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Advanced Science in Alzheimer’s Disease
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Advanced Science in Alzheimer’s Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 1889

Special Issue Editor

Dr. Silvia Boschi

E-Mail Website
Guest Editor
Aging Brain and Memory Clinic, Department of Neuroscience, “Rita Levi Montalcini”, Memory Clinic, University of Torino, Via Cherasco 15, 10126 Turin, Italy
Interests: Alzheimer’s disease; dementia; neurodegeneration; neuronal biomarkers

Special Issue Information

Dear Colleagues,

Contemporary research into Alzheimer’s disease (AD) increasingly focuses on elucidating its molecular intricacies. At the molecular level, AD is distinguished by the aggregation of amyloid-beta peptides and hyperphosphorylated tau proteins, resulting in the formation of insoluble plaques and neurofibrillary tangles, respectively. This pathological hallmark disrupts neuronal function, synaptic transmission, and, ultimately, cognitive abilities. Molecular investigations aim to elucidate the precise mechanisms governing the synthesis, clearance, and cytotoxicity of these proteins, as well as their interactions with cellular processes such as inflammation, oxidative stress, and mitochondrial dysfunction. Moreover, genetic studies have pinpointed risk variants associated with AD, shedding light on molecular pathways implicated in disease pathogenesis. Leveraging advanced molecular techniques, including genome editing, proteomics, and high-resolution imaging, researchers strive to decipher the molecular underpinnings of AD progression. Insights derived from these efforts hold promise for the development of targeted therapies aimed at arresting or reversing molecular aberrations, thus offering prospects for efficacious interventions in the battle against AD.

Dr. Silvia Boschi
Guest Editor

Manuscript Submission Information

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Keywords

  • neuroinflammation
  • synaptic dysfunction
  • oxidative stress
  • neurofibrillary tangles
  • mitochondrial dysfunction
  • biomarkers

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Published Papers (3 papers)

