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2.
Int. j. cardiovasc. sci. (Impr.) ; 35(2): 161-171, Mar.-Apr. 2022. tab, graf
Article in English | LILACS-Express | LILACS | ID: biblio-1364975

ABSTRACT

Abstract Background: There are divergences in the literature regarding the experimental model (Wistar-WIS or Wistar Kyoto-WKY) to be used as a Spontaneously Hypertensive Rat (SHR) control. The characterization of these models in terms of cardiovascular parameters provides researchers with important tools at the time of selection and application in scientific research. Objective: The aim of this study was to evaluate the use of WIS and WKY as a Spontaneously Hypertensive Rat (SHR) control by assessing the long-term behavior of blood pressure and cardiac structure and function in these strains. Methods: To this end, WIS, WKY, and SHR underwent longitudinal experiments. Blood pressure and body mass were measured every two weeks from the 8th to the 72nd. Echocardiographic analysis was performed in all groups with 16, 48, and 72 weeks of life. After having applied the normality test, the Two-Way ANOVA of repeated measures followed by the Tukey post hoc test was used. A significance level of 5% was established. Results: The WIS group showed higher body mass (p<0.05), while the WKY and SHR presented higher body mass variation over time (p<0.05). SHR exhibited increased values of systolic, diastolic, and mean blood pressure when compared to WKY and WIS, whereas the WKY generally showed higher values than WIS (p<0.05). Regarding the cardiac function, SHR showed reduced values, while the WKY presented an early decrease when compared to WIS with aging (p<0.05). Conclusion: WIS is a more suitable normotensive control for SHR than WKY in experiments to test blood pressure and cardiac structure and function.


Subject(s)
Animals , Male , Rats , Hypertension/genetics , Hypertension, Renovascular , Rats, Inbred SHR , Rats, Inbred WKY , Rats, Wistar , Epigenesis, Genetic , Arterial Pressure , Heart Function Tests
3.
Arch. argent. pediatr ; 120(1): e8-e16, feb 2022. tab
Article in English, Spanish | LILACS, BINACIS | ID: biblio-1353524

ABSTRACT

La hipertensión arterial (HTA) es un factor de riesgo modificable de enfermedad cardiovascular (ECV) y debe incluirse dentro del estudio de los orígenes del desarrollo de la salud y enfermedad (DOHaD). Durante el desarrollo intrauterino y perinatal, diferentes factores ambientales impactan en la programación temprana de las enfermedades crónicas no transmisibles (ECNT). En esta revisión se resume la evidencia que vincula los cambios adaptativos y la plasticidad del feto a factores ambientales desfavorables alterando el fenotipo adulto en el desarrollo de HTA. Estos cambios adaptativos responden a cambios epigenéticos que favorecen el desarrollo de HTA y ECV en la edad adulta con implicancias intergeneracionales. Por último, se mencionan estrategias preventivas para limitar o revertir algunas de las variables que pueden producir alteraciones en la programación del desarrollo que conducen a HTA en etapas más tardías de la vida.


Hypertension (HTN) is a modifiable risk factor for cardiovascular disease (CVD) and should be included in the study of developmental origins of health and disease (DOHaD). During intrauterine and perinatal development, different environmental factors have an impact on the early programming of noncommunicable diseases (NCDs). This review provides a summary of the evidence that connects the fetus' plasticity and adaptive changes to unfavorable environmental factors that alter the adult phenotype in the development of HTN. Such adaptive changes result from epigenetic changes that favor the development of HTN and CVD in adulthood with intergenerational implications. Lastly, we mention preventive strategies to limit or reverse any variable that may alter developmental programming leading to HTN later in life.


Subject(s)
Humans , Female , Pregnancy , Cardiovascular Diseases , Noncommunicable Diseases , Hypertension/etiology , Risk Factors , Epigenesis, Genetic
4.
Article in English | WPRIM | ID: wpr-922251

ABSTRACT

In neuronal system, epigenetic modifications are essential for neuronal development, the fate determination of neural stem cells and neuronal function. The dysfunction of epigenetic regulation is closely related to occurrence and development of neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, Huntington's disease. Abnormally elevated DNA methylation inhibits the expression of some DNA repair-related genes and affects the progression of Huntington's disease. In the brain of Alzheimer's disease patients, the levels of H3K27ac and H3K9ac histone modifications increased. In addition, the alteration of RNA methylation in animal models of Alzheimer's disease and Parkinson's disease showed discrepancy trends. Therefore, epigenetic modifications may serve as potential therapeutic targets for neurodegenerative diseases. Here, we summarize the recent progress of the roles of epigenetic modifications in neurodegenerative diseases.


