Background: Recent studies have highlighted a possible oral-systemic connection between decreased oral function, particularly reduced occlusal support, and cognitive decline. However, studies examining the relationship between occlusal support and peripheral biomarkers such as salivary amyloid-β42 (Aβ 42 ) remain limited. Objective: This study examined the association between occlusal support and cognitive decline by analyzing salivary Aβ 42 levels in older adults. Methods: A cross-sectional study was conducted among 62 participants categorized by occlusal support using the Eichner Index. Meanwhile, cognitive function and daily living abilities were assessed using the Mini-Mental State Examination (MMSE) and Lawton Instrumental Activities of Daily Living Scale (IADL). Salivary Aβ 42 levels were quantified using enzyme linked immunosorbent type assays. Results: Participants with reduced occlusal support exhibited lower MMSE and IADL scores, and higher salivary Aβ 42 levels (p < 0.05). Furthermore, salivary Aβ 42 concentrations increased across cognitive status categories and remained significant after adjustment for demographic, systemic, and oral health factors (ANCOVA p = 0.003). Multivariable regression identified unstimulated salivary flow rate as the strongest independent predictor of salivary Aβ 42 levels (β = −0.498, p < 0.001) Conclusions: Preserving occlusal support rather than solely focusing on replacing missing teeth may be relevant to cognitive health maintenance in older adults. These findings also support the potential role of salivary Aβ 42 as a non-invasive extracerebral biomarker of neurodegenerative disease, such as Alzheimer's disease.
Background Natural medicines have low toxicity, multi-target effects and long-term clinical use. They inhibit amyloid-β (Aβ) deposition, regulate tau phosphorylation, and exert anti-inflammatory and antioxidant activities, matching Alzheimer's disease (AD) complex pathogenesis. Supported by the World Health Organization, they are promising alternatives to current symptomatic AD drugs that cannot stop disease progression. Objective AD poses a growing global neurodegenerative burden, but systematic bibliometric analysis of natural medicines against AD remains lacking. This study aimed to reveal research trends, core contributors, hotspots and mechanisms from 1999 to 2025. Methods Literature data were retrieved from the Web of Science Core Collection (WOSCC) database (1999–2025) using a combined subject term search strategy. VOSviewer 1.6.20 was used for collaborative network analysis (countries, institutions, authors) and keyword co-occurrence analysis; CiteSpace 6.3.R1 was applied for keyword burst detection. Results Global publications on natural medicines against AD showed phased growth: slow growth (1999–2009), rapid growth (2011–2018), and explosive growth (2020–present). China led in publications; India had the strongest international collaboration. Top co-cited journals included Journal of Ethnopharmacology , and key cited literatures focused on natural medicines’ anti-AD effects. Keyword analysis revealed core hotspots: oxidative stress, amyloid-beta, neuroinflammation, and emerging technologies. Core anti-AD mechanisms of natural medicines included inhibiting Aβ aggregation, regulating tau phosphorylation, anti-neuroinflammation, and gut-brain axis modulation. Numerous typical compounds showed potential but faced slow clinical translation. Conclusions China is a core contributor. Research has shifted to molecular mechanisms and clinical translation, with network pharmacology, molecular docking and gut-brain axis as frontiers. Future efforts require interdisciplinary cooperation and large-sample trials.
Background The donepezil transdermal patch is a useful option for Alzheimer's disease (AD) patients with poor oral adherence. However, treatment discontinuation due to skin irritation or management difficulties remains a clinical challenge. Objective To identify predictive factors for the successful continuation of the donepezil transdermal patch in a real-world setting. Methods A retrospective review included 26 AD patients newly prescribed or switched to the donepezil patch at a dementia center. Patients were divided into continuation (n = 15) and discontinuation (n = 11) groups based on a 12-week cutoff. We evaluated baseline demographics, Mini-Mental State Examination (MMSE), Clinical Dementia Rating-Sum of Boxes (CDR-SB), Alzheimer's Disease Assessment Scale-Cognitive Subscale for Activities of Daily Living (ADL-Cog), and caregiver burden using the 8-item Zarit Burden Interview (Zarit-8). Multivariate logistic regression identified risk factors for discontinuation. Results Univariate analysis showed no significant differences between groups in age (p = 0.855), MMSE (p = 0.677), CDR-SB (p = 0.762), and ADL-Cog (p = 0.826). Although the mean Zarit-8 score was higher in the discontinuation group (14.00 ± 10.70 versus 7.86 ± 5.55, p = 0.171), this lacked statistical significance. However, multivariate regression revealed a higher Zarit-8 score was a significant independent predictor of discontinuation after adjusting for age (p = 0.038, OR = 1.134). Conclusions Caregiver burden, rather than patient cognitive function or impairment in activities of daily living, significantly predicts discontinuation of the transdermal patch. To the best of our knowledge, no previous studies have utilized the Zarit burden scale as a clinical predictor of pharmacological adherence. Assessing caregiver reserve before introduction is crucial for maintaining adherence.
