Alzheimer's & Dementia最新文献

Reply to “Associations of semaglutide with first-time diagnosis of Alzheimer's disease in patients with type 2 diabetes: Target trial emulation using nationwide real-world data in the US”

IF 13 1区医学 Q1 CLINICAL NEUROLOGY

Alzheimer's & Dementia

Pub Date : 2025-02-14 DOI: 10.1002/alz.14620

Michael G. Rydberg

<p>I read with great interest Wang et al.’s excellent article on the association of semaglutide with new diagnosis of Alzheimer's disease (AD).<span><sup>1</sup></span> The authors utilized a rigorous target trial emulation framework to assess the risk of new AD diagnosis after the initiation of semaglutide compared to seven other anti-diabetic medication classes in patients with type 2 diabetes. The primary outcome was a new diagnosis of AD after initiation of anti-diabetic medication. Notably, eligibility criteria required that patients had no use of any anti-diabetic medications within the prior 6 months. The authors performed propensity score matching to attempt to eliminate confounding between treatment groups.</p><p>The results were impressive, with a hazard ratio of receiving a new diagnosis of AD within 3 years of 0.33 for semaglutide compared to insulin. The results were consistent across different medication classes and patient subgroups. Interestingly, examination of the Kaplan–Meier curves indicates an almost immediate split (within days) for semaglutide versus insulin, sodium–glucose cotransporter 2 inhibitors, metformin, sulfonylureas, and thiazolidinediones. The Kaplan–Meier curve for semaglutide versus other glucagon-like peptide-1 receptor agonists (GLP-1Ras) even appears to diverge by ≈ 90 days.</p><p>Despite the exciting preclinical evidence and observational studies suggesting a potential benefit of semaglutide in preventing or delaying dementia, the immediate separation of the Kaplan–Meier curves is biologically implausible given the pathogenesis of AD, and highly suggestive of unmeasured confounding,<span><sup>2</sup></span> despite the rigorous methods used by the authors. As noted in the description of the AHEAD 3-45 Study, “the AD continuum begins with a long asymptomatic or preclinical stage, during which amyloid beta (Aβ) is accumulating for more than a decade prior to widespread cortical tauopathy, neurodegeneration, and manifestation of clinical symptoms.”<span><sup>3</sup></span> These authors note that “individuals with preclinical AD have an increased risk of cognitive decline over 3–5 years” compared to those without.<span><sup>3</sup></span></p><p>Therefore, seeing a reduction in incident AD within days or weeks of a new medication is highly suggestive of residual confounding. Despite the appropriately rigorous matching, it is probable that residual confounding remains, as patients who receive semaglutide versus insulin or a thiazolidinedione are almost certainly inherently different (in baseline education levels, socioeconomic status, or patient engagement with the medical field, which may alter patient desire for semaglutide). Physician differences between those prescribing semaglutide versus medications such as sulfonylureas or thiazolidinediones are possible as well, given that these are generally poor choices for the initial treatment of type 2 diabetes. Patients receiving some of these medications may be re

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引用次数: 0

Response to the letter titled reply to “Associations of semaglutide with first-time diagnosis of Alzheimer's disease in patients with type 2 diabetes: Target trial emulation using nationwide real-world data in the US”

IF 13 1区医学 Q1 CLINICAL NEUROLOGY

Alzheimer's & Dementia

Pub Date : 2025-02-14 DOI: 10.1002/alz.14611

Rong Xu

We appreciate the opportunity to address the comments by Dr Rydberg regarding our study.¹ The author raised a very interesting question regarding the early separation of the survival curves, given that Alzheimer's disease often takes many years to develop. Patients in our study population were at high risk for developing AD with an average age of 58 years. In addition, all participants had type 2 diabetes as well as a high burden of comorbidities, including hypertension, obesity, cardiovascular disease, and depression—factors that are well-established risk factors for AD. In addition, the matched semaglutide and comparison groups are heterogeneous even though they were well-matched. Patients with different characteristics (e.g., age, gender, obesity) have varying risks for progressing to AD. Early divergence in outcomes between the two groups suggested that semaglutide slowed the progression of AD in patients with very high risk, likely through damped neuroinflammation, enhanced neuroprotection, and other mechanisms. The survival curve for the semaglutide group remained flatter than that of the comparison group throughout the 3-year follow-up period, suggesting that semaglutide could have slowed the progression of AD for patients with varying risks, rather than just those with very high risk. However, these are our speculations, the actual underlying mechanisms remain unknown and warrant further investigation. We acknowledge the limitations inherent in electronic health record (EHR)-based observational studies and the inability to draw causal conclusions. Our findings provide real-world data supporting the potential benefits of semaglutide for AD prevention, particularly in high-risk populations, and call for future randomized clinical trials to confirm the causal relationship between semaglutide and AD prevention.

