To better address the severe challenges of Alzheimer's disease (AD) prevention and control in China, the national government has published the National Action Plan for Addressing the elderly people with dementia. In order to accelerate the achievement of its core objectives, the Chinese Expert Consensus on Multidisciplinary Rehabilitation Interventions for Alzheimer's Disease has been formulated by integrating multidisciplinary expert opinions and evidence-based findings, using the Delphi method combined with GRADE evidence grading. This consensus advocates a “hospital-community-family” tripartite collaborative management model to standardize systematic and multidimensional approaches for the prevention, treatment, rehabilitation, and care of AD.This consensus deliver evidence-based guidance for tripartite stakeholders (healthcare providers, community networks, and family care systems) to operationalize healthy aging strategies through standardized AD management protocols.. For preventive strategies, AD risk factors are categorized into low-, medium-, and high-risk tiers to guide the formulation of personalized prevention and intervention strategies. For therapeutic management, treatment regimens are stratified by AD clinical stages (mild/moderate/severe), incorporating Western pharmacotherapy, traditional Chinese medicine and neuromodulation techniques. Rehabilitation requires individualized protocols based on multidimensional assessments encompassing functional disability evaluations, personal preferences, and familial support systems, with active rehabilitation prioritized during early/mid-stages and passive interventions dominating advanced AD care. Rehabilitation measures include cognitive therapies (including cognitive training, cognitive stimulation, and cognitive rehabilitation), lifestyle modifications (featuring nutritional guidance and exercise regimens that combine aerobic, strength, and mind-body training), humanistic approaches (such as reminiscence and immersive technologies), art-based therapies (applying music, dance, and visual arts), nature-assisted therapies (through horticultural and animal-assisted interaction), as well as sensory modulation techniques (utilizing light therapy and aromatherapy). For moderate-to-advanced stage AD patients presenting with behavioral and psychological symptoms of dementia or profound cognitive-functional decline, care strategies should implement person-centered care frameworks to preserve self-identity, deliver integrated palliative support, and manage comorbidities through multidisciplinary coordination.

Objective: This study aims to explore the application of toys and games in non-pharmacological interventions of Alzheimer's disease, and analyze the current research status, in order to provide guidance for future studies. Methods: This paper adopts literature review and thematic analysis methods. Literature searches were conducted on CNKI, Wanfang, Google Scholar, SCOPUS, Pubmed, and Science Direct using keywords such as "Alzheimer's disease," "dementia," "non-pharmacological intervention," "toys," and "games." Relevant literature from 2020 to 2024 was collected and subjected to thematic analysis. Results: The research indicates that non-pharmacological interventions for Alzheimer's disease are continuously emerging, among which a significant form of treatment is to use toys and games to enhance patients' quality of life. These toys and games stimulate cognitive and sensory functions, improve patients' social interaction abilities, promote physical activity, and alleviate negative emotions such as depression and anxiety. Conclusion: Currently, the toys used in occupational therapy for Alzheimer's disease patients mostly come from existing children's toys on the market or are simple toys developed by researchers in psychology and medicine, lacking research on how to design more tools for occupational therapy for Alzheimer's disease patients from a design perspective. Future research can start from the field of design to explore its principles and methods, in order to provide more beneficial insights and guidance for non-pharmacological interaction of Alzheimer's disease patients.

Cognitive impairment is the primary symptom of Alzheimer's disease (AD), manifesting as memory loss and changes in other cognitive functions. Currently, cognitive tools such as the mini-mental state examination (MMSE) and the montreal cognitive assessment (MoCA) are widely used to evaluate overall cognitive function in patients. However, these scales are time-consuming and require experienced clinicians to conduct face-to-face testing. This review aims to introduce MemTrax, a computerized continuous recognition task, and its application in cognitive assessment. In this test, subjects are required to complete a picture recognition task within approximately 90 seconds to assess their cognitive functions, mainly episodic memory, including memory processing, storage, retrieval, and reaction time.Previous studies have confirmed that its efficacy in identifying normal individuals, mild cognitive impairment (MCI), and AD patients is superior to MoCA. Moreover, combining with other biomarkers can further enhance its diagnostic efficacy, and it is also potential for assessment of treatment efficacy. Here we also introduce the application of MemTrax in various types of cognitive disorder diseases. Finally, this article proposes that MemTrax can be used as a digital tool to establish a systematic neuroscience database in the future, combining machine learning and other biomarkers to predict early dementia, as well as for large-scale cognitive screening and continuous cognitive monitoring.

Objective: We aimed to explore the association of liver fibrosis markers with cognitive decline. Methods: In this cross-sectional study, there were 8669 participants over 60 years old from 51 Community Health Centers in the Luohu District of Shenzhen from 2017 to 2018. All participants were divided into a cognitive low-risk group (n=8202) and a cognitive high-risk group (n=467) according to their scores of mini-mental state examination and education status. Blood routine examination and liver function markers were tested from fasting blood samples. The liver fibrosis markers FIB-4 and APRI were calculated with parameters such as ALT, AST, and PLT using specific formulas. We used the t-test, Mann-Whitney test, and Chi-square test to analyze the differences in general statistical characteristics and live fibrosis markers between the two groups, and binary Logistic regression analysis was used to analyze each parameter. The association between the liver fibrosis markers and alcohol drinking habits was tested by Spearman rank correlation. Results: FIB-4 was significantly higher in the cognitive high-risk group than the cognitive low-risk group [1.40 (1.13,1.78) vs. 1.49 (1.21,1.88), Z=3.595, P<0.001] but FIB-4 was not an independent risk factor of cognitive decline [OR (95%CI): 0.718 (0.444~1.159), P=0.175]. For alcohol drinkers, FIB-4 was significantly positively correlated with the age of starting drinking (r_s=0.089, P=0.005) and frequency of drinking (r_s=0.149, P<0.001). There was a positive correlation between APRI and frequency of drinking (r_s=0.078, P=0.013) as well. For people abstaining from alcohol, FIB-4 exhibited a positive correlation with the age of abstinence (r_s=0.172, P=0.014). Conclusion: FIB-4 was elevated in people with cognitive decline, and increased frequency of drinking was correlated with raised FIB-4 and APRI, and giving up drinking as soon as possible might be beneficial to prevent the cognitive decline by liver health.

Alzheimer's disease (AD) is the most common neurodegenerative disease worldwide and a leading cause of dementia. Currently, there are no highly effective treatments for this condition. The imbalance between the production and clearance of Aβ(amyloid-beta) protein is considered a primary pathogenic mechanism of AD. Enhancing the clearance of Aβ in the brain during the early stages can delay the onset and progression of AD. In recent years, with the introduction of the concept of the glymphatic system and the discovery of meningeal lymphatic vessels, the directional transport of fluids within the central nervous system has become a research hotspot. The glymphatic system plays a crucial role in clearing amyloid-beta protein and holds promise as a novel approach to combat neurodegenerative diseases. This review aims to summarize the current research progress on the role of the brain's glymphatic system in AD treatment and explore its potential applications in disease management.