Background Previous studies have shown that tea consumption frequency or sleep quality is independently associated with cognitive function, but the combined association remains unclear. Objective To investigate the individual and combined associations between tea consumption frequency and sleep quality with cognitive function and analyze whether this association is modified by gender and age. Methods The cross-sectional study involved 646 participants from 17 villages in Jimo District, Qingdao, in 2022. Data on tea consumption frequency were collected via a questionnaire. Cognitive function and sleep quality were assessed through the Montreal Cognitive Assessment and Pittsburgh Sleep Quality Index, respectively. Linear regression models were used to analyze associations, with a combined variable for tea consumption frequency and sleep quality constructed to evaluate their combined association. Stratified analysis and interaction tests assessed the moderating effects of gender and age. Results Higher consumption frequency of green tea (β (95% CI): 0.97 (0.23, 1.70)) or black tea (β (95% CI): 0.78 (0.08, 1.48)) was positively associated with cognitive function. Moreover, higher consumption frequency of green tea combined with good sleep quality was significantly associated with optimal cognitive function (β (95% CI): 1.17 (0.10, 2.31)). Stratified analysis revealed no significant modifying effects of gender or age on the aforementioned associations. Conclusion Increased consumption frequency of green tea, alongside maintaining good sleep quality, is associated with enhanced cognitive function. These findings highlight the value of modifiable lifestyle factors in promoting cognitive health.
Background Amyloid-β (Aβ) accumulation begins before cognitive impairment, highlighting the need for scalable blood-based biomarkers to identify individuals at risk during the preclinical stage of Alzheimer's disease. Objective To evaluate whether plasma %p-tau217 detects Aβ-PET positivity and whether longitudinal plasma %p-tau217 change is associated with early Aβ accumulation in cognitively unimpaired participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI). Methods This retrospective longitudinal study included 98 cognitively unimpaired ADNI participants with plasma %p-tau217, plasma Aβ 42/40 , Aβ-PET, and clinical/genetic data. Aβ-PET positivity was defined as Centiloid (CL) ≥ 40. Among participants with baseline Aβ-PET <40 CL, participant-specific annual slopes for Aβ-PET CL and plasma biomarkers were estimated from matched longitudinal measurements using linear mixed-effects models. Regression and receiver operating characteristic analyses assessed associations with Aβ-PET change and discrimination of Aβ-PET positivity and Aβ accumulator status. Results Plasma %p-tau217 showed excellent discrimination of Aβ-PET positivity (area under the curve (AUC) = 0.962) and yielded a higher AUC than plasma Aβ 42/40 . In participants with baseline Aβ-PET <40 CL, longitudinal plasma %p-tau217 slope was the only plasma biomarker independently associated with annual Aβ-PET CL increase in fully adjusted models (β = 1.38; FDR-adjusted p < 0.001). Plasma %p-tau217 slope also yielded a higher AUC for Aβ accumulator status than baseline plasma %p-tau217. Conclusions Plasma %p-tau217 is a strong blood-based biomarker for detecting Aβ-PET positivity in cognitively unimpaired individuals. Longitudinal plasma %p-tau217 change provides additional information beyond baseline plasma biomarkers and may support enrichment or monitoring strategies in Alzheimer's disease prevention trials, pending validation in larger independent cohorts.