The author declares no conflicts of interest. Author disclosures are available in the Supporting Information.

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引用次数: 0

Prevalence of idiopathic normal pressure hydrocephalus in older adult population in Shanghai, China: A population-based observational study

IF 13 1区医学 Q1 CLINICAL NEUROLOGY

Alzheimer's & Dementia

Pub Date : 2025-02-14 DOI: 10.1002/alz.14525

Xuhao Fang, Xinxin Xu, Chunyan Liu, Shihong Li, Yao Deng, Feng Tang, Li Zhang, Yan Xing, Renling Mao, Jin Hu

<div> <section> <h3> INTRODUCTION</h3> <p>Idiopathic normal pressure hydrocephalus (iNPH), a condition that primarily affects the elderly, has an unclear prevalence rate in China.</p> </section> <section> <h3> METHODS</h3> <p>A cross-sectional survey involving 1491 seniors aged 60 and above in Shanghai was conducted. Clinical symptoms and brain imaging data were collected for the diagnosis of suboptimal probable iNPH (s-probable iNPH). The crude prevalence was calculated and the estimated prevalence was inferred.</p> </section> <section> <h3> RESULTS</h3> <p>The crude prevalence of s-probable iNPH was 3.09% and 2.62% respectively, using DESH score ≥6 and Radscale score ≥7 as the primary imaging diagnostic criteria. The estimated prevalence of Shanghai was 2.59% among people over 60 years old and it rose to 7.99% among people aged over 90, and it was estimated that 134,152 and 11,708, respectively, had s-probable iNPH among the corresponding age group.</p> </section> <section> <h3> DISCUSSION</h3> <p>The prevalence of s-probable iNPH fluctuates based on the radiological scoring systems and the defined thresholds employed, and it tends to rise with advancing age.</p> </section> <section> <h3> Highlights</h3> <div> <ul> <li><sup>**</sup>Significant Prevalence<sup>**</sup>: The study identified a substantial prevalence of iNPH in older adults, with rates increasing significantly with age, particularly among those aged 90–99 years and centenarians.</li> <li><sup>**</sup>Diagnostic Approach<sup>**</sup>: The research utilized novel diagnostic methodologies by integrating the DESH score or Radscale score with stringent clinical symptoms, providing a closer approximation to the true prevalence of iNPH.</li> <li><sup>**</sup>Gender Disparity<sup>**</sup>: A marked gender difference was observed, with the prevalence of iNPH being significantly higher in males compared to females across all age groups.</li> <li><sup>**</sup>Clinical Implications<sup>**</sup>: The findings underscore the importance of considering iNPH in the differential diagnosis of dementia, particularly among older male patients presenting with cognitive impairment and gait disturbances.</li> <li><sup>**</sup>Public Health Impact<sup>**</sup>: The estimated numb

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引用次数: 0

A brain DNA co-methylation network analysis of psychosis in Alzheimer's disease 阿尔茨海默病精神病的脑 DNA 共甲基化网络分析

IF 13 1区医学 Q1 CLINICAL NEUROLOGY

Alzheimer's & Dementia

Pub Date : 2025-02-12 DOI: 10.1002/alz.14501

Morteza Kouhsar, Luke Weymouth, Adam R. Smith, Jennifer Imm, Claudia Bredemeyer, Yehani Wedatilake, Ali Torkamani, Sverre Bergh, Geir Selbæk, Jonathan Mill, Clive Ballard, Robert A. Sweet, Julia Kofler, Byron Creese, Ehsan Pishva, Katie Lunnon

INTRODUCTION

The presence of psychosis in Alzheimer's disease (AD) is suggested to be associated with distinct molecular and neuropathological profiles in the brain.