Subject(s)
Animals , DNA Methylation , Epigenesis, Genetic , Humans , Neurodegenerative Diseases/genetics , Parkinson Disease/genetics , Protein Processing, Post-Translational
5.
Chinese Journal of Lung Cancer ; (12): 705-713, 2021.
Article in Chinese | WPRIM | ID: wpr-922131

ABSTRACT

Patients with oncogenic driver alterations of non-small cell lung cancer (NSCLC) can benefit from targeted therapy, but acquired resistance is inevitable ultimately. Epigenetic modifications, including DNA methylation, histone modifications, non-coding RNA-mediated regulate and chromatin remodeling, are important mechanisms of acquired resistance in targeted therapy of NSCLC. In recent years, studies have found that epigenetic modifications can effectively reverse drug resistance. Targeted therapy combined with epigenetic modifications may become a promising therapeutic strategy. Here, we review the progress of epigenetic mechanism in acquired resistance of targeted therapy in NSCLC, hoping to provide ideas for screening dominant population and overcoming resistance.
.


Subject(s)
Carcinoma, Non-Small-Cell Lung/genetics , DNA Methylation , Epigenesis, Genetic , Humans , Lung Neoplasms/genetics
6.
Acta Physiologica Sinica ; (6): 980-990, 2021.
Article in Chinese | WPRIM | ID: wpr-921303

ABSTRACT

The normal development of follicles involves a series of complex life processes such as ordered transcriptional activation and inhibition, which is crucial for female reproductive ability. Histone methylation can change the chromatin state in cells and affect the transcription activity of genes. Current studies indicate that epigenetic modifications such as histone methylation play an important regulatory role in follicular development in female mammals. This paper summarized the relationship between H3K4, H3K9 methylation and germ cell development, their regulatory effects, including their dynamical changes during follicular development, and the progress of H3K4me3 and other histone methylation binding to promoter regions of different genes to regulate gene expression and thus affect germ cell epigenetic reprogramming, oocyte transcription, meiosis and other processes. This review will provide a reference for the study of mechanisms related to histone methylation modification and the development and maturation of gonadal parenchymal cells.


Subject(s)
Animals , DNA Methylation , Epigenesis, Genetic , Female , Histones , Mammals , Ovarian Follicle/growth & development , Protein Processing, Post-Translational
7.
Chinese Medical Journal ; (24): 2901-2910, 2021.
Article in English | WPRIM | ID: wpr-921119

ABSTRACT

Recent research efforts have provided compelling evidence of genome-wide DNA methylation alterations in pediatrics. It is currently well established that epigenetic clocks, composed of DNA methylation sites, can estimate the gestational and chronological age of cells and tissues from different ages. Also, extensive research is aimed at their correlation with early life exposure and pediatric diseases. This review aimed to systematically summarize the epigenetic clocks in the pediatric population. Publications were collected from PubMed and Web of Science databases up to Apr 2021. Epigenetic clocks, DNA methylation clocks, epigenetic age acceleration or deceleration, pediatric and the pediatric population were used as search criteria. Here, we first review the currently applicative pediatric epigenetic clocks. We then highlight the interpretation for epigenetic age deviations in the pediatric population and their association with external factors, developmental trajectories, and pediatric diseases. Considering the remaining unknown of pediatric clocks, research strategies into them are also discussed. In all, pediatric epigenetic clocks may act as potent tools to understand development, growth and diseases in early life.


Subject(s)
Aging , Child , DNA Methylation/genetics , Epigenesis, Genetic/genetics , Epigenomics , Humans
8.
Chinese Journal of Biotechnology ; (12): 2223-2231, 2021.
Article in Chinese | WPRIM | ID: wpr-887791

ABSTRACT

Nuclear bodies are membrane-free nuclear substructures that are localized in the mammalian nuclear matrix region. They are multiprotein complexes that recruit other proteins to participate in various cellular activities, such as transcription, RNA splicing, epigenetic regulation, tumorigenesis and antiviral defense. It is of great significance to clarify the functions and regulatory mechanisms of nuclear bodies to probe related diseases and virus-host interactions. This review takes several nuclear bodies associated proteins as examples, summarizes the formation process, structure and functions of nuclear bodies, and focuses on their important roles in antiviral infection. It is expected to provide new insight into host antiviral mechanisms.


