Objectives To investigate the relationships of serum albumin with in vivo Alzheimer disease (AD) pathologies, including cerebral β-amyloid (Aβ) protein deposition, neurodegeneration of AD-signature regions, and cerebral white matter hyperintensities (WMH), in the human brain. Methods A total of 396 older adults without dementia underwent comprehensive clinical assessments, measurement of serum albumin level, and multimodal brain imaging, including [¹¹C] Pittsburgh compound B-PET, ¹⁸F-fluorodeoxyglucose-PET, and MRI. Serum albumin was categorized as follows: 4.5 g/dL (high albumin; used as a reference category). Aβ positivity, AD-signature region cerebral glucose metabolism (AD-CM), AD-signature region cortical thickness (AD-CT), and WMH volume were used as outcome measures. Results Serum albumin level (as a continuous variable) was inversely associated with Aβ deposition and Aβ positivity. The low albumin group showed a significantly higher Aβ positivity rate compared to the high albumin group (odds ratio 3.40, 95% confidence interval 1.67–6.92, p = 0.001), while the middle albumin group showed no difference (odds ratio 1.74, 95% confidence interval 0.80–3.77, p = 0.162). Neither serum albumin level (as a continuous variable) nor albumin categories were related to AD-CM, AD-CT, or WMH volume. Conclusions Low serum albumin may increase the risk of AD dementia by elevating amyloid accumulation. In terms of AD prevention, more attention needs to be paid to avoid a low serum albumin level, even within the clinical normal range, by clinicians.

An emerging body of literature has indicated that moderate alcohol intake may be protective against Alzheimer disease (AD) dementia. However, little information is available regarding whether moderate alcohol intake is related to reductions in amyloid-beta (Aβ) deposition, or is protective via amyloid-independent mechanisms in the living human brain. Here we examined the associations of moderate alcohol intake with in vivo AD pathologies, including cerebral Aβ deposition, neurodegeneration of AD-signature regions, and cerebral white matter hyperintensities (WMHs) in the living human brain. The present study was part of the Korean Brain Aging Study for Early Diagnosis and Prediction of Alzheimer’s Disease (KBASE), an ongoing prospective cohort study that started in 2014. As of November 2016, 414 community-dwelling individuals with neither dementia nor alcohol-related disorders (280 cognitively normal [CN] individuals and 134 individuals with mild cognitive impairment [MCI]) between 56 and 90 years of age (mean age 70.9 years ± standard deviation 7.8; male, n [%] = 180 [43.5]) were recruited from 4 sites (i.e., 2 university hospitals and 2 public centers for dementia prevention and management) around Seoul, South Korea. All the participants underwent comprehensive clinical assessments comprising lifetime and current histories of alcohol intake and multimodal brain imaging, including [¹¹C] Pittsburgh compound B positron emission tomography (PET), [¹⁸F] fluorodeoxyglucose (FDG) PET, and magnetic resonance imaging (MRI) scans. Lifetime and current alcohol intake were categorized as follows: no drinking, <1 standard drink (SD)/week, 1–13 SDs/week, and 14+ SDs/week. A moderate lifetime alcohol intake (1–13 SDs/week) was significantly associated with a lower Aβ positivity rate compared to the no drinking group, even after controlling for potential confounders (odds ratio 0.341, 95% confidence interval 0.163–0.714, p = 0.004). In contrast, current alcohol intake was not associated with amyloid deposition. Additionally, alcohol intake was not related to neurodegeneration of AD-signature regions or cerebral WMH volume. The present study had some limitations in that it had a cross-sectional design and depended on retrospective recall for alcohol drinking history. In this study, we observed in middle- and old-aged individuals with neither dementia nor alcohol-related disorders that moderate lifetime alcohol intake was associated with lower cerebral Aβ deposition compared to a lifetime history of not drinking. Moderate lifetime alcohol intake may have a beneficial influence on AD by reducing pathological amyloid deposition rather than amyloid-independent neurodegeneration or cerebrovascular injury.

Background: Alzheimer’s disease (AD) is the most common form of dementia, which makes the lives of patients and their families difficult for various reasons. Therefore, early detection of AD is crucial to alleviating the symptoms through medication and treatment. Objective: Given that AD strongly induces language disorders, this study aims to detect AD rapidly by analyzing the language characteristics. Materials and Methods: The mini-mental state examination for dementia screening (MMSE-DS), which is most commonly used in South Korean public health centers, is used to obtain negative answers based on the questionnaire. Among the acquired voices, significant questionnaires and answers are selected and converted into mel-frequency cepstral coefficient (MFCC)-based spectrogram images. After accumulating the significant answers, validated data augmentation was achieved using the Densenet121 model. Five deep learning models, Inception v3, VGG19, Xception, Resnet50, and Densenet121, were used to train and confirm the results. Results: Considering the amount of data, the results of the five-fold cross-validation are more significant than those of the hold-out method. Densenet121 exhibits a sensitivity of 0.9550, a specificity of 0.8333, and an accuracy of 0.9000 in a five-fold cross-validation to separate AD patients from the control group. Conclusions: The potential for remote health care can be increased by simplifying the AD screening process. Furthermore, by facilitating remote health care, the proposed method can enhance the accessibility of AD screening and increase the rate of early AD detection.

Park HY, et al. J Korean Med Sci. 2024 Mar;39(12):e123. https://doi.org/10.3346/jkms.2024.39.e123

Jeon SY, et al. J Korean Med Sci. 2025 Jul;40:e215. https://doi.org/10.3346/jkms.2025.40.e215

Objective This review overviewed the recent paradigm shifts in the diagnosis and management of Alzheimer’s disease (AD), emphasizing the 2024 Alzheimer’s Association (AA) revised criteria, advances in cerebrospinal fluid (CSF) and blood-based biomarkers (BBMs), and practical considerations for anti-amyloid monoclonal antibody therapy.Methods We conducted a narrative appraisal of consensus frameworks (2018 National Institute on Aging–Alzheimer’s Association [NIA-AA] amyloid, tau, and neurodegeneration [AT(N)] and the 2024 AA criteria), clinical practice guidance from AA released in 2025, regulatory status of CSF and BBMs. Intended-use settings (triage vs. confirmatory) of BBMs and implementation of anti-amyloid anti-body treatments (lecanemab or donanemab) in real-world practice in Korea were also reviewed.Results The 2024 AA criteria define AD biologically and designate A and T as core biomarkers; Core 1 biomarkers can establish AD irrespective of symptoms, whereas Core 2 biomarkers refine staging. A two-cutoff BBM strategy (positive/intermediate/negative) reduces misclassification and guides confirmatory CSF/positron emission tomography (PET) or retesting. BBMs now approach CSF/PET accuracy for amyloid detection, enable triage and, in selected settings, confirmation, and show utility for monitoring treatment response. Integration of clinical stages (1–6) with biological stages (A–D) clarifies syndrome–pathology discordance. Special scenarios—maintenance after induction, APOE ε4 homozygotes, Down syndrome, and serious mental illness—require individualized risk–benefit assessment. In South Korea, constrained access to tau PET and some BBMs necessitates Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision–anchored evaluation with selective biomarker testing.Conclusion Biomarker-oriented diagnosis and anti-amyloid therapies are reshaping AD care. Priorities include rigorous validation of BBMs across populations, equitable access to core biomarkers, safety strategies, and real-world evidence to implement maintenance and special-population care pathways.