METHODS

We assessed brain DNA methylation in AD donors with psychosis (AD+P) and without psychosis (AD−P) using the EPIC array. Weighted gene correlation network analysis identified modules of co-methylated genes in a discovery cohort (PITT-ADRC: N = 113 AD+P, N = 40 AD−P), with validation in an independent cohort (BDR: N = 79 AD+P, N = 117 AD−P), with Gene Ontology and cell-type enrichment analysis. Genetic data were integrated to identify methylation quantitative trait loci (mQTLs), which were co-localized with GWAS for related traits.

RESULTS

We replicated one AD+P associated module, which was enriched for synaptic pathways and in excitatory and inhibitory neurons. mQTLs in this module co-localized with variants associated with schizophrenia and educational attainment.

DISCUSSION

This represents the largest epigenetic study of AD+P to date, identifying pleiotropic relationships between AD+P and related traits.

Highlights

DNA methylation was assessed in the prefrontal cortex in subjects with AD+P and AD−P.
WGCNA identified six modules of co-methylated loci associated with AD+P in a discovery cohort.
One of the modules was replicated in an independent cohort.
This module was enriched for synaptic genes and in excitatory and inhibitory neurons.
mQTLs mapping to genes in the module co-localized with GWAS loci for schizophrenia and educational attainment.

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引用次数: 0

Parallel changes in cognition, neuropsychiatric symptoms, and amyloid in cognitively unimpaired older adults and those with mild cognitive impairment 认知功能未受损的老年人和轻度认知功能受损的老年人在认知、神经精神症状和淀粉样蛋白方面的平行变化

IF 13 1区医学 Q1 CLINICAL NEUROLOGY

Alzheimer's & Dementia

Pub Date : 2025-02-12 DOI: 10.1002/alz.14568

Alyssa N. De Vito, Zachary J. Kunicki, Hannah E. Joyce, Edward D. Huey, Richard N. Jones, for the Alzheimer's Disease Neuroimaging Initiative

INTRODUCTION

Alzheimer's disease (AD) diagnosis centers on cognitive impairment despite other early indicators like neuropsychiatric symptoms (NPSs) and amyloid beta (Aβ) accumulation. This study examined how cognition, NPS, and Aβ changes are interrelated over time in individuals without dementia.

METHODS

Participants were 1247 individuals from the Alzheimer's Disease Neuroimaging Initiative (ADNI)-2 and -3 cohorts with at least 48 months of follow-up. Cognitive domains were assessed via ADNI composite measures, NPS via the neuropsychiatric inventory, and Aβ via standardized uptake value ratio (SUVR) composite scores. Co-occurring changes were evaluated with parallel process models.

RESULTS

NPS was longitudinally associated with performance in each cognitive domain. Negative baseline Aβ-cognition associations were observed in three cognitive domains. No Aβ-NPS associations were observed.

DISCUSSION

This study demonstrated strong longitudinal relationships between NPS and cognition in preclinical and prodromal stages of AD. Future studies should incorporate NPS into models of disease trajectories to improve early detection and prediction of disease progression.

Highlights

Co-occurring changes in Aβ, cognition, and neuropsychiatric symptoms are understudied.
We found relationships between neuropsychiatric symptoms and cognition.
We found baseline, but not longitudinal, Aβ and cognition associations.
Changes in neuropsychiatric symptoms should be included in early detection models of ADRD.

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引用次数: 0

Influence of alpha-synuclein on glucose metabolism in Alzheimer's disease continuum: Analyses of α-synuclein seed amplification assay and FDG-PET

IF 13 1区医学 Q1 CLINICAL NEUROLOGY

Alzheimer's & Dementia

Pub Date : 2025-02-12 DOI: 10.1002/alz.14571

Elijah Mak, Scott A. Przybelski, Heather J. Wiste, Angela J. Fought, Christopher G. Schwarz, Matthew L. Senjem, Clifford R. Jack Jr., Val J. Lowe, Ronald C. Petersen, Bradley F. Boeve, John T. O'Brien, Kejal Kantarci, for the Alzheimer's Disease Neuroimaging Initiative

INTRODUCTION

We investigated the association between alpha-synuclein (α-syn) pathology and brain glucose metabolism across the cognitive spectrum of Alzheimer's disease (AD) co-pathologies.