Subject(s)
Animals , Cell Nucleus , Epigenesis, Genetic , Intranuclear Inclusion Bodies/metabolism , Nuclear Proteins/metabolism
9.
Protein & Cell ; (12): 29-38, 2021.
Article in English | WPRIM | ID: wpr-880916

ABSTRACT

Prostate cancer is the most commonly diagnosed non-cutaneous cancers in North American men. While androgen deprivation has remained as the cornerstone of prostate cancer treatment, resistance ensues leading to lethal disease. Forkhead box A1 (FOXA1) encodes a pioneer factor that induces open chromatin conformation to allow the binding of other transcription factors. Through direct interactions with the Androgen Receptor (AR), FOXA1 helps to shape AR signaling that drives the growth and survival of normal prostate and prostate cancer cells. FOXA1 also possesses an AR-independent role of regulating epithelial-to-mesenchymal transition (EMT). In prostate cancer, mutations converge onto the coding sequence and cis-regulatory elements (CREs) of FOXA1, leading to functional alterations. In addition, FOXA1 activity in prostate cancer can be modulated post-translationally through various mechanisms such as LSD1-mediated protein demethylation. In this review, we describe the latest discoveries related to the function and regulation of FOXA1 in prostate cancer, pointing to their relevance to guide future clinical interventions.


Subject(s)
Amino Acid Sequence , Epigenesis, Genetic , Epithelial-Mesenchymal Transition , Gene Expression Regulation, Neoplastic , Hepatocyte Nuclear Factor 3-alpha/metabolism , Histone Demethylases/metabolism , Histones/metabolism , Humans , Male , Mutation , Prostate/pathology , Prostatic Neoplasms/pathology , Protein Binding , Protein Processing, Post-Translational , Receptors, Androgen/metabolism , Signal Transduction , Transcription, Genetic
10.
Protein & Cell ; (12): 7-28, 2021.
Article in English | WPRIM | ID: wpr-880895

ABSTRACT

Mammalian fertilization begins with the fusion of two specialized gametes, followed by major epigenetic remodeling leading to the formation of a totipotent embryo. During the development of the pre-implantation embryo, precise reprogramming progress is a prerequisite for avoiding developmental defects or embryonic lethality, but the underlying molecular mechanisms remain elusive. For the past few years, unprecedented breakthroughs have been made in mapping the regulatory network of dynamic epigenomes during mammalian early embryo development, taking advantage of multiple advances and innovations in low-input genome-wide chromatin analysis technologies. The aim of this review is to highlight the most recent progress in understanding the mechanisms of epigenetic remodeling during early embryogenesis in mammals, including DNA methylation, histone modifications, chromatin accessibility and 3D chromatin organization.


Subject(s)
Animals , Chromatin Assembly and Disassembly , DNA Methylation , DNA Transposable Elements , Embryo, Mammalian , Embryonic Development/genetics , Epigenesis, Genetic , Epigenome , Female , Fertilization/physiology , Gene Expression Regulation, Developmental , Histone Code , Histones/metabolism , Male , Mice , Oocytes/metabolism , Spermatozoa/metabolism
11.
Article in Chinese | WPRIM | ID: wpr-878706

ABSTRACT

The self-renewal and differentiation of hematopoietic stem cells(HSCs)are highly regulated by epigenetic modification,in which histone acetylation can activate or silence gene transcription.Histone deacetylase inhibitors(HDACIs)can inhibit the activity of histone deacetylase in HSCs to increase histone acetylation.A variety of HDACIs,such as trichostatin A and valproic acid,are used to expand HSCs in vitro,especially cord blood HSCs,combined with cytokines in serum-free culture to obtain more long-term repopulating cells.HDACIs promote the transcription of pluripotent genes related to stem cell self-renewal and inhibit the expression of genes related to differentiation,so as to promote the expansion and inhibit differentiation of HSCs.The expansion of cord blood HSCs by small molecular HDACIs in vitro is expected to improve the quantity of cord blood HSCs.The further research will focus on high-throughput screening for the most powerful HDACIs and the highly selective HDACIs,exploring the combination of epigenetic modifiers of different pathways.


