Intima-media Thickness (CIMT) and Montreal Cognitive Assessment IndonesianVersion (MoCA-Ina) scores of the two groups. Result: The comparison of the total MoCA-Ina scores between the two groups was not statistically significant ( p = .332). However, the orientation domain in the SLE group was statistically lower than the HS group (5.83 ± 0.41 vs 6 ± 0.00, p = .002). The SLE group was found to have a thicker anterior and posterior IMT of right carotid artery ( p < .001, p = .031) and a thicker anterior IMT of left carotid artery ( p < .001). There was a significant inverse correlation between the total MoCA-Ina score and the posterior IMT of the left carotid artery (r = −0.272, p = .035) of SLE patients. Atherosclerosis plaque of the right carotid artery was not associated with total MoCA-Ina score; however, there was a significant association with the attention domain ( p = .023) and the visuospatial domain of MoCA-Ina ( p = .018). Conclusion: SLE patients have lower orientation domain of MoCA-Ina and thicker CIMT than healthy subjects. Atherosclerosis plaque of the carotid artery was associated with attention and visuospatial domains of MoCA-Ina.

The trail-making test (TMT) is a commonly used executive function test in various populations worldwide. It is also used to assess the dementia population, who experience impairment in executive function. In Indonesia, the psychometric properties of TMT for local populations have been reported to be satisfactory. However, there was a lack of studies on the validity and reliability of the TMT for the dementia population. In this study, we examined the validity and reliability of TMT and established population-specific norms for dementia. We analyzed data from 71 TMT scores and three other neuropsychological tests (DSST, DS test, and MOCA) to examine its psychometric properties. The internal consistency analysis was used to assess the reliability of the TMT, while the generalized structured component analysis (GSCA) was conducted to examine TMT’s validity in assessing executive function. The reliability test indicated that the TMT has high reliability (ω = 0.639), while GSCA revealed that TMT has high construct validity with three other neuropsychological tests (TMT-A=0.72 and TMT-B=0.573). Additionally, this study provides standardized norms of TMT for the dementia population.

Monoclonal antibodies (mAbs) have made significant progress in the treatment of Alzheimer's disease (AD). However, mAbs are associated with adverse effects, including Amyloid‐Related Imaging Abnormality (ARIA), which manifests as edema or effusion (ARIA‐E) and hemorrhage (ARIA‐H). The mechanisms behind these effects are not yet fully understood. Moreover, spontaneous ARIA has been insufficiently explored, and mAb therapies, particularly lecanemab, have mainly focused on patients with the APOE‐ε4 allele carrier. This review aims to address this gap by examining the mechanisms of spontaneous ARIA, ARIA induced by mAbs, and the influence of genetic variants on ARIA development. The autoantibody‐Aβ‐mediated immune response targets excessive Aβ deposits, increasing immune activity through microglial reactivity. The heightened immune response, driven by Aβ accumulation in blood vessels, promotes angiopathy and inflammation, potentially contributing to spontaneous ARIA. The APOE‐ε4 allele carrier is more strongly associated with ARIA‐E because it redistributes Aβ deposition from the brain to blood vessels, influencing microglial reactivity. The redistribution enhances vascular integrity and reduces the risk of ARIA‐H. However, it also increases the likelihood of ARIA‐E due to Aβ accumulation in the vasculature, triggering inflammation. In contrast, the development of ARIA‐H is linked to increased TREM2 expression and microglial reactivity, leading to impaired vascular integrity and disrupted matrix remodeling, which worsens the condition. Additionally, the adverse effects of mAbs may extend beyond the APOE‐ε4 allele, possibly impacting other genetic variants involved in microglial reactivity, Aβ redistribution, and vascular integrity.