METHODS

Fluorodeoxyglucose positron emission tomography (FDG-PET) data from 829 Alzheimer's Disease Neuroimaging Initiative participants (648 cognitively impaired [CI], 181 unimpaired [CU]) were compared between α-syn seed amplification assay (SAA) positive and negative groups. Interactions with cerebrospinal fluid (CSF) AD biomarkers were examined.

RESULTS

SAA+ was associated with widespread hypometabolism among CI individuals, particularly in posterior cortical regions, independent of CSF amyloid and tau levels in the occipital lobes. Regional hypometabolism mediated the effect of α-syn SAA on disease severity in CI individuals, independent of CSF amyloid and tau levels. There were no influences of SAA on FDG-PET in CU individuals.

DISCUSSION

This study supports a model in which α-syn aggregation influences metabolic dysfunction, which then influences clinical disease severity, independent of AD. SAA+ could help optimize participant selection and outcome measures for clinical trials in AD.

Highlights

α-synuclein seed amplification positivity (SAA+) was associated with hypometabolism in cognitively impaired individuals.
Hypometabolism mediated the influence of α-synuclein on disease severity.
Occipital hypometabolism in SAA+ was independent of cerebrospinal fluid levels of Alzheimer's disease pathology.
These findings can optimize future clinical trials targeting α-synuclein pathology.

{"title":"Influence of alpha-synuclein on glucose metabolism in Alzheimer's disease continuum: Analyses of α-synuclein seed amplification assay and FDG-PET","authors":"Elijah Mak, Scott A. Przybelski, Heather J. Wiste, Angela J. Fought, Christopher G. Schwarz, Matthew L. Senjem, Clifford R. Jack Jr., Val J. Lowe, Ronald C. Petersen, Bradley F. Boeve, John T. O'Brien, Kejal Kantarci, for the Alzheimer's Disease Neuroimaging Initiative","doi":"10.1002/alz.14571","DOIUrl":"https://doi.org/10.1002/alz.14571","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> INTRODUCTION</h3>\u0000 \u0000 <p>We investigated the association between alpha-synuclein (α-syn) pathology and brain glucose metabolism across the cognitive spectrum of Alzheimer's disease (AD) co-pathologies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> METHODS</h3>\u0000 \u0000 <p>Fluorodeoxyglucose positron emission tomography (FDG-PET) data from 829 Alzheimer's Disease Neuroimaging Initiative participants (648 cognitively impaired [CI], 181 unimpaired [CU]) were compared between α-syn seed amplification assay (SAA) positive and negative groups. Interactions with cerebrospinal fluid (CSF) AD biomarkers were examined.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> RESULTS</h3>\u0000 \u0000 <p>SAA+ was associated with widespread hypometabolism among CI individuals, particularly in posterior cortical regions, independent of CSF amyloid and tau levels in the occipital lobes. Regional hypometabolism mediated the effect of α-syn SAA on disease severity in CI individuals, independent of CSF amyloid and tau levels. There were no influences of SAA on FDG-PET in CU individuals.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> DISCUSSION</h3>\u0000 \u0000 <p>This study supports a model in which α-syn aggregation influences metabolic dysfunction, which then influences clinical disease severity, independent of AD. SAA+ could help optimize participant selection and outcome measures for clinical trials in AD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Highlights</h3>\u0000 \u0000 <div>\u0000 <ul>\u0000 \u0000 <li>α-synuclein seed amplification positivity (SAA+) was associated with hypometabolism in cognitively impaired individuals.</li>\u0000 \u0000 <li>Hypometabolism mediated the influence of α-synuclein on disease severity.</li>\u0000 \u0000 <li>Occipital hypometabolism in SAA+ was independent of cerebrospinal fluid levels of Alzheimer's disease pathology.</li>\u0000 \u0000 <li>These findings can optimize future clinical trials targeting α-synuclein pathology.</li>\u0000 </ul>\u0000 </div>\u0000 </section>\u0000 </div>","PeriodicalId":7471,"journal":{"name":"Alzheimer's & Dementia","volume":"21 2","pages":""},"PeriodicalIF":13.0,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/alz.14571","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143389113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