Objective: To investigate the effect of Guide Care management model on self-management of Parkinson's disease patients.Methods: A total of 90 patients with Parkinson's disease who were hospitalized in the Department of Geriatric Neurology of our hospital from November 2021 to December 2022 were selected as the research objects. According to the random principle, they were divided into an experimental group and a control group, with 45 cases in each group. The control group was given routine nursing intervention, while the experimental group was given Guided Care management model intervention. The self-management ability, quality of life, disease progression, anxiety and depression of the two groups were evaluated. The intervention lasted for 6 weeks. Results: After intervention, the scores of three dimensions of self-management (daily behavior management, management cognition and disease management) in the experimental group were higher than those in the control group. The total scores of self-management and daily behavior management in the experimental group were higher than those in the control group (P< 0.001). The scores of UPDRS in both groups decreased before treatment, and the scores of motor examination, activities of daily living, mental behavior and emotion in the experimental group were significantly lower than those in the control group (P< 0.001). After intervention, the PDQ-39 scores of the two groups were significantly decreased, and the score of the experimental group was significantly lower than that of the control group (P< 0.05). After intervention, the SAS and SDS scores of the experimental group were significantly lower than those of the control group (P< 0.05). Conclusion: The Guide Care management model can improve the self-management ability of patients with Parkinson's disease and improve the clinical prognosis..

Objective: To explore the relationship between apolipoprotein A1 (ApoA1), apolipoprotein B (ApoB) and executive function in people with early cognitive impairment (EMCI), late mild cognitive impairment (LMCI), and early Alzheimer's disease (AD) patients, and to establish a group of Normal Control (NC) as a control group, in order to provide help for clinical intervention in the AD patients. Methods: A total of 142 people aged 50-80 years were recruited from Chengdu Fourth People's Hospital, including 35 cases of EMCI, 17 cases of LMCI, 26 cases of AD and 64 cases of NC. Each patient collected the following scales for executive function assessments using The Shape Trail Test part A (STT-A), The Shape Trail Test part B (STT-B), The Animal Fluency Test (AFT), The Symbol Digit Modalities Test (SDMT), Digit Span Test (DST) at baseline. The laboratory collected morning fasting blood to detect ApoA1 and ApoB levels. Spearman correlation test was used to analyze the correlation between ApoA1, ApoB and executive function, and linear regression analysis of the influencing factors of ApoA1 and ApoB on executive function. Results: The years of education in AD group were significantly lower than that in the NC group (P<0.05); In the NC group，the time spent on STT-A and STT-B were significantly lower than that in the EMCI group, LMCI group and AD group(P<0.05); in the EMCI group, the time spent on STT-A was significantly lower than that in the AD group(P<0.05), and the AFT and SDMT scores were significantly lower than those in the NC group(P<0.05) ; in the AD group, the AFT score was significantly lower than that in the NC group and LMCI group(P<0.05) ; the SDMT and DST score was significantly lower than that in the NC group (P<0.05) ; the ApoA1 level in the AD group was significantly lower than that in the NC group and EMCI group(P<0.05) ; there was no statistically significant difference in the ApoB levels among the four groups. ApoA1 levels were positively correlated with AFT, SDMT, and DST (P<0.05), and negatively correlated with STT-A and STT-B (P<0.05) ; ApoB levels had no correlation with executive functions; after adjusting for confounding factors, the multiple linear regression results of ApoA1 and executive function showed that ApoA1 significantly positively affected SDMT (P<0.05). After diagnosis stratification, the results of linear regression between ApoA1 and SDMT showed that ApoA1 could significantly positively affect SDMT in the NC group, LMCI group, and AD group (P<0.05). Conclusion: The connection between ApoB and executive function has not been found;. ApoA1 is mainly significantly related to information processing speed in the NC group, LMCI group, and AD group, indicating that the combination of ApoA1 and information processing speed can become an important tool for exploring cognitive impairment..

The meningeal lymphatic vessels (mLVs) play a crucial role in the complex circulation and exchange of soluble contents between the cerebrospinal fluid (CSF) and the interstitial fluid (ISF). It has been confirmed that mLVs can drain intracranial CSF and immune cells to extracranial deep cervical lymph nodes (dCLNs), thereby establishing a direct link between the central nervous system (CNS) and the peripheral immune system. Given the limited therapeutic options for Alzheimer's disease (AD), enhancing brain lymphatic flow to improve the clearance of toxic waste has emerged as a new approach to alleviating cognitive impairment. This article briefly introduces the discovery process, structure, and location of mLVs, and thoroughly discusses their physiological functions. It focuses on the relationship between mLVs and the pathogenesis of AD, aiming to provide reference for emerging therapeutic mechanisms of AD.

Objective: To investigate the associations of five obesity indicators, body mass index (BMI), body round index (BRI), visceral adiposity index (VAI), lipid accumulation product (LAP), and a body shape index (ABSI), with the risk of mild cognitive impairment (MCI) in middle-aged and older adults. Methods: This cross-sectional study recruited participants from Wuhan and Shiyan cities in Hubei province during 2019 and 2022. After excluding individuals with self-reported dementia or Parkinson's disease and missing general characteristics, a total of 6,917 participants were included in this study. Multiple linear regression and logistic regression models were used to evaluate the associations of body mass index and novel obesity indicators with the cognitive function. Restricted cubic spline model was used to explore the nonlinear relationships between obesity indicators and MCI. Results: Among the 6917 participants in this study, 3338 (48.3%) were males and 3579 (51.7%) were females. A total of 670 (9.7%) participants were identified as MCI. Increased BRI and ABSI were associated with decreased MMSE score and raised MCI risk (P trend < 0.001). After adjusting for confounding, compared to the Q1 subgroup, individuals in the BRI, ABSI and LAP Q4 subgroup respectively showed increased MCI risk [OR (95% CI)=1.58 (1.23,2.03), 2.54 (1.68, 3.86), 1.38 (1.08, 1.76)]. RCS confirmed the linear dose-response relationships of BRI and ABSI with MCI risk (both P for non-linear associations were > 0.05). However, BMI and VAI were not found to be correlated with MCI risk. Conclusion: High BRI, ABSI and LAP may be risk factors for cognitive decline, and BRI and ABSI may present a potential dose-response relationship with MCI risk.

Vascular dementia (VaD) is a severe syndrome of cognitive impairment caused by ischemic stroke, hemorrhagic stroke, and cerebrovascular lesions that cause hypoperfusion of memory, cognitive, and behavioral brain regions. Among the types of dementia, VaD is the second most common cause after Alzheimer's disease, but the pathogenesis of VaD is still unclear. Astrocytes are the most abundant glial cells in the central nervous system.Astrocytes have the ability to produce and release specific neurotransmitters, and express corresponding neurotransmitter receptors,which can respond to a variety of neuroactive substances.In recent years, a large number of studies have been carried out on the role of astrocytes in the central nervous system (CNS), and this article reviews the current role and mechanism of astrocytes in the progression of VaD based on the research background and research significance.We hope to provide a useful reference for understanding the pathogenesis of VaD and exploring new treatment methods and bring new breakthroughs in the treatment of clinical VaD.