Background and Objectives: Cerebral vasospasm is the most common complication of subarachnoid hemorrhage (SAH) that is related to high mortality and morbidity. Early biomarkers predicting those conditions are still limited. This study aims to analyze spectrin degradation products (SBDPs) as potential biomarkers for SAH patients, which can be used to monitor clinical outcomes. Materials and Methods: We conducted a prospective observational study in acute SAH within 72 h of onset. All patients underwent placement of continuous cerebrospinal drainage, and liquor was taken four times and analyzed using ELISA to measure SBDP150, SBDP145, and SBDP120 levels and analyzed using Friedman test and post hoc Wilcoxon analysis. The relationship between SBDP levels and vasospasm, as well as functional outcomes (using the Glasgow Outcome Scale–Extended, GOSE), was assessed. Results: We enrolled thirty-five patients: thirty patients with lumbar drainage (LD) and five with extra ventricular drainage (EVD). Friedman’s analysis showed significant changes over time for SBDP120 (p = 0.0001) and SBDP145 (p = 0.0001), but not for SBDP150 (p = 0.218). Levels of SBDP120 on day 3 (p = 0.001), SBDP120 on day 5 (p = 0.022), and SBDP145 on day 3 (p = 0.005) in EVD group were higher than in the LD group. SBDP145 on day 5 was significantly higher in patients with vasospasm (p = 0.041 in all patients, p = 0.028 in LD patients), indicating its potential as an early biomarker for vasospasm. SBDP145 on day 7 (p = 0.014) is the strongest predictor of unfavorable GOSE at 90 days in all patients. In LD patients, SBDP145 on day 7 (p = 0.002), SBDP120 on day 7 (p = 0.009), and SBDP120 on day 10 (p = 0.043) were significantly associated with poor GOSE at 90 days. Conclusions: A higher level of SBDP145 on day 5 can predict vasospasm risk, while an elevated level of SBDP145 and SBDP120 on day 7 is a potential predictor of poor functional outcomes. SBDPs may serve as valuable biomarkers for SAH management.

One common type of vascular dementia (VaD) is poststroke dementia (PSD). Vascular dementia can occur in one-third of stroke patients. The worsening of cognitive function can occur quickly if not detected and treated early. One of the potential medical modalities for observing this disorder by considering costs and safety factors is electroencephalogram (EEG). It is thought that there are differences in the spectral dynamics of the EEG signal between the normal group and stroke patients with cognitive impairment so that it can be used in detection. Therefore, this study proposes an EEG signal characterization method using EEG spectral power complexity measurements to obtain features of poststroke patients with cognitive impairment and normal subjects. Working memory EEGs were collected and analyzed from forty-two participants, consisting of sixteen normal subjects, fifteen poststroke patients with mild cognitive impairment, and eleven poststroke patients with dementia. From the analysis results, it was found that there were differences in the dynamics of the power spectral in each group, where the spectral power of the cognitively impaired group was more regular than the normal group. Notably, (1) significant differences in spectral entropy (SpecEn) with a value Dem < SpecEn_MCI < SpecEn_Normal), and (3) a post hoc multiple comparison test showed significant differences between groups at the F7 electrode. This study shows that spectral complexity analysis can discriminate between normal and poststroke patients with cognitive impairment. For further studies, it is necessary to simulate performance validation so that the proposed approach can be used in the early detection of poststroke dementia and monitoring the development of dementia.

Post-stroke dementia (PSD) is a type of vascular dementia (VaD) that might be occurred in post-stroke patients. Memory, language and behavior tests can be used for the analysis of cognitive impairment caused by PSD. Often a supporting clinical examination such as an electroencephalogram (EEG) is used to support the diagnosis or analyze the characteristic changes that occur in the brain. Conventional analysis or visual inspection of EEG signals can be very difficult, since the nature of the signal tends to be non-stationer. Therefore, this study proposes a quantitative analysis for the characterization of EEG signals in stroke survivors with dementia. It is thought that it has different characteristics with the normal subject so that this study can be used as a reference in supporting dementia detection in post-stroke survivors. The quantitative analysis used in this study is coherence analysis. Coherence analysis was performed on EEG signals recorded from six poststroke patients with dementia and then compared with ten normal healthy subjects. Analysis of coherence between brain areas includes inter and intra-hemispheric coherence. Validation was carried out by using the independent t-test where the confidence level was 95%, indicating that the p-value <0.05 had a significant difference. The test results show that in general the coherence of the electrode pairs in patients with dementia is lower than in the normal healthy group. It is notably, i) In interhemispheric, the C3-C4, T3-T4, and T5-T6 pairs generate significant differences, ii) the highest decrease in intrahemispheric coherence was found in C3-T5 with p = 0.0005. The coherence study presented in this paper is expected to be used for early detection of PSD in the future.