White matter injury, plasma Alzheimer's disease, and neurodegenerative biomarkers on cognitive decline in community-dwelling older adults: A 10-year longitudinal study

IF 13 1区医学 Q1 CLINICAL NEUROLOGY

Alzheimer's & Dementia

Pub Date : 2025-02-12 DOI: 10.1002/alz.14594

Qili Hu, Xiaowen Zhou, Zhenxu Xiao, Qianhua Zhao, Ding Ding, Jun Zhang

INTRODUCTION

This study aimed to investigate the synergistic impact of white matter injury, Alzheimer's disease, and neurodegenerative pathology on long-term cognitive decline and dementia risk in older adults.

METHODS

We included 262 dementia-free participants with baseline and follow-up interviews (2010–2021). At baseline, peak width of skeletonized mean diffusivity (PSMD) was assessed from diffusion tensor imaging. Plasma phosphorylated tau 217 (p-tau217) and neurofilament light chain (NfL) were measured using a single-molecule immune-array assay. Cognitive function was evaluated using Mini-Mental State Examination (MMSE) and domain-specific cognitive tests.

RESULTS

Participants with high-level PSMD, p-tau217, and NfL showed the fastest decline of MMSE (β = −0.30) and the highest dementia incidence of 3.54/100 person-years. A combination model with three markers demonstrated a good predictive value for dementia, incorporating age, sex, education, and apolipoprotein E (area under the curve = 0.93, 95% confidence interval = 0.86, 0.99).

DISCUSSION

Combining co-pathology markers may identify individuals with a high risk of cognitive decline.

Highlights

Peak width of skeletonized mean diffusivity (PSMD) was correlated with long-term cognitive decline, and this correlation was modified by plasma phosphorylated tau (p-tau)217 and neurofilament light chain (NfL).
Participants with high levels of PSMD, p-tau217, and NfL showed the fastest cognitive decline and the highest risk of dementia.
A combination of the three markers exhibited a good predictive value of incident dementia over a 10-year follow-up period.

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引用次数: 0

The Dementia SomaSignal Test (dSST): A plasma proteomic predictor of 20-year dementia risk

IF 14 1区医学 Q1 CLINICAL NEUROLOGY

Alzheimer's & Dementia

Pub Date : 2025-02-12 DOI: 10.1002/alz.14549

Michael R. Duggan, Clare Paterson, Yifei Lu, Hannah Biegel, Heather E. Dark, Jenifer Cordon, Murat Bilgel, Naoto Kaneko, Masaki Shibayama, Shintaro Kato, Makio Furuichi, Iwao Waga, Keita Hiraga, Masahisa Katsuno, Yukiko Nishita, Rei Otsuka, Christos Davatzikos, Guray Erus, Kelsey Loupy, Melissa Simpson, Alexandria Lewis, Abhay Moghekar, Priya Palta, Rebecca F. Gottesman, Susan M. Resnick, Josef Coresh, Stephen A. Williams, Keenan A. Walker

There is an unmet need for tools to quantify dementia risk during its multi-decade preclinical/prodromal phase, given that current biomarkers predict risk over shorter follow-up periods and are specific to Alzheimer's disease.

鉴于目前的生物标志物可在较短的随访期内预测痴呆症风险，而且只针对阿尔茨海默氏症，因此在痴呆症的临床前/前驱期阶段，对量化痴呆症风险的工具的需求尚未得到满足。

引用次数: 0

Tracer kinetic model detecting heterogeneous blood–brain barrier permeability to water and contrast agent in Alzheimer's disease and dementia with Lewy bodies 检测阿尔茨海默病和路易体痴呆症患者血脑屏障对水和造影剂的异质性通透性的示踪动力学模型

IF 13 1区医学 Q1 CLINICAL NEUROLOGY

Alzheimer's & Dementia

Pub Date : 2025-02-12 DOI: 10.1002/alz.14529

Ziming Xu, Yong Ji, Chen Wen, Jinghuan Gan, Zhichao Chen, Rui Li, Xiaoqi Lin, Jiaqi Dou, Yajie Wang, Shuai Liu, Zhihong Shi, Hao Wu, Hao Lu, Huijun Chen

INTRODUCTION

Blood–brain barrier (BBB) breakdown is essential in Alzheimer's disease (AD) and dementia with Lewy bodies (DLB), whereas the variability in BBB permeability to water and contrast agent is less clear.