Subject(s)
Epigenesis, Genetic , Fetal Blood , Hematopoietic Stem Cells , Histone Deacetylase Inhibitors/pharmacology , Valproic Acid/pharmacology
12.
Chinese Medical Journal ; (24): 1031-1042, 2021.
Article in English | WPRIM | ID: wpr-878118

ABSTRACT

Type 1 diabetes (T1D) is an autoimmune disease that resulted from the severe destruction of the insulin-producing β cells in the pancreases of individuals with a genetic predisposition. Genome-wide studies have identified HLA and other risk genes associated with T1D susceptibility in humans. However, evidence obtained from the incomplete concordance of diabetes incidence among monozygotic twins suggests that environmental factors also play critical roles in T1D pathogenesis. Epigenetics is a rapidly growing field that serves as a bridge to link T1D risk genes and environmental exposures, thereby modulating the expression of critical genes relevant to T1D development beyond the changes of DNA sequences. Indeed, there is compelling evidence that epigenetic changes induced by environmental insults are implicated in T1D pathogenesis. Herein, we sought to summarize the recent progress in terms of epigenetic mechanisms in T1D initiation and progression, and discuss their potential as biomarkers and therapeutic targets in the T1D setting.


Subject(s)
Diabetes Mellitus, Type 1/genetics , Epigenesis, Genetic/genetics , Genetic Predisposition to Disease/genetics , Humans , Incidence , Twins, Monozygotic
13.
Frontiers of Medicine ; (4): 383-403, 2021.
Article in English | WPRIM | ID: wpr-888735

ABSTRACT

Cancer development is a complicated process controlled by the interplay of multiple signaling pathways and restrained by oxygen and nutrient accessibility in the tumor microenvironment. High plasticity in using diverse nutrients to adapt to metabolic stress is one of the hallmarks of cancer cells. To respond to nutrient stress and to meet the requirements for rapid cell proliferation, cancer cells reprogram metabolic pathways to take up more glucose and coordinate the production of energy and intermediates for biosynthesis. Such actions involve gene expression and activity regulation by the moonlighting function of oncoproteins and metabolic enzymes. The signal - moonlighting protein - metabolism axis facilitates the adaptation of tumor cells under varying environment conditions and can be therapeutically targeted for cancer treatment.


Subject(s)
Energy Metabolism , Epigenesis, Genetic , Humans , Metabolic Networks and Pathways , Neoplasms/genetics , Tumor Microenvironment
14.
Article in Chinese | WPRIM | ID: wpr-888404

ABSTRACT

The progress of epigenetic research has led to the discovery and confirmation of age-related markers based on DNA methylation. These DNA methylation indices are called "epigenetic clock/age". The concept of "epigenetic clock/age" and the establishment of its evaluation system are helpful to solve some of the long-standing problems in the field of life and medicine. When facing the current global aging, it is of great significance to refer to the comprehensive health parameters to determine the biological age and life span of an individual, and thus to design a plan to slow down the process of life cycle. This paper has summarized the concept and development of "epigenetic clock/age" in recent years.


Subject(s)
Aging/genetics , Biomarkers , DNA Methylation , Epigenesis, Genetic , Humans
15.
Article in English | WPRIM | ID: wpr-879956

ABSTRACT

Epigenetics concerns gene regulatory mechanisms beyond DNA sequence,such as DNA methylation,histone modification,chromatin remodeling,and non-coding RNA. Epigenetic mechanisms play a key role in development,cell fate decision and tumorigenesis. Chromatin modifications and its high order structure across our genome are major forms of epigenetic information,and its establishment and maintenance are closely related to cell metabolism. Metabolic changes in cancer cells include aerobic glycolysis,increased glucose uptake,abnormally active glutamine metabolism,and the use of non-conventional energy supply. These changes meet the vigorous energy and matter needs for the development and spread of cancer,and help tumor cells adapt to hypoxia microenvironment for their survival,proliferation,invasion and migration. There is a complex relationship between epigenetic modifications and cell metabolism in tumor. On the one hand,metabolites in tumor cells may act as cofactors,modification donors or antagonists of epigenetic enzymes,thus modulating the epigenetic landscape. On the other hand,epigenetic modifications can directly regulate the expression of metabolic enzymes,transporters,signaling pathway and transcription factors to affect cell metabolism. This article reviews the crosstalk between epigenetics and cancer metabolism,to explore their potential future applications in the treatment of tumors.