Recent studies have shown that Kallikrein-related peptidases (KLKs) play crucial roles in the pathological progression of Alzheimer's disease (AD). This review systematically summarizes the latest research advances in AD-related KLKs (KLK1, KLK6, KLK7, KLK8, and KLK10). Studies have revealed that KLK6 affects amyloid-β (Aβ) generation by inhibiting α-secretase and enhancing γ-secretase activity; KLK7, as an Aβ-degrading enzyme secreted by astrocytes, shows accelerated Aβ deposition in AD model mice when deficient; KLK8 influences the PI3K/Akt/GSK-3β signaling pathway, leading to decreased Akt phosphorylation and increased GSK-3β expression, thereby promoting Tau protein hyperphosphorylation, with significantly higher expression levels observed in female AD patients compared to males. Furthermore, KLKs impair blood-brain barrier function through mechanisms including extracellular matrix protein cleavage and reduction of endothelial cell inflammation. Meanwhile, KLK6 and KLK8 exhibit significantly elevated expression levels in the cerebrospinal fluid and blood of AD patients, suggesting their potential value as biomarkers. A deeper understanding of KLKs' mechanisms in AD will provide new insights into the early diagnosis and treatment of the disease.

Alzheimer's disease (AD) and osteoporosis (OP) are both age-related degenerative diseases,which mainly occur in the elderly population over the age of 60, and are becoming an increasingly common combination in the aging population. It has been proved that a variety of factors can stimulate and accelerate the occurrence of AD and OP in clinical practice. This review mainly studies the common pathogenesis of AD and OP, and discusses the pathogenesis factors such as vitamin D and vitamin K levels, signaling pathways, apolipoprotein and neuroinflammation in AD mouse models. In addition,potential treatments for these two diseases are described.

Alzheimer's disease has become a great concern in the current aging society. In order to better treat this disease, it is crucial to study and understand its pathogenic mechanisms. Equally important is how to detect Alzheimer's disease early and more accurately. Here, we summarized the pathogenic mechanisms of Alzheimer's disease and compared its different detection methods.

Objective: To investigate the characteristic of sporadic Creutzfeldt-Jakob disease(sCJD), improve the knowledge of sCJD for clinicians. Methods: We collected the clinical data, brain neuroimages and laboratory test results of a case of sCJD and reviewed relative articles. Results: The patient showed limb rigidity, involuntary movements, myoclonic jerks, speech disorders, rapidly progressive cognitive impairment, and later autonomic dysfunction, and passed away 8 months after the onset. Conclusion: The early symptoms of sCJD are atypical, varied and heterogeneous, with a high fatality rate. The diagnosis of CJD requires attention to distinguishing it from various diseases, and dynamic examination of cerebrospinal fluid, brain MRI, electroencephalogram, and even biopsy to avoid misdiagnosis and missed diagnosis.

There have been many different opinions on the pathogenesis of Alzheimer's disease (AD), and the β-amyloid protein (Aβ) theory has always been dominant. However, many treatments targeting on Aβ have had little effect, which has led researchers to re-examine this theory. More and more research findings have made people realize that although the accumulation of Aβ plaques in the brain is closely related to cognitive decline, it may only be a manifestation of AD, not the root cause of this disease. The body's inability to clear the accumulation of proteins including Aβ due to various reasons such as chronic inflammation with brain damage may be a deeper cause of this disease. These important cell functions include endocytosis, macropinocytosis, innate phagocytosis and autophagy, and mitochondria that provide energy to these high-energy consumption applications may be the determining factor affecting these functions. Therefore, simply removing Aβ plaques may have little effect in the treatment of Alzheimer's disease. More efforts should be placed on how to improve essential cell functions like innate phagocytosis and autophagy, as well as to improve mitochondrial function to increase energy production.

Objective: Investigate the diagnostic value of cerebrospinal fluid (CSF) growth-associated protein 43 (GAP-43) in AD and the predictive value of AD transition from mild cognitive impairment (MCI) to dementia through a cross-sectional and longitudinal observational study. Methods: 787 subjects with CSF GAP-43 data were divided into normal group (n=247), MCI group (n=413) and dementia group (n=127) based on cognitive status. Kruskal-Wallis test was used to compare the differences of CSF GAP-43 between groups. Multiple logistic model was used to test the correlation between CSF GAP-43 and different cognitive states. The diagnostic efficacy of CSF GAP-43 level for AD was evaluated by receiver-operating curves (ROC) and the area under curves (AUC). The diagnostic efficacy of AD was compared with that of CSF core markers (Aβ, t-tau, p-tau). Patients with MCI were divided into stable MCI (sMCI) and progressive MCI (pMCI) according to whether they progressed to dementia within 5 years. Mann-Whitney u test was used to compare CSF GAP-43 between groups. Cox regression model was used to test the correlation between CSF GAP-43 and the progression of MCI to dementia. The predictive value of CSF GAP-43 levels in predicting MCI progression to dementia was evaluated by ROC curve. The association of CSF GAP-43 level with the risk of progression to dementia was evaluated using Kaplan-Meier survival curves. Results: The results of cross-sectional study showed that the level of CSF GAP-43 was significantly higher in the dementia group than in the normal group and the MCI group (P<0.0001). CSF GAP-43 was an independent risk factor for the onset of AD dementia (P=0.002). The AUC of CSF GAP-43, Aβ, p-tau and t-tau for the diagnosis of AD were 0.64, 0.68, 0.64 and 0.63. Follow-up analysis showed that the level of CSF GAP-43 in pMCI patients was significantly higher than that in sMCI patients (P<0.0001), and CSF GAP-43 was an independent risk factor for the progression of MCI to dementia (P=0.012). The AUC for CSF GAP-43 predicting MCI progression to dementia was 0.75 (P<0.0001, 95%CI: 0.69~0.80). The risk of progression to dementia was 3.45 times greater in MCI patients with high CSF GAP-43 levels than in MCI patients with low CSF GAP-43 levels (P<0.0001, 95%CI: 2.17~5.43).Conclusion: CSF GAP-43 level can be used in the diagnosis of AD dementia, and its diagnostic efficacy is comparable to that of CSF core biomarkers (Aβ, t-tau, p-tau). CSF GAP-43 can predict the progression of MCI to dementia and is an independent risk factor for the progression of MCI to dementia.

