Obesity is one of the factors associated with cognitive impairment. However, obesity may differently affect cognitive function in different age groups, and scarce data are available from low- and middle-income countries. This cross-sectional study aimed to identify the association between obesity and cognitive impairment among 143 elderly individuals in Yogyakarta. We recorded the sociodemographic factors and some comorbidities, also measured the body mass index as a parameter of obesity, cognitive function using Montreal Cognitive Assessment—Indonesia, mood condition and depression status using geriatric depression scale-short form, as well as the daily life function using Activity of Daily Living and Instrumental Activity of Daily Living. After adjustment for the sociodemographic and comorbidities, we found that subjects with older age were more likely to have cognitive impairment (odds ratio [OR] 3.544, 95%CI: 1.36–9.22, p < 0.01) and compared with elderly individuals with normal weight, obese elderly individuals were 40% less likely to have cognitive impairment (OR 0.604, 95%CI: 0.39–0.95, p < 0.05). This study suggests that obesity in elderly individuals is less frequently associated with cognitive impairment. These findings support the reverse causation mechanism related to body mass index (BMI) and cognitive impairment in low/middle-income countries.

People with dementia (PWD) may exhibit symptoms that negatively affect their relationships with their families or friends which could cause social strain. The Negative Relationship Quality (NRQ) questionnaire can be used to measure social strain in PWD. There has never been an Indonesian adaptation of the NRQ. This preliminary study aimed to measure the validity and reliability of the NRQ among PWD in Indonesia (NRQ-INA). This study used a cross-sectional design. Forward–backward translation methods were conducted first. Pearson’s correlation and factor analysis were employed for the validity test. Cronbach’s alpha and test–retest were used to determine reliability. The NRQ-INA has four parallel items related to social strain that are divided into three subscales and asked to spouse/partner, family members, and friends, leading to a total of 12 questions. The results of validity testing from 60 respondents showed that all items in the NRQ-INA were strongly valid with correlation coefficients (r) of >0.8 (p < 0.01). Factor analysis showed a convergence with the variance explained of more than 50% for all items in each subscale, which also indicated that NRQ-INA had acceptable construct validity to measure social strain. Cronbach’s alpha values (α) were 0.926, 0.942, and 0.938 for the subscales of spouse, friends, and family members, respectively. The correlations of test–retest reliability for all items were >0.7 (p < 0.01), demonstrating a reliable NRQ-INA measurement. In conclusion, NRQ-INA had a good validity and reliability to measure social strain in PWD. Further study of the concurrent validity among PWD is still needed.

Alzheimer’s disease is one of the most prevalent neurodegenerative diseases among older people. Generally, there are two main pathologies of Alzheimer’s disease, including the accumulation of amyloid beta and the hyperphosphorylation of the microtubule-associated Tau protein in the brain. Recently, more studies have discovered that changes in the immune system can be one of the causes of amyloid-beta deposits. Amyloid-beta is a product of the breakdown of the glycoprotein amyloid precursor protein, a transmembrane protein that is cleaved by β-secretase and γ-secretase. In the brain, amyloid-beta deposits can trigger microglia activation, which helps eliminate the deposits. However, microglia activation may induce neuroinflammation by releasing pro-inflammatory cytokines and damage the blood-brain barrier, which can cause an influx of peripheral immune cells, including the adaptive immune system, into the brain. The role of the adaptive immune system in Alzheimer’s disease pathology is quite complicated and may alter due to aging. Aging can directly alter the immune system by reducing protective immunity through reduced production of naïve T cells and increased memory T cells. The increase in memory T cells, which have already recognized specific antigens, such as amyloid beta, may act as amyloid beta-reactive T cells and induce activation and release of amyloid beta-specific antibodies from B cells. This condition increases neuroinflammatory processes. Several drugs that directly target the immune system showed promising results as Alzheimer’s disease progressed. However, due to limited data, inconsistent results, and late adverse outcome effects, these drugs still require further research.