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Research

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30 pages, 2234 KiB  
Article
Investigating Genetic Overlap between Alzheimer’s Disease, Lipids, and Coronary Artery Disease: A Large-Scale Genome-Wide Cross Trait Analysis
by Artika Kirby, Tenielle Porter, Emmanuel O. Adewuyi and Simon M. Laws
Int. J. Mol. Sci. 2024, 25(16), 8814; https://doi.org/10.3390/ijms25168814 - 13 Aug 2024
Viewed by 360
Abstract
There is evidence to support a link between abnormal lipid metabolism and Alzheimer’s disease (AD) risk. Similarly, observational studies suggest a comorbid relationship between AD and coronary artery disease (CAD). However, the intricate biological mechanisms of AD are poorly understood, and its relationship [...] Read more.
There is evidence to support a link between abnormal lipid metabolism and Alzheimer’s disease (AD) risk. Similarly, observational studies suggest a comorbid relationship between AD and coronary artery disease (CAD). However, the intricate biological mechanisms of AD are poorly understood, and its relationship with lipids and CAD traits remains unresolved. Conflicting evidence further underscores the ongoing investigation into this research area. Here, we systematically assess the cross-trait genetic overlap of AD with 13 representative lipids (from eight classes) and seven CAD traits, leveraging robust analytical methods, well-powered large-scale genetic data, and rigorous replication testing. Our main analysis demonstrates a significant positive global genetic correlation of AD with triglycerides and all seven CAD traits assessed—angina pectoris, cardiac dysrhythmias, coronary arteriosclerosis, ischemic heart disease, myocardial infarction, non-specific chest pain, and coronary artery disease. Gene-level analyses largely reinforce these findings and highlight the genetic overlap between AD and three additional lipids: high-density lipoproteins (HDLs), low-density lipoproteins (LDLs), and total cholesterol. Moreover, we identify genome-wide significant genes (Fisher’s combined p value [FCPgene] < 2.60 × 10−6) shared across AD, several lipids, and CAD traits, including WDR12, BAG6, HLA-DRA, PHB, ZNF652, APOE, APOC4, PVRL2, and TOMM40. Mendelian randomisation analysis found no evidence of a significant causal relationship between AD, lipids, and CAD traits. However, local genetic correlation analysis identifies several local pleiotropic hotspots contributing to the relationship of AD with lipids and CAD traits across chromosomes 6, 8, 17, and 19. Completing a three-way analysis, we confirm a strong genetic correlation between lipids and CAD traits—HDL and sphingomyelin demonstrate negative correlations, while LDL, triglycerides, and total cholesterol show positive correlations. These findings support genetic overlap between AD, specific lipids, and CAD traits, implicating shared but non-causal genetic susceptibility. The identified shared genes and pleiotropic hotspots are valuable targets for further investigation into AD and, potentially, its comorbidity with CAD traits. Full article
(This article belongs to the Special Issue Advanced Science in Alzheimer’s Disease)
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14 pages, 2242 KiB  
Article
A Comparative Analysis of Two Automated Quantification Methods for Regional Cerebral Amyloid Retention: PET-Only and PET-and-MRI-Based Methods
by Sunghwan Kim, Sheng-Min Wang, Dong Woo Kang, Yoo Hyun Um, Eun Ji Han, Sonya Youngju Park, Seunggyun Ha, Yeong Sim Choe, Hye Weon Kim, Regina EY Kim, Donghyeon Kim, Chang Uk Lee and Hyun Kook Lim
Int. J. Mol. Sci. 2024, 25(14), 7649; https://doi.org/10.3390/ijms25147649 - 12 Jul 2024
Viewed by 517
Abstract
Accurate quantification of amyloid positron emission tomography (PET) is essential for early detection of and intervention in Alzheimer’s disease (AD) but there is still a lack of studies comparing the performance of various automated methods. This study compared the PET-only method and PET-and-MRI-based [...] Read more.
Accurate quantification of amyloid positron emission tomography (PET) is essential for early detection of and intervention in Alzheimer’s disease (AD) but there is still a lack of studies comparing the performance of various automated methods. This study compared the PET-only method and PET-and-MRI-based method with a pre-trained deep learning segmentation model. A large sample of 1180 participants in the Catholic Aging Brain Imaging (CABI) database was analyzed to calculate the regional standardized uptake value ratio (SUVR) using both methods. The logistic regression models were employed to assess the discriminability of amyloid-positive and negative groups through 10-fold cross-validation and area under the receiver operating characteristics (AUROC) metrics. The two methods showed a high correlation in calculating SUVRs but the PET-MRI method, incorporating MRI data for anatomical accuracy, demonstrated superior performance in predicting amyloid-positivity. The parietal, frontal, and cingulate importantly contributed to the prediction. The PET-MRI method with a pre-trained deep learning model approach provides an efficient and precise method for earlier diagnosis and intervention in the AD continuum. Full article
(This article belongs to the Special Issue Advanced Science in Alzheimer’s Disease)
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Review

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15 pages, 2314 KiB  
Review
Interconnections between the Gut Microbiome and Alzheimer’s Disease: Mechanisms and Therapeutic Potential
by Ahmad M. Sait and Philip J. R. Day
Int. J. Mol. Sci. 2024, 25(16), 8619; https://doi.org/10.3390/ijms25168619 - 7 Aug 2024
Viewed by 361
Abstract
Alzheimer’s disease (AD) is a neurodegenerative disease that is known to accumulate amyloid-β (Aβ) and tau protein. Clinical studies have not identified pathogenesis mechanisms or produced an effective cure for AD. The Aβ monoclonal antibody lecanemab reduces Aβ plaque formation for the treatment [...] Read more.
Alzheimer’s disease (AD) is a neurodegenerative disease that is known to accumulate amyloid-β (Aβ) and tau protein. Clinical studies have not identified pathogenesis mechanisms or produced an effective cure for AD. The Aβ monoclonal antibody lecanemab reduces Aβ plaque formation for the treatment of AD, but more studies are required to increase the effectiveness of drugs to reduce cognitive decline. The lack of AD therapy targets and evidence of an association with an acute neuroinflammatory response caused by several bacteria and viruses in some individuals has led to the establishment of the infection hypothesis during the last 10 years. How pathogens cross the blood–brain barrier is highly topical and is seen to be pivotal in proving the hypothesis. This review summarizes the possible role of the gut microbiome in the pathogenesis of AD and feasible therapeutic approaches and current research limitations. Full article
(This article belongs to the Special Issue Advanced Science in Alzheimer’s Disease)
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