Objective: Holmes tremor (HT) is a rare movement disorder. HT may also be associated with other neurological symptoms, including cognitive dysfunction. This study aims to investigate the pathophysiological mechanisms, diagnostic approaches, and therapeutic strategies for HT, thereby providing guidance for clinical management. Methods: The diagnosis of HT primarily relies on clinical features and neuroimaging techniques, such as MRI. Treatment options include pharmacological interventions (e.g., levodopa, trihexyphenidyl) and surgical approaches (e.g., deep brain stimulation, thalamotomy). A systematic review of the literature was conducted to summarize the clinical features, pathophysiological mechanisms, and treatment outcomes of HT. Results: HT symptoms typically emerge between 4 weeks and 2 years after neurological injury, associated with abnormal synaptic reorganization and collateral axonal sprouting following neuronal damage. The efficacy of pharmacological treatments varies among individuals, with levodopa showing effectiveness in approximately 54% of patients, though overall efficacy remains limited. Other medications, such as antiepileptic drugs and dopamine agonists, are also commonly used, but their effectiveness can be highly variable, with some patients showing poor response to these drugs. Surgical interventions, including deep brain stimulation, thalamotomy, lesionectomy of the original pathological focus, and ablation of specific nuclei, have demonstrated some efficacy but exhibit individual variability. There is currently no unified treatment consensus, and large-scale multicenter studies validating the long-term outcomes of novel therapies are lacking. Conclusion: The treatment of HT remains challenging, and its pathophysiological mechanisms are not yet fully understood. Future research should further investigate the pathophysiological mechanisms of HT, particularly its relationship with cognitive dysfunction, and optimize treatment strategies. Conducting multicenter studies to validate the long-term efficacy of novel therapies holds promise for improving the quality of life and prognosis of HT patients.

Alzheimer's disease is a neurodegenerative disorder characterized by β-amyloid deposition and pathological phosphorylation of tau protein. Traditional population-level sequencing has been limited in resolving the highly heterogeneous cellular populations and their spatiotemporal dynamics in brain tissue due to resolution constraints. In recent years, single-cell sequencing technologies—including single-cell RNA sequencing, single-cell assay for transposase-accessible chromatin sequencing, single-cell whole-genome sequencing, and spatial transcriptomics—have overcome these limitations. These technologies enable systematic exploration of subpopulation heterogeneity and pathological response mechanisms in neurons, microglia, astrocytes, and oligodendrocytes at single-cell resolution, offering novel insights into the cellular and molecular mechanisms underlying Alzheimer's disease. Studies demonstrate that single-cell RNA sequencing combined with spatial topological information can map cell-specific distributions of β-amyloid plaques and neurofibrillary tangles. Multi-omics integrative analyses have revealed the epigenetic mechanisms by which APOE ε4 regulates microglial phagocytic function and delineated the brain-gut axis and neuroinflammatory network atlas. Although single-cell technologies still face challenges in sensitivity, cost, spatial resolution, and data analysis, their integration with artificial intelligence algorithms and high-throughput microfluidic platforms is driving a paradigm shift in Alzheimer's Disease research—from pathological description to systems biology and precision medicine. Future advancements in detection efficiency, multi-omics integration, three-dimensional spatial mapping, and clinical validation are essential to enable ultra-early diagnosis and personalized therapies for Alzheimer's Disease. This review systematically summarizes the progress of single-cell sequencing technologies in elucidating key cell types in AD and discusses their technical limitations and future prospects.

Alzheimer’s disease (AD) is a prevalent neurodegenerative disorder. Air pollution, characterized by its complex composition, diverse pollutant types, and significant spatiotemporal variability, poses both localized and long-range threats due to atmospheric transport. Certain pollutants exhibit persistence and bioaccumulative properties, exerting profound impacts on human health and social equity. These effects are further modulated by natural geographical and meteorological conditions, rendering them uniquely complex. An increasing body of evidence identifies air pollution as a significant environmental risk factor for AD. In response to growing interest, this paper provides a comprehensive review of the epidemiological evidence, pathophysiological mechanisms, and emerging methodological approaches related to air pollution's role in AD. Furthermore, it explores how compounded social determinants interact with environmental exposure to influence AD risk.

Objective: Frontotemporal dementia（FTD） and Alzheimer's disease（AD） exhibit overlapping clinical symptoms and neuroimaging features, complicating differential diagnosis and increasing misdiagnosis risks. This study aimed to explore gray matter volume（GMV） patterns between FTD and AD using 3D high-resolution T1-weighted MRI and machine learning to establish an objective diagnostic method. Methods: Voxel-based morphometry（VBM） was applied to analyze whole-brain GMV differences in 20 FTD and 35 AD patients. The relationships between GMV exhibiting significant differences and cognitive scores（MMSE, MoCA, CDT, ADAS-cog, CDR, ADL） were assessed. A support vector machine（SVM） classifier was constructed using GMV features from significant regions. Results: Significant GMV differences in FTD versus AD were observed in the right hemisphere（FWE-corrected, cluster level, P<0.05）, including the occipital（superior/middle/inferior gyri）, parietal（superior parietal lobule, supramarginal gyrus, angular gyrus）, and temporal lobes（superior/middle/inferior gyri）. GMV in the right occipital and temporal regions was significantly and positively associated with MMSE, MoCA and CDT scores（beta = 0.263-0.399, P<0.05）. The SVM model achieved moderate classification accuracy（60.00%, AUC = 0.6729）. Conclusion: VBM combined with cognitive assessment identified neuroimaging biomarkers distinguishing FTD from AD. Although the SVM model shows moderate performance, these findings provide objective evidence for clinical differentiation. This work not only advances understanding of neuroanatomy but also lays a foundation for optimizing machine learning models to improve diagnostic accuracy, demonstrating promising clinical translation potential.

Objective: The aim of the current study was to explore the specific intrinsic functional connectivity between the the retrosplenial cortex (RSC) and the hippocampal subfields in healthy adults and to characterize the alterations in functional connectivity between the RSC and the hippocampal subfields in amnestic mild cognitive impairment (aMCI) and Alzheimer's disease (AD) patients. Methods: Demographic data, neuropsychological assessments, and resting-state functional magnetic resonance imaging (fMRI) data were collected from 60 AD participants, 60 participants with aMCI, and 60 sex-matched normal controls (NCs). The bilateral RSC, other parts of the posterior cingulate cortex (PCC), and hippocampus (HPC) subfields (including the bilateral cornu ammonis fields (CA1-CA3), the dentate gyrus (DG), and subiculum (SUB)) were selected to investigate functional connectivity alterations in aMCI and AD. Results: Resting-state functional connectivity analysis demonstrated heterogeneity in the degree of connectivity between the HPC and different parts of the total PCC, with considerably greater functional connectivity of the RSC with the HPC compared with other parts of the PCC. Furthermore, the bilateral RSC exhibited widespread intrinsic functional connectivity with all HPC subfields. Compared to the NCs, the aMCI and AD groups showed different magnitudes of decreased functional connectivity between the RSC and the contralateral DG. Additionally, diminished functional connectivity between the left RSC and right DG was correlated with clinical disease severity in aMCI subjects. Conclusion: These findings confirm and extend previous studies suggesting that the RSC is extensively and functionally connected with HPC subfields and that these functional connections are selectively affected in the AD continuum, with prominent disruptions in functional connectivity between the RSC and contralateral DG underpinning episodic memory impairment associated with the disease.