Background The heterogeneous performance of dementia and Alzheimer's disease risk scores makes it difficult to identify tools suitable for supporting risk reduction and prevention strategies. Although multiple factors may contribute, we hypothesized that differences in age specification and study design are the primary contributors to this variability. Objective: To evaluate how age specification and length of follow-up affect the performance of three midlife risk scores: CogDrisk-ML, CAIDE, and UKBDRS. Methods Longitudinal data were drawn from the ARIC, UK Biobank, and Whitehall II cohorts. Participants free of dementia at baseline were included. Baseline variables were used to calculate each risk score. Risk prediction was evaluated using Cox proportional hazards models with three age specifications: UKBDRS (continuous), CogDrisk-ML (categorical: 40–49, 50–54, 55–59, 60–64 years), and CAIDE (categorical age: <47, 47–53, >53 years). Predictive accuracy was assessed using Harrell's C-statistics and 95% confidence intervals (CIs). Results Across all cohorts and risk scores, excluding age from risk scores resulted in similar C-statistics. In age- and sex-only models, continuous age produced the highest Harrell's C-statistics (95% CI) [ARIC: 0.71 (0.68, 0.73); UK Biobank: 0.78 (0.77, 0.79), and Whitehall II: 0.75 (0.62, 0.88)], followed by categorical age specifications. Compared with continuous age, categorical specifications reduced C-statistics, with the largest reduction for CAIDE. Shorter follow-up yielded higher but less precise C-statistics. Conclusions Age specification strongly influences dementia risk model performance, especially with shorter follow-up, with continuous age yielding the highest accuracy. Our findings emphasize that differences in dementia risk prediction performance are driven primarily by age specification and cohort age structure rather than intrinsic superiority of individual risk tools.
Late-life depression may mask Alzheimer's disease (AD). We report a 78-year-old man with treatment-refractory depressive and anxiety symptoms accompanied by paroxysmal somatic attacks, unresponsive to psychotropic treatment and modified electroconvulsive therapy. Ultimately, biomarker evaluation confirmed AD pathology, and donanemab was initiated. Follow-up amyloid positron emission tomography demonstrated marked amyloid clearance, particularly in the frontal lobe, accompanied by concurrent improvement in depressive symptoms, cognition, and reduced somatic attacks. This case suggests that anti-amyloid therapy may benefit AD patients presenting with refractory neuropsychiatric symptoms, potentially related to frontal amyloid clearance, underscoring the importance of AD screening in resistant late-life depression.
Background With the widespread use of antiretroviral therapy, people living with HIV (PLWH) are experiencing increased life expectancy, accompanied by a growing burden of age-related comorbidities. Cognitive impairment and dementia have been increasingly reported among PLWH; however, epidemiological evidence regarding their association remains inconsistent. Objective This systematic review and meta-analysis aimed to evaluate the association between HIV infection and the risk of dementia and cognitive impairment. Methods We systematically searched PubMed, Embase, Web of Science, and the Cochrane Library from inception to March 4, 2026 for cohort studies investigating the association between HIV infection and dementia or cognitive impairment. Study selection, data extraction, and quality assessment using the Newcastle-Ottawa Scale were independently conducted by two reviewers. Heterogeneity across studies was assessed using Q test and I 2 statistics. Pooled relative risks (RRs) with 95% confidence intervals (CIs) were calculated using fixed- or random-effects models as appropriate. Subgroup, sensitivity, and publication bias analyses were performed. Results A total of 9 articles were eligible for this analysis. The pooled results showed that HIV infection was significantly associated with an increased risk of dementia and cognitive impairment (RR=2.07, 95% CI: 1.35, 3.17). Substantial heterogeneity was observed across studies ( I 2 =93.7%). Subgroup analyses suggested that publication year, baseline immunological status, and age distribution might partially explain the observed heterogeneity. Sensitivity analysis confirmed the robustness of the findings, and no significant publication bias was detected. Conclusions This meta-analysis suggests that HIV infection is associated with an increased risk of dementia and cognitive impairment.
Background Bulk transcriptomic studies of Alzheimer's disease are difficult to interpret because the diseased brain is not only transcriptionally altered, but structurally remodeled. Neuronal and synaptic loss, reactive gliosis, and vascular or extracellular-matrix changes can all shift measured expression. Objective To reanalyze GSE5281 with glial marker-derived adjustment and integrate residual gene sets with Alzheimer's disease S-PrediXcan/transcriptome-wide association study (TWAS) results to prioritize genes relevant to disease pathogenesis and target discovery. Methods We used age, composite glial score, and surrogate-variable adjustment to define residual upregulated and downregulated genes, then evaluated these sets in brain-tissue TWAS outputs using Stouffer meta-Z statistics, permutation/bootstrap set-level testing, and gene-level leave-one-out influence analysis. Results The residual sets did not show significant set-level enrichment. AD_RESIDUAL_DOWN showed Stouffer Z = 0.862, permutation p = 0.6982, and bootstrap 95% CI = −3.18 to 5.38. AD_RESIDUAL_UP showed Stouffer Z = −1.564, permutation p = 0.5002, and bootstrap 95% CI = −5.43 to 2.26. However, gene-level analysis identified 41 influential gene-disease entries. GALNT6 was the strongest signal in the residual upregulated set and the strongest overall gene-level signal. C1QTNF4 and NTSR2 were the largest influence signals in the residual downregulated set, while EPHX2 ranked among the influential genes. Conclusions These findings support glial-adjusted residual transcriptomics with leave-one-out TWAS influence analysis as a computational prioritization strategy for Alzheimer's disease, rather than as evidence of broad pathway-level genetic enrichment.