Subject(s)
Carcinogenesis , DNA Methylation , Epigenesis, Genetic , Gene Expression Regulation , Humans , Neoplasms/genetics , Tumor Microenvironment
16.
Actual. osteol ; 16(1): 47-66, Ene - abr. 2020. ilus
Article in Spanish | LILACS | ID: biblio-1140035

ABSTRACT

La "razón de ser" de nuestros huesos y esqueletos constituye un dilema centralizado en los conceptos biológicos de "estructura" y "organización", cuya solución necesitamos comprender para interpretar, diagnosticar, tratar y monitorear correctamente las osteopatías fragilizantes. Últimamente se ha reunido conocimiento suficiente para proponer aproximaciones razonables a ese objetivo. La que exponemos aquí requiere la aplicación de no menos de 6 criterios congruentes: 1) Un criterio cosmológico, que propone un origen común para todas las cosas; 2) Un criterio biológico, que explica el origen común de todos los huesos; 3) Un enfoque epistemológico, que desafía nuestra capacidad de comprensión del concepto concreto de estructura y del concepto abstracto de organización, focalizada en la noción rectora de direccionalidad espacial; 4) Una visión ecológica, que destaca la importancia del entorno mecánico de cada organismo para la adecuación de la calidad mecánica de sus huesos a las "funciones de sostén" que les adjudicamos; 5) Una correlación entre todo ese conocimiento y el necesario para optimizar nuestra aptitud para resolver los problemas clínicos implicados y 6) Una jerarquización del papel celular en el manejo de las interacciones genético-ambientales necesario para asimilar todo el problema a una simple cuestión de organización direccional de la estructura de cada hueso. Solo aplicando estos 6 criterios estaríamos en condiciones de responder a la incógnita planteada por el título. La conclusión de esta interpretación de la conducta y función de los huesos debería afectar el fundamento de la mayoría de las indicaciones farmacológicas destinadas al tratamiento de la fragilidad ósea. (AU)


The nature of the general behavior of our bones as weight-bearing structures is a matter of two biological concepts, namely, structure and organization, which are relevant to properly interpret, diagnose, treat, and monitor all boneweakening diseases. Different approaches can be proposed to trace the corresponding relationships. The one we present here involves six congruent criteria, namely, 1) a cosmological proposal of a common origin for everything; 2) a biological acknowledgement of a common origin for all bones; 3) the epistemological questioning of our understanding of the concrete concept of structure and the abstract notion of organization, focused on the lead idea of directionality; 4) the ecological insight that emphasizes the relevance of the mechanical environment of every organism to the naturally-selected adjustment of the mechanical properties of their mobile bones to act as struts or levers; 5) The clinical aspects of all the alluded associations; 6) The central role of bone cells to control the genetics/ environment interactions of any individual as needed to optimize the directionality of the structure of each of his/her bones to keep their mechanical ability within physiological limits. From our point of view, we could only solve the riddle posed by the title by addressing all of these six criteria. The striking conclusion of our analysis suggests that the structure (not the mass) of every bone would be controlled not only to take care of its mechanical ability, but also to cope with other properties which show a higher priority concerning natural selection. The matter would be that this interpretation of bone behavior and 'function' should affect the rationales for most pharmacological indications currently made to take care of bone fragility. (AU)


Subject(s)
Humans , Bone and Bones/physiology , Bone Diseases, Metabolic/diagnosis , Osteogenesis Imperfecta/diagnosis , Osteogenesis Imperfecta/therapy , Osteoporosis/diagnosis , Osteoporosis/therapy , Bone and Bones/anatomy & histology , Bone and Bones/cytology , Bone and Bones/ultrastructure , Bone Diseases, Metabolic/therapy , Epigenesis, Genetic
17.
Protein & Cell ; (12): 792-808, 2020.
Article in English | WPRIM | ID: wpr-880882

ABSTRACT

Over 17 and 160 types of chemical modifications have been identified in DNA and RNA, respectively. The interest in understanding the various biological functions of DNA and RNA modifications has lead to the cutting-edged fields of epigenomics and epitranscriptomics. Developing chemical and biological tools to detect specific modifications in the genome or transcriptome has greatly facilitated their study. Here, we review the recent technological advances in this rapidly evolving field. We focus on high-throughput detection methods and biological findings for these modifications, and discuss questions to be addressed as well. We also summarize third-generation sequencing methods, which enable long-read and single-molecule sequencing of DNA and RNA modification.


Subject(s)
Animals , DNA/metabolism , DNA Methylation , Epigenesis, Genetic , Epigenomics , Humans , RNA/metabolism , Transcriptome
18.
Article in Chinese | WPRIM | ID: wpr-828538

ABSTRACT