Objective: To explore the effect of APOEɛ4 gene carrier status on amyloid deposition in the brain of Alzheimer's disease patients in Chinese population. Methods：A retrospective collection was conducted on 932 cognitively normal individuals and patients diagnosed with mild cognitive impairment or Alzheimer's disease who visited the Memory Clinic of Huashan Hospital affiliated with Fudan University from August 2018 to March 2023. Among them, there were 532 cognitive normal individuals and 400 cognitive impaired individuals, including 211 mild cognitive impairment and 189 Alzheimer's disease patients. All participants were subjected to cognitive assessment, genotype determination, and [18F] Florbetapir PET imaging quantitative analysis of A β deposition in the brain, which is converted into centiloid value. The centiloid value of each group were compared based on cognitive status, APOEɛ4 gene carrying status, gender, and other factors. Performing partial correlation analysis on the centiloid value and cognitive scores of APOEɛ4 gene carrying or non carrying group. Results: The centiloid value of the APOEɛ4 gene carrying group is higher than that of the non carrying group, and the difference is significant (26.7 ± 38.3 vs 3.7 ± 26.6, P<0.001）. In the population with cognitive impaired, the centiloid value of both male and female APOEɛ4 gene carriers were higher than those of non carriers of the same gender (36.2 ± 40.3 vs 9.7 ± 30.7, 39.2 ± 37.5 vs 17.7 ± 38.8, respectively), P<0.001）. However, there is no significant difference in centiloid value between males and females in carriers or non carriers with cognitive impaired (36.2 ± 40.3 vs 39.2 ± 37.5, 9.7 ± 30.7 vs 17.7 ± 38.8, P>0.05）. The difference in centiloid value between the cognitive normal group and the cognitive impaired group is statistically significant (0.2 ± 21.0 vs 23.5 ± 38.6, P<0.001）. In subjects with cognitive impaired or cognitive normal, there is a significant difference in centiloid value between APOEε4 carriers and non carriers (P<0.001).The difference in centiloid value between cognitive impaired and cognitive normal populations is also significant (P<0.001) in APOEε4 gene carriers or non carriers. Under the control of age, education year, and gender, there is a moderate negative correlation between the centiloid value and cognitive scores in both the APOEɛ4 gene carrying and non carrying groups (r=-0.435 and -0.449, respectively,P<0.001）. Conclusion: The deposition of amyloid protein in the brain of APOEɛ4 gene carriers is significantly higher than that of non carriers, and there is a negative correlation between amyloid protein deposition and cognition in APOEɛ4 gene carriers and non carriers.

Objective: To expolre the changes in cerebral white matter microstructure and cerebral blood flow (CBF) in patients with plateau Alzheimer's disease (AD) using multimodal MRI. Methods: A total of 18 AD patients with long-term plateau residence and 20 healthy subjects were prospectively enrolled. 3.0T MRI scanner was used to acquire diffusion tensor imaging (DTI), T1-weighted, and arterial spin labeling (ASL) sequences. DPABI Pro post-processing software was applied to obtain tract-based spatial statistics (TBSS) images based on fiber tractography and region of interest (ROI) images.Comprehensive analysis of the characteristics of white matter microstructure changes in plateau AD patients was performed by combining CBF data and cognitive scales. Results: 1. TBSS results showed that the regions of white matter fiber tract damage in plateau AD patients were basically consistent with those in plainland AD patients. Compared with the normal control (NC) group, ROI analysis revealed that axial diffusivity (AD), mean diffusivity (MD), and radial diffusivity (RD) in the AD group were significantly increased in multiple brain regions (P < 0.05). 2. In plateau AD patients, decreased CBF coexisted with abnormal DTI findings in regions including the temporal lobe, corona radiata, parietal lobe, precuneus, cingulate gyrus, prefrontal lobe, and thalamus. 3. In plateau AD patients, AD and MD values of the cingulate gyrus were positively correlated with ADL scores; AD and MD values of the thalamus were significantly negatively correlated with MMSE scores; RD value of the hippocampus was negatively correlated with MMSE scores. Conclusions: Widespread and significant damage to global cerebral white matter and fiber tracts is observed in plateau AD patients, with regional specificity characterized by extensive involvement of the visual cortex, thalamus, and motor cortex. Additionally, there is substantial overlap between regions of decreased CBF and abnormal DTI indices in plateau AD patients, reflecting that the "blood flow-microstructure" synergistic damage mechanism caused by neurovascular coupling (NVC) impairment may exacerbate the pathological progression of plateau AD, and is closely related to global cognitive function and daily living ability.

Accurate early diagnosis of Alzheimer’s disease (AD) represents a major challenge against the backdrop of global aging. This paper reviews research advances combining generative Artificial Intelligence (AI) with multimodal neuroimaging (including MRI and PET) to achieve early and accurate diagnosis of AD. This review systematically analyzes the applications of generative models in AD diagnosis across key areas: brain image data augmentation, pathological feature representation learning, and brain network modeling. We provide a detailed analysis of how these technologies effectively overcome critical challenges such as neuroimaging data scarcity and class imbalance. These technologies enhance the models’ classification performance on AD datasets and its ability to predict the progression of AD. Specifically, in the analysis of functional and structural brain networks, generative AI offers a new paradigm for understanding AD pathological mechanisms and enabling early prediction by constructing high-fidelity networks. Furthermore, this paper discusses the clinical translation prospects of these technologies in personalized prognosis and treatment monitoring, as well as the technical and ethical challenges in implementation. This review provides a comprehensive framework to understand the potential and development trends of generative AI, multimodal neuroimaging, and their derived functional brain network features in the auxiliary diagnosis of early AD.

Objective: To evaluate the effectiveness of caregiver group support skills training on coaches' attitudes towards dementia care and their sense of competence. Methods: A total of 56 participants in the dementia caregiver group support skills training (referred to as "coaches"; 10 male and 46 female) completed assessments of their dementia care attitudes and sense of competence before and after the training. Paired t-tests were used to compare the differences in scores for dementia care attitudes and sense of competence before and after the training. Multivariate analysis was conducted to explore the demographic factors associated with the changes in dementia care attitudes and sense of competence. Results: After the training, coaches showed a significant increase in scores for the "hope" and "personhood validation" factors of the dementia care attitude scale, as well as the total scale score (P < 0.05). Additionally, scores for the "professionalism," "relationship building," "managing caregiving challenges," and "maintaining personhood" factors of the dementia care competence scale, as well as the total scale score, significantly increased after the training (P < 0.05). Multivariate analysis indicated that only the occupation was associated with changes in the total score and "relationship building" factor of dementia care competence before and after the training; no other sociodemographic characteristics were associated with the changes in dementia care attitudes and other factors of competence scale. Conclusion: Caregiver group support skills training can improve coaches’ attitudes towards dementia care and enhance their sense of competence in caregiving.