Background Dementia prevalence is rising globally, with the greatest increase occurring in low- and middle-income countries where access to advanced diagnostic tools remains limited. Circulating lipid parameters have been increasingly investigated as accessible biomarkers for dementia risk and cognitive decline. Objective To systematically review and synthesize existing evidence on the relationship between circulating lipid parameters and dementia risk, Alzheimer's disease, and cognitive decline, with particular consideration of their potential utility in resource-limited settings. Methods A systematic literature review was conducted in accordance with PRISMA guidelines. Studies published between 2000 and May 2025 evaluating associations between lipid profiles and cognitive outcomes, dementia, or neurodegenerative disease were included and narratively synthesized. Results Evidence across studies suggests that lipid dysregulation is associated with dementia-related outcomes, although findings remain heterogeneous. Elevated total cholesterol, low-density lipoprotein cholesterol, and triglycerides were frequently associated with increased risk of dementia, Alzheimer's disease, or cognitive decline, whereas high-density lipoprotein cholesterol generally showed protective associations. Several studies also identified prognostic value in composite lipid ratios and lipid variability measures. However, the strength and direction of associations varied according to age, sex, timing of lipid assessment, and study population. Conclusions Circulating lipid parameters alone are insufficient as definitive diagnostic biomarkers. However, when interpreted in a population-specific and life-course context, they may contribute to early risk stratification and complement neuropsychological screening, particularly in resource-limited settings where access to advanced neuroimaging and cerebrospinal fluid testing is restricted.
Background Depression in Alzheimer's disease (AD) is common, distressing, difficult to treat and inadequately understood. Objective We compared gene expression in neurons and microglia from AD patients +/- depression, stratified according to depression polygenic risk score (PRS-D) and looked for differential pathway regulation. Methods We identified AD patients with ( n = 95) or without depression ( n = 25) whose brains had been donated to a UK brain bank. Exclusion criteria included other disorders known to affect cognition, previous major psychiatric disorder and a neuropathological diagnosis of a non-AD dementia. Depression was defined as a clinical depression diagnosis or Geriatric Depression Scale/Center for Epidemiologic Studies Depression Scale >7. PRS-D was calculated using LDpred2. In the AD + depression group, only the top ( n = 29) and bottom tertile ( n = 30) of PRS-D were analyzed by microarray. Tissue from superior frontal gyrus (SFG) and anterior insula (AIns) was sorted into neuronal and microglial fractions, and gene expression measured using a ClariomS Pico microarray. Results After quality control, microarray data were available for AIns microglia ( n = 51), AIns neurons ( n = 59), SFG microglia ( n = 60) and SFG neurons ( n = 63). No individual genes had a p < 0.05, adjusted for false discovery rate. Gene set enrichment analysis identified significantly upregulated and downregulated pathways in both brain regions and cell types. More pathways were differentially expressed in microglia than in neurons. Many of these pathways related to infection or inflammation but also included olfactory transduction and Parkinson's disease. Conclusions In conclusion we have identified pathways that may contribute to the development of depression in AD. A majority were identified predominantly in microglia.
We report the case of a 46-year-old woman who presented with progressing, early-onset cognitive decline associated with atypical features due to a PSEN1 mutation. This case extends the known spectrum of clinical, radiological and pathological findings associated with this mutation.
