Role of primary aging hallmarks in Alzheimer´s disease

Zhao, Jianmin; Huai, Jisen

doi:10.7150/thno.79535

Cited by 25 publications

(14 citation statements)

References 674 publications

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“…In contrast, the searches for SNPs able to influence the expression of function in the genes coding for epigenetic regulators and concurrently associated with neurodegenerative diseases, especially AD, are almost absent. On the other hand, the emerging paradigms demonstrate that dynamic and latent epigenetic alterations are widely incorporated into the AD pathological pathways [25,39,108]. Thus, the goal of our work was to detect the SNPs able to affect the epigenetic mechanisms in AD.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, the goal of our work was to detect the SNPs able to affect the epigenetic mechanisms in AD. As it is known that the majority of the SNPs (up to 90%) associated with the trait reside in the regulatory region of the genome (promoters, enhancers, and so on) and influence gene expression [109][110][111], we focused on the search for this particular regulatory SNPs (rSNPs) using our own earlier developed functional approaches based on the search for allelic specificity of events in multi-omics data [108,109,112].…”

Section: Discussionmentioning

confidence: 99%

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Exploring the Genetic Predisposition to Epigenetic Changes in Alzheimer’s Disease

Bryzgalov

Korbolina

Merkulova

2023

IJMS

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Alzheimer’s disease (AD) is a prevalent type of dementia in elderly populations with a significant genetic component. The accumulating evidence suggests that AD involves a reconfiguration of the epigenetic landscape, including DNA methylation, post-translational modification of histone proteins, and chromatin remodeling. Along with environmental factors, individual specific genetic features play a considerable role in the formation of epigenetic architecture. In this study, we attempt to identify the non-coding regulatory SNPs (rSNPs) able to affect the epigenetic mechanisms in AD. To this end, the multi-omics approach is used. The GEO (Gene Expression Omnibus) available data (GSE153875) for AD patients and controls are integrated to reveal the rSNPs that display allele-specific features in both ChIP-seq profiles of four histone modifications and RNA-seq. Furthermore, we analyze the presence of rSNPs in the promoters of genes reported to be differentially expressed between AD and the normal brain (AD-related genes) and involved in epigenetic regulation according to the EpiFactors database. We also searched for the rSNPs in the promoters of the genes coding for transcription regulators of the identified AD-related genes. These regulators were selected based on the corresponding ChIP-seq peaks (ENCODE) in the promoter regions of these genes. Finally, we formed a panel of rSNPs localized to the promoters of genes that contribute to the epigenetic landscape in AD and, thus, to the genetic predisposition for this disease.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Exploring the Genetic Predisposition to Epigenetic Changes in Alzheimer’s Disease

Bryzgalov

Korbolina

Merkulova

2023

IJMS

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“…Both amyloid beta (A) plaques and neurofibrillary tangles containing hyperphosphorylated Tau are pathological markers of the disease, and both soluble oligomers and aggregated proteins contribute to neuronal toxicity. Substantial research on DNAm and AD etiology reveals that the most prominent DNAm change in AD occurs at hypomethylated or unmethylated levels [55]. For example, neurons from cortical tissue withdrew from dead patients with AD showed a lower immunoreactivity of 5-methylcytosine compared to normal controls of similar age, suggesting a marked loss of 5-methylcytosine in AD-affected brains [56].…”

Section: Epigenetic Clock In Risk Prediction Of Complex Diseasementioning

confidence: 99%

Epigenetic Clocks: In Aging-Related and Complex Diseases

Margiotti,

Monaco,

Fabiani

et al. 2023

Cytogenet Genome Res

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There is evidence that complex disease and mortality are associated with DNA methylation (DNAm) and age acceleration. Numerous epigenetic clocks, including Horvath, Hannum, DNA PhenoAge, DNA GrimAge, and DunedinPoAm continue to be developed in this young scientific field. The most well-known epigenetic clocks are presented here, along with information about how they relate to chronic disease. We examined all the literature until January 2023, investigating associations between measures of age acceleration and complex and age-related diseases. We focused on the scientific literature and researches that are most strongly associated with epigenetic clocks and that have shown promise as biomarkers for obesity, cardiovascular illness, type 2 diabetes, and neurodegenerative disease. Understanding the complex interactions between accelerated epigenetic clocks and chronic diseases may have significant effects on both the early diagnosis of disease and health promotion. Additionally, there is a lot of interest in developing treatment plans that can delay the onset of illnesses or, at the very least, alter the underlying causes of such disorders

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“…Alzheimer’s disease (AD) is the most common neurodegenerative disease, leading to gradual cognitive impairment and personality abnormalities [ 1 ]. The prevalence of AD is increasing year by year as the world population ages [ 2 , 3 ].…”

Section: Introductionmentioning

confidence: 99%

Antibody Assay and Anti-Inflammatory Function Evaluation of Therapeutic Potential of Different Intravenous Immunoglobulins for Alzheimer’s Disease

Fei

Pei

Pan

et al. 2023

IJMS

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Alzheimer’s disease (AD) is a common neurodegenerative disease that currently has no known cure. Intravenous immunoglobulin (IVIG), which contains AD-related antibodies and has anti-inflammatory properties, has shown potential as a treatment for AD. However, the efficacy of clinical trials involving AD patients treated with IVIG has been inconsistent. Our previous study found that different IVIGs had significantly varied therapeutic effects on 3xTg-AD mice. In order to investigate the relationship between the composition and function of IVIG and its efficacy in treating AD, we selected three IVIGs that showed notable differences in therapeutic effects. Then, the concentrations of specific antibodies against β-amyloid (Aβ)42, tau, and hyperphosphorylated tau (p-tau) in three IVIGs, as well as their effects on systemic inflammation induced by lipopolysaccharide (LPS) in Balb/c mice, were analyzed and compared in this study. The results indicated that these IVIGs differed greatly in anti-Aβ42/tau antibody concentration and anti-p-tau ratio, and improved LPS-stimulated peripheral inflammation, liver and kidney injury, and neuroinflammation in Balb/c mice to varying degrees. Combined with our previous results, the efficacy of IVIG against AD may be positively correlated with its level of AD-related antibodies and anti-inflammatory ability. AD-related antibody analysis and functional evaluation of IVIG should be given sufficient attention before clinical trials, as this may greatly affect the therapeutic effect of AD treatment.

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Role of primary aging hallmarks in Alzheimer´s disease

Cited by 25 publications

References 674 publications

Exploring the Genetic Predisposition to Epigenetic Changes in Alzheimer’s Disease

Exploring the Genetic Predisposition to Epigenetic Changes in Alzheimer’s Disease

Epigenetic Clocks: In Aging-Related and Complex Diseases

Antibody Assay and Anti-Inflammatory Function Evaluation of Therapeutic Potential of Different Intravenous Immunoglobulins for Alzheimer’s Disease

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