Deutetrabenazine, a deuterated derivative of tetrabenazine, has emerged as an effective treatment for Huntington's chorea and tardive dyskinesia. By selectively inhibiting vesicular monoamine transporter 2 (VMAT2), it reduces the synaptic release of dopamine and other monoamines, thereby alleviating involuntary movement symptoms. Compared to its precursor, deutetrabenazine demonstrates an improved safety profile, with significantly lower incidences of sedation and depression, enhancing patient adherence and suitability for long-term use. It is especially well-tolerated in vulnerable populations such as children and the elderly, showing better emotional stability and pharmacokinetic advantages. While its therapeutic potential is being explored in other neurodegenerative conditions like Parkinson's and Alzheimer's diseases, its current indications remain limited. Long-term administration poses challenges such as drug resistance and mood-related side effects, underscoring the need for psychological monitoring and individualized treatment plans. Furthermore, its high cost and inconsistent insurance coverage constrain global accessibility. Future strategies involving neuromodulation technologies, optimized reimbursement policies, and precision medicine approaches may expand its clinical utility and improve availability worldwide.

Objective: To evaluate and summarize the relevant evidence for the management of mild cognitive impairment in patients with Parkinson's disease, and provide evidence-based support for the development of scientific and effective management of mild cognitive impairment in Parkinson's disease. Methods: According to the "6S" model of evidence-based resources, the author systematically searched guidelines, expert consensus, clinical decision, evidence summary and systematic review on the management of mild cognitive impairment in Parkinson's disease patients from domestic and foreign guide websites, professional association websites and databases. The search period is up to December 2024. Literature quality assessment, evidence extraction and summary were conducted by two researchers trained in evidence-based systems. Results: A total of 14 literatures were included, including 6 guidelines, 5 expert consensus articles and 3 systematic reviews. The 34 evidences were summarized from 7 aspects: assessment object and time, assessment content and screening tool, risk factor management, safety management, medication management, non-drug intervention and follow-up management. Conclusion: This study systematically summarizes evidences in the field of mild cognitive impairment management in patients with Parkinson's disease, which can provide scientific reference for clinical nursing staff's practice. Nursing staff should select evidence based on the actual clinical situation and individual factors of patients to guide Parkinson's patients to improve mild cognitive impairment.

Objective: To analyze the differences in the triglyceride-glucose index (TyG) and its combination with obesity indicators in the assessment of cognitive function, and to further explore their mediating effects between physical activity (PA) and cognitive function. Methods: Questionnaires of the physical examination population in Youyi Road Community Health Service Centre for Baoshan District, Shanghai from April to December 2020 were collected. A total of 3937 subjects were included. The association between PA and cognitive function, the association between TyG and its combined obesity indicators and cognitive function were analyzed using generalized linear regression models, and gender stratified analysis was conducted. The mediating effects of TyG and its combined obesity indicators in the relationship between PA and cognitive function were evaluated using the mediation models. Results: After full adjustment, there was a significant association between PA and cognitive function (β=0.337, P < 0.05), and the trend of the analysis results in men was consistent with that of the total population (β=0.374, P < 0.05). There was no significant association between TyG and the mini-mental state examination (MMSE) score in the total population. Compared with TyG-body mass index (TyG-BMI) and TyG-waist circumference (TyG-WC), the association between TyG-waist-to-height ratio (TyG-WHtR) and MMSE score was significantly enhanced (β=-0.588, P < 0.001), and the results of the gender subgroup analysis were consistent with those of the total population. TyG-BMI, TyG-WC and TyG-WHtR all played significant mediating roles between PA and cognitive function, among which the mediating effect of TyG-WHtR was the strongest (9.81%, P < 0.05). Conclusion: There is a significant association between PA, TyG and its combination with obesity indicators and cognitive function. TyG-BMI, TyG-WC and TyG-WHtR all played significant mediating roles between PA and cognitive function, and TyG-WHtR plays the strongest mediating role in the association. The TyG-obesity combined indexes provide basis for formulating cognitive function protection strategies for individuals with metabolic abnormalities..

Objective: To conduct a meta-analysis on the incidence of frailty in patients with Alzheimer's Disease (AD), in order to provide a scientific basis for the prevention of frailty in AD patients. Methods: By systematically searching CNKI, Wanfang, VIP Chinese databases, PubMed, Web of Science, Embase and Cochrane Library English databases, the epidemiological evidence of the incidence of frailness in AD patients was comprehensively obtained. The literature search period was set from the establishment of the database to March 10, 2025, and literature screening, data extraction and bias risk assessment were carried out by two researchers respectively. Statistical software Stata14.0 was used to conduct a meta-analysis of the included studies. Results: Thirteen studies were included, covering 2806 patients with Alzheimer's disease, and the analysis suggested an overall incidence of frailty of 34% (95%CI: 27%~41%). Study area, measurement tool, study time, sample size and other factors have an impact on the incidence of frailty in patients with Alzheimer's disease. Conclusion: The incidence of frailties in patients with Alzheimer's disease is high. Attention should be paid to frailties in patients with Alzheimer's disease, and early detection and intervention measures should be taken to reduce the occurrence of frailties in this population.

In the context of an aging society, the management of chronic diseases in patients with dementia has become a public health issue that requires urgent attention. This article expounds the current situation of chronic disease management for dementia, analyzes the characteristics of dementia, the process of chronic disease management for dementia, and the management characteristics in medical care institutions. It proposes a series of targeted countermeasures and suggestions from multiple aspects,including improving cognitive abilities, optimizing medication management, managing behavioral and psychological symptoms of dementia (BPSD), building care systems, promoting health, and prevention. These efforts aim to provide new ideas and references for the chronic disease management of dementia patients, aiming to provide more comprehensive and effective chronic disease management services for patients with dementia, improve their quality of life, reduce the burden on families and society, and provide work ideas and references for the management of chronic diseases in elderly dementia patients in China.

Objective: To systematically evaluate the efficacy and safety of repetitive transcranial magnetic stimulation (rTMS) in the treatment of vascular dementia(VaD). Methods: Randomized controlled trials (RCTs) investigating rTMS for VaD were retrieved from Chinese and English databases from inception to May 2025. After screening based on predefined inclusion and exclusion criteria, a meta-analysis was performed using RevMan 5.4 software. Results: A total of 15 eligible RCTs involving 1,296 patients were included. The meta-analysis demonstrated that, compared with the control group, rTMS significantly improved clinical response rate [RR=1.26,95%CI(1.18,1.35),P<0.00001], Montreal Cognitive Assessment (MoCA) score [MD=1.84,95%CI(1.27,2.41),P<0.00001], Mini-Mental State Examination (MMSE) score [MD=3.81,95%CI(3.43,4.19),P<0.00001], Hasegawa Dementia Scale (HDS) score [MD=3.48,95%CI(2.94,4.03),P<0.00001], National Institutes of Health Stroke Scale (NIHSS) score [MD=-1.23,95%CI(-1.47,-0.99),P<0.00001], and Activities of Daily Living (ADL) score [MD=6.72,95%CI(5.70,7.74),P<0.00001]. All differences were statistically significant. Adverse effects of rTMS were mild, with good patient tolerance and high safety. Conclusion: rTMS demonstrates significant efficacy in improving cognitive function, activities of daily living, andneurological deficits in VaD patients, while maintaining high treatment safety.