Background While central nervous system (CNS)-active medication polypharmacy is prevalent among adults with early-onset dementia (EOD), its impact on nursing home (NH) admission is unclear. Objective To examine whether CNS-active medication polypharmacy is associated with risk for NH admission among patients with EOD. Methods A retrospective cohort study using 2012–2021 MarketScan Databases was conducted with adults aged 30 to 64 years diagnosed with Alzheimer's disease and related dementias (ADRD). CNS-active medication polypharmacy was assessed during a fixed 6-month period after an indexed ADRD diagnosis and defined as concurrent use of ≥3 CNS-active medications on the American Geriatrics Society Beers Criteria list that overlapped for ≥30 consecutive days. Cox hazards models were used to estimate the hazard ratio (HR) of NH admission between patients with versus without CNS-active medication polypharmacy, with adjustment for baseline covariates via inverse probability of treatment weighting. Results Of the 18,029 patients with EOD identified, those with CNS-active medication polypharmacy (versus those without) had an increased risk of NH admission (HR, 1.34 [95% CI, 1.16–1.56]). The risk was pronounced in patients aged >50 years, male patients, patients with a diagnosis of Alzheimer's disease or senile dementia, and patients having baseline use of anti-dementia medications. Conclusions In this commercially insured population of adults with EOD, receipt of CNS-active medication polypharmacy was associated with risk for NH admission. The finding, however, should be interpreted with caution, as it may reflect differences in the underlying disease severity and clinical indications treated by the studied CNS-active medications.
Lecanemab has demonstrated amyloid reduction and slowed clinical decline in early Alzheimer's disease trials. Herein, we report retrospective case series results on lecanemab treatment in our clinic. Overall, 61 individuals were included. For the 33 patients with Kokmen Mental Status Exam baseline and post-baseline scores, 67% had either improved or stable scores. Nine incident amyloid-related imaging abnormalities were observed with all but one patient continuing treatment. Six patients were safely transitioned from aducanumab to lecanemab treatment upon market withdrawal of aducanumab. In a real-world clinical practice setting, the lecanemab effectiveness and safety profile were similar to that observed in clinical studies.
Alzheimer's disease (AD) is a neurodegenerative disease that leads to cognitive impairment and dementia, and retinal imaging is being explored as a biomarker. We examined the differences in retinal thickness by optical coherence tomography (OCT) between 47 participants with mild cognitive impairment due to Alzheimer's disease (Aβ+MCI) and 23 age-matched controls, as well as associations between cognition and OCT. There was no significant difference in retinal thickness between groups. However, retinal measures were robustly associated with global cognition and executive function in those with Aβ+MCI. Further studies with larger samples are needed to understand the clinical utility of OCT in AD.
Evidence has grown that the core pathology of age-related dementias, including Alzheimer's disease, is microvascular—small, symptomless bleeds from cerebral capillaries, accelerated by the hypertension of age. Each such bleed, this evidence suggests, damages a patch of brain, causing the death of neurons. This review asks how this vulnerability of the brain emerged from evolution, to cause age-related dementia? And has the vulnerability spurred the evolution of mitigating mechanisms? It is argued that seven features of human evolution contribute to the cause of dementia: the dependence of our tissues, especially the brain, on oxygen; the toxicity of the molecule (heme) that binds to oxygen to enable its transport; the pulsatility of the heart; the danger of glutamate as an excitatory neurotransmitter; the irreparability of elastin; the low level of adult neurogenesis in humans; and the breakdown, in late life, of the blood-brain barrier. Also discussed are mechanisms that have evolved to counter these threats to the brain, including the generation of a reserve of brain tissue. We argue that the vulnerabilities of the brain to damage that accumulates throughout life, and leads to dementia in the aged, were established early in the evolution of vertebrates. Several can be understood as unavoidable yet damaging outcomes of highly advantageous steps in evolution. Human cognition fails when and because, with age, the damage that results from these vulnerabilities overwhelms the evolved protections and exhausts any reserve of brain tissue. Implications of these vulnerabilities for the delay and management of dementia are discussed.
Background Mild cognitive impairment (MCI) is an important transitional stage between normal cognitive aging and dementia. Biomarker-based biological age may better capture physiological aging processes than chronological age, yet its association with the risk of developing MCI remains insufficiently studied. Objective We aimed to examine the association between Gompertz Law-Based Biological Age (Light BioAge) and incident MCI in a middle-aged and older Chinese population, and to explore whether social activeness modifies this association. Methods We used data from the China Health and Retirement Longitudinal Study, a nationally representative cohort. Light BioAge was calculated from chronological age, serum creatinine, fasting glucose, and C-reactive protein. Incident MCI was defined using age- and education-standardized cognitive assessments. Cox regressions were used to analysis. Results Among 9410 participants free of MCI at baseline, 1047 developed MCI during follow-up. Light BioAge was negatively associated with risk of MCI (hazards ratio (HR) = 0.99, 95% CI: 0.98–0.99). Compared to high Light BioAge, those in the moderate and low groups showed significantly lower risks of MCI (HR = 0.78, 95% CI: 0.65–0.94 and HR = 0.79, 95% CI: 0.65–0.97, respectively). The association were consistent across sex and different levels of social activeness, with no significant interaction observed. Conclusions Lower biological age, as estimated by Light BioAge, is independently associated with a reduced risk of MCI in middle-aged and older adults. The use of biomarker-based aging indicators may help identify individuals at higher risk of cognitive decline for early preventive strategies.