METHODS

We investigated BBB permeability to water and contrast agent simultaneously using a novel tracer kinetic model for dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) in 42 AD patients, 22 DLB patients, and 22 healthy controls. All participants underwent clinical, cognitive, and MRI assessments.

RESULTS

AD patients exhibited a significant reduction in the water exchange rates across the BBB, whereas DLB patients showed a significant increase in BBB permeability to contrast agent. Moreover, BBB permeability to both water and contrast agent in multiple brain regions demonstrated correlations with clinical severity.

DISCUSSION

The simultaneous evaluation of BBB permeability to water and contrast agent based on the proposed model highlights the heterogeneous patterns of BBB breakdown in AD and DLB.

Highlights

We measured blood–brain barrier (BBB) permeability to water and contrast agent based on dynamic contrast-enhanced magnetic resonance imaging.
Alzheimer's disease (AD) is characterized by lower water exchange rates across the BBB.
Dementia with Lewy bodies exhibits higher BBB permeability to contrast agent.
BBB permeability is related to cognitive impairment and disease burden.
BBB permeability to water was negatively associated with that to contrast agent.

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引用次数: 0

Transcriptome analysis of early- and late-onset Alzheimer's disease in Korean cohorts

IF 13 1区医学 Q1 CLINICAL NEUROLOGY

Alzheimer's & Dementia

Pub Date : 2025-02-12 DOI: 10.1002/alz.14563

Sang-Won Han, Jiyun Hwang, Tamina Park, Jung-Min Pyun, Joo-Yeon Lee, Jeong Su Park, Paula J. Bice, Shiwei Liu, Sunmin Yun, Jibin Jeong, Shannon L. Risacher, Andrew J. Saykin, Min Soo Byun, Dahyun Yi, Joohon Sung, Dong Young Lee, SangYun Kim, Kwangsik Nho, Young Ho Park

INTRODUCTION

The molecular mechanisms underlying early-onset Alzheimer's disease (EOAD) and late-onset Alzheimer's disease (LOAD) remain incompletely understood, particularly in Asian populations.

METHODS

RNA-sequencing was carried out on blood samples from 248 participants in the Seoul National University Bundang Hospital cohort to perform differential gene expression (DGE) and weighted gene co-expression network analysis. Findings were replicated in an independent Korean cohort (N = 275).

RESULTS

DGE analysis identified 18 and 88 dysregulated genes in EOAD and LOAD, respectively. Network analysis identified a LOAD-associated module showing a significant enrichment in pathways related to mitophagy, 5′ adenosine monophosphate-activated protein kinase signaling, and ubiquitin-mediated proteolysis. In the replication cohort, downregulation of SMOX and PLVAP in LOAD was replicated, and the LOAD-associated module was highly preserved. In addition, SMOX and PLVAP were associated with brain amyloid beta deposition.

DISCUSSION

Our findings suggest distinct molecular signatures for EOAD and LOAD in a Korean population, providing deeper understanding of their diagnostic potential and molecular mechanisms.

Highlights

Analysis identified 18 and 88 dysregulated genes in early-onset Alzheimer's disease (EOAD) and late-onset Alzheimer's disease (LOAD), respectively.
Expression levels of SMOX and PLVAP were downregulated in LOAD.
Expression levels of SMOX and PLVAP were associated with brain amyloid beta deposition.
Pathways including mitophagy and 5′ adenosine monophosphate-activated protein kinase signaling were enriched in a LOAD module.
A LOAD module was highly preserved across two independent cohorts.

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引用次数: 0