Objective: To assessment of the incidence and risk factors of cognitive decline in maintenance hemodialysis (MHD) patients. Methods: A total of 89 MHD patients and 30 Non-dialysis individuals with matched age and sex in the same community were enrolled. The cognitive functions of MHD patients and Non-dialysis individuals were evaluated by mini-mental State Examination (MMSE). The values below 27 indicative of cognitive impairment, which was corrected by the educational background. The clinical data, previous medical history, biochemical indicators of malnutrition, bone mineral metabolism and inflammation were evaluated. Logistic regression analysis was performed to find out the risk factors of cognitive decline in MHD patients. Results: Out of 89 enrolled MHD patients, 43.8% were classified with cognitive impairment, significantly higher than that in the healthy individuals group (13.3%, P=0.003). In the cognitive impairment group, age and MCV were significantly higher than that of the normal cognitive group, and the HDL was significantly lower than that of the normal cognitive group (P<0.05). Further analysis found that the scores in all fields of the cognitive impairment group were significantly lower than those with normal cognitive function, especially in attention, computational power and language ability (P<0.05). The results of logistic regression analysis showed that age(β=-0.110, P=0.008), MCV(β=-0.168, P=0.022) and HDL(β=3.071, P=0.038) were the independent risk factors affecting cognitive impairment in MHD patients. Conclusion: The incidence of cognitive impairment in MHD patients was significantly higher than that in matched healthy individuals in the same community. Age, MCV and HDL were independent risk factors for cognitive impairment in MHD patients.

Alzheimer's disease (AD) is a complex neurodegenerative disorder caused by multiple factors, characterized primarily by the deposition of amyloid β-protein (Aβ) plaques and the formation of phosphorylated Tau protein neurofibrillary tangles in the brain, which together lead to memory loss and cognitive impairment. In recent years, microRNAs(miRNAs), as an essential class of non-coding RNA molecules, have demonstrated a pivotal role in the pathogenesis of AD. miRNAs tightly regulate the generation and clearance of Aβ by targeting key genes such as APP and BACE1. Meanwhile, specific miRNAs can significantly influence the phosphorylation state of Tau protein, exerting a profound impact on neuronal stability and survival. However, despite the enormous potential of miRNAs in AD research, numerous challenges remain. For instance, the differences in miRNA expression patterns between AD patients and healthy controls, as well as their biological significance and translational relevance, require further validation. Additionally, there is currently a lack of unified and accurate criteria for assessing the reliability of miRNAs as biomarkers, and miRNA-based therapies have not yet been approved for clinical use. Therefore, future research needs to further delve into the specific mechanisms of miRNAs in AD, systematically evaluate their potential as therapeutic targets, and actively overcome existing technical and methodological challenges, in order to provide new theoretical foundations and practical strategies for the diagnosis and treatment of AD.

Objective: To obtain the clinical basis for non-drug intervention in mild cognitive impairment (MCI) by exploring the efficacy of auricular acupuncture combined working memory (WM) training in patients with MCI. Methods: A total of 40 MCI patients who were hospitalized in the Department of Geriatrics at Hangzhou Wuyunshan Hospital from January to December 2023 were included and randomly divided into an observation group of 20 patients who received 3-week WM training and a control group of 20 patients who did not receive training by drawing lots. The Montreal Cognitive Assessment (MoCA) was used to evaluate the patients' cognitive function. Results: Before training, there was no significant difference in cognitive function between the two groups(P>0.05). In the observation group, the visual-spatial and executive ability and MoCA total scores of patients followed up for 6 months after training were higher than those before training, and the difference was statistically significant (P<0.05). After training, followed up for 6 months, the visual-spatial and executive function and MoCA total scores of patients in the observation group were higher than those in the control group, and the difference was statistically significant (P<0.05). Conclusion: Auricular acupoint stimulation combined with WM training can improve some cognitive functions in MCI population.

Objective: To evaluate clinical phenotypes and nocturnal sleep structure characteristics with mild cognitive impairment due to Alzheimer's disease (AD). Methods: Based on cerebrospinal fluid or positron emission tomography imaging to detect the concentration or deposition status of β-amyloid protein (Aβ) to distinguish between MCI due to AD and control group. All patients underwent polysomnography monitoring (PSG), APOE gene testing, Montreal Cognitive Assessment (MoCA), Hamilton Anxiety Scale (HAMA), and Hamilton Depression Scale (HAMD) assessments. Results: ① Significant differences were found in clinical characteristics such as sleep disturbance, body mass index (BMI), education years, occupations, combined with risk factors, and APOEε4 gene mutation (P<0.05); ② There were statistically significant differences in MoCA and HAMA scores between these two groups (P<0.05); ③Significant differences in N1/total sleep time (TST)%, N2/TST%, N3/TST% and rapid eye movement sleep time (REM)/TST%, average blood oxygen concentration during night-sleep time, sleep-related apnea-hypopnea index (AHI), obstructive sleep apnea (OSA) index between these two groups (P<0.05); ④Clinical phenotypes including sleep disorders, APOEε4 mutation, multiple risk factors, cognitively demanding occupations and sleep microstructural parameters were significantly correlated with MCI due to AD (P<0.05); ⑤Gender, sleep disturbance, APOEε4 gene mutation, BMI and polysomnographic indices (N1/TST%, N2/TST%, REM/TST% and OSA index) were key factors in MCI due to AD (P<0.05); ⑥N1/TST%, N2/TST%, REM/TST% and OSA index demonstrated significant linear correlations with MoCA scores (P<0.01). Conclusion: Patients with MCI due to AD exhibited distinct clinical features, including a higher prevalence of sleep disorders, elevated APOEε4 allele carrier rates, lower prevalence of multiple risk factors, a higher proportion of cognitively demanding occupations and lower BMI. Sleep parameters, including N1/TST%, N2/TST%, REM/TST% and OSA index, demonstrated significant correlations with cognitive impairment. Characteristic changes in the proportion of N1, N2 and REM sleep among MCI patients may serve as potential biomarkers for early identification of MCI due to AD.