Background Timely detection of cognitive concerns can facilitate further assessment, referral, and management; however, cognitive impairment often remains under-detected in primary care settings, representing a missed opportunity for early detection for Alzheimer's disease and related dementias. Objective We aimed to develop and internally validate a machine learning-based cross-sectional concurrent classification model that utilizes routine health check data only, supporting concurrent identification of individuals with Ascertain Dementia 8 (AD8)-defined suspected cognitive impairment who warrant further clinical cognitive evaluation. Methods This cross-sectional study included 7440 adults (aged ≥65 years) from the 2021 Elderly Health Check Program in Shenzhen, China. Suspected cognitive impairment was defined as an AD8 score ≥2. Following data splitting, feature selection was processed via the Boruta algorithm. Five algorithms—logistic regression, random forest, XGBoost, SVM, and EasyEnsemble—were evaluated. Performance was assessed using ROC, PR, accuracy, sensitivity, specificity, PPV, NPV, NNS, DCA, calibration plots, and Brier score. Results The EasyEnsemble model outperformed other algorithms on the independent testing set, with an ROC-AUC of 0.696 (Bootstrap-corrected mean: 0.677; 95% CI: 0.643–0.713). At the clinically optimized threshold of 0.034, the model achieved a sensitivity of 60.6%, a specificity of 73.4% and a NNS of 51.9. DCA indicated a positive net benefit across a threshold range approximately from 0.03 to 0.20, suggesting potential clinical utility for triage in this setting. Conclusions This cross-sectional model provides a pragmatic, low-cost tool for concurrent case-finding of individuals with AD8-defined suspected cognitive impairment in primary care. However, further external validation in diverse geographic regions is mandatory before clinical implementation.
Brain-derived neurotrophic factor (BDNF) is a neurotrophin regulating neuroplasticity and is reduced in Alzheimer's disease (AD). Whether BDNF relates to AD pathophysiology in dementia-free individuals and under what conditions remain unknown. Pain, a prevalent midlife condition and AD risk factor, engages BDNF signaling. We examined whether frequent pain moderated associations between BDNF and AD plasma biomarkers (ptau217, BD-tau) in early midlife (Mean age=45.8). Among individuals with frequent pain, higher BDNF was associated with lower BD-tau and ptau217. No associations emerged among pain-free individuals. These findings suggest BDNF-indexed neuroplasticity may buffer against AD pathology and neurodegeneration in the context of pain.
Background Resilience is an important positive construct supporting people with dementia; however, validated self-report instruments for this population remain limited, and no Turkish version is currently available. Objective This study aimed to adapt the Bangor Dementia Resilience Scale (BDRS) into Turkish and to evaluate its psychometric properties in individuals with mild cognitive impairment (MCI) and early-stage dementia. Methods This cross-sectional psychometric study included 118 individuals with MCI or early-stage dementia. The translation and cultural adaptation process followed established guidelines. Structural validity was examined using exploratory factor analysis (EFA). Convergent validity was assessed using Pearson correlations between the Turkish version of the BDRS (T-BDRS) scores and quality of life (QoL-AD), as well as clinical variables including Mini-Mental State Examination, Neuropsychiatric Inventory, and Katz Activities of Daily Living. Reliability was evaluated using Cronbach's alpha, McDonald's omega, item–total correlations, and test–retest reliability (n = 30). Results EFA supported a five-factor structure explaining 68.32% of the total variance. The internal consistency of the total scale was excellent (Cronbach's α = 0.946; ω = 0.946). Item–total correlations ranged from 0.604 to 0.787. Test–retest reliability demonstrated excellent stability (ICC = 0.993). Convergent validity was supported by a strong positive correlation with QoL-AD (r = 0.819, 95% CI: 0.744–0.872, p < 0.001). Conclusions The T-BDRS demonstrated satisfactory validity and reliability for assessing resilience in individuals with MCI and early-stage dementia. It represents a promising tool for research and clinical practice, supporting the assessment of positive psychosocial outcomes in dementia care.