Objective: To comprehensively evaluate the effectiveness of driving ability as a predictor for Alzheimer's disease (AD), explore relevant data collection and analysis methods, and identify valid early warning indicators. Methods: Computerized searches were conducted in databases including CNKI, CBM, Wanfang, VIP, PubMed, and Web of Science to identify studies using driving ability for AD prediction. Literature meeting inclusion criteria was screened, and data quality was assessed. Relevant information was extracted, and heterogeneous data were integrated. Principal component analysis (PCA) was used to evaluate the importance of indicators in the driving-based warning system. Meta-analysis was performed to assess the effect of AD on driving ability. Subgroup analysis was conducted to reduce intergroup heterogeneity, with stratification based on age, gender, and Mini-Mental State Examination (MMSE) scores to examine differences in effects across groups. A multifactorial interaction subgroup analysis was further proposed to minimize intergroup heterogeneity, analyzing the combined influence of age, gender, and MMSE scores on statistical outcomes. Results: After screening, 12 studies were included. PCA results identified the three most significant indicators: spatial control (9.13%), emotional adaptation (8.78%), and navigation execution (8.36%). Meta-analysis and subgroup analysis revealed that older female patients with low MMSE scores exhibited the most severe driving-related cognitive impairment (SMD = -0.75, P < 0.001). Additionally, among male AD patients, the high-score MMSE group showed a greater absolute effect size (ΔSMD = -0.22, P < 0.001). Multifactorial interaction subgroup analysis explained 78% of the heterogeneity (Q = 12.37, P = 0.006). Conclusion: This study provides preliminary evidence that abnormal driving behavior can serve as a novel biomarker for early AD detection, with spatial orientation, emotional stability, and navigation ability identified as core indicators. However, the warning system must account for population differences (higher sensitivity in older females) and individual baseline variations (longitudinal self-referencing).

Objective: To explore the impact of geriatric syndrome on cognitive function in patients with mild cognitive impairment. Methods: This study included 422 elderly people who completed outpatient physical examinations at Hangzhou Wuyunshan Hospital from January to December 2022. All subjects were evaluated using the Montreal Cognitive Assessment (MoCA) and the Comprehensive Geriatric Assessment (CGA). The clinical data and geriatric syndromes of the two groups were compared, and the impact of geriatric syndromes on cognitive function in patients with mild cognitive impairment was observed. Results: A total of 422 elderly patients were enrolled, with 157 in the observation group (MoCA < 26) and 265 in the control group (MoCA ≥ 26). The observation group had significantly lower decreased grip strength, decreased calf circumference, 3-meter stand and walk, normal gait speed, comorbidity index, number of teeth, dentures, dental problems affecting eating, gum pain, and sleep disturbances than the control group (P < 0.05). Binary logistic regression analysis showed that comorbidity index (OR = 2.093, P = 0.012), decreased grip strength (OR = 19.488, P < 0.001), dental problems affecting eating (OR = 4.591, P = 0.001), gum pain (OR = 2.798, P = 0.009), and sleep disturbances (OR = 2.253, P = 0.031) were risk factors for cognitive function in patients with MCI. The number of teeth (OR = 0.740, P < 0.001) and wearing dentures (OR = 0.021, P < 0.001) were protective factors for cognitive function in patients with MCI. Conclusion: Geriatric syndrome has a certain degree of impact on the cognitive function of MCI patients. CGA should be emphasized in the MCI population and attention should be paid to geriatric syndrome to improve the quality of life of the elderly.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by a long preclinical phase and a cascade of pathological events. With recent advances in blood and imaging biomarkers, the dynamic tracking of AD progression has become increasingly feasible. However, most studies have focused on single-modality markers, with limited integration across biological systems and time scales. This review adopts a time-dynamic perspective to summarize the longitudinal evolution of key blood biomarkers (e.g., Aβ42/40 ratio, p-tau217, NfL, GFAP) and imaging markers (e.g., Aβ-PET, Tau-PET, MRI) across the AD continuum. We compare the timing of initial abnormalities, progression patterns, and correlations with cognitive decline. Furthermore, we highlight integrative modeling approaches, including event-based models, and deep learning frameworks, which enable multi-modal risk prediction and individualized disease staging. The clinical potential of such integration in early screening, disease trajectory forecasting, and therapeutic decision-making is discussed, along with current limitations and future directions. This review provides a framework for developing dynamic, biology-driven precision diagnostic strategies in AD.

Objective: To examine the clinical manifestations, imaging features, potential pathological mechanisms, differential diagnosis, and clinical significance of atypical Alzheimer's disease (AD), with the objective of enhancing comprehension of atypical AD and elevating the standard of clinical diagnosis. Methods: The clinical manifestations, laboratory findings and imaging features, and differential diagnosis of three patients with atypical AD were reviewed, and their pathological mechanisms were analyzed accordingly. Results: There was a decrease in Aβ and an increase in Tau in all three patients' cerebrospinal fluid (CSF) tests. The patient with frontal variant of AD (FvAD) started with memory loss and mental behavior abnormalities, and the brain Magnetic Resonance Imaging (MRI) showed symmetrical atrophy of bilateral frontal lobe, temporal lobe, parietal cortex and hippocampus. The patient with logopenic variant primary progressive aphasia (LvPPA) has the onset of speech clumsiness. Brain MRI shows that the left lateral fissure is wider than the right, and bilateral hippocampal atrophy is relatively mild. The patient with posterior cortical atrophy (PCA) presented with memory loss and visuospatial impairment. Brain MRI showed bilateral partooccipital lobe atrophy, widening of the right lateral fissure, and relatively mild bilateral hippocampal atrophy. Conclusions: Atypical AD are starting with speech impairment, mental behavior abnormalities, and visuospatial disorders. Because the dysmnesia symptoms of atypical AD are not typical, it is not easy to identify them early, and it is easy to be confused with frontotemporal dementia, cortical basal ganglia degeneration and Lewy body dementia. The clinical diagnosis requires a comprehensive consideration of detailed medical history and neurological examination, combined with neuropsychiatric scales, imaging, and biomarkers.

To report a case of Alzheimer's disease (AD) mainly manifesting as corticobasal syndrome, share the diagnosis and treatment experience, and improve clinicians' understanding of this atypical type of AD. The medical history, results of neurocognitive assessment tests, and cranial structure and molecular neuroimaging data of a patient with corticobasal syndrome due to Alzheimer’s disease (AD-CBS) were collected, and discussions were made referring to relative articles. The patient mainly presented with motor dysfunction, apraxia and alien limb phenomenon of the left limb, accompanied by progressive cognitive impairments and sensory somatic cortical disorder. Cranial magnetic resonance imaging (MRI) showed obvious atrophy of the right parietal lobe, and cranial positron emission tomography (PET) showed abnormal deposition of Aβ and tau in the cerebral cortex, which was consistent with the characteristic manifestations of AD-CBS. Corticobasal syndrome (CBS) is mainly characterized by asymmetric atrophy of the cortex and extrapyramidal symptoms clinically. Due to the relatively late onset of cognitive impairment compared to motor dysfunctions, it is prone to misdiagnosis. Early diagnosis and medication can help slow the progression of AD-CBS. Meanwhile, due to the diverse causes of CBS, neuroimaging and laboratory examinations are required for differential diagnosis in clinical practice, and the possibility of co-pathology should be considered, raising the importance of long-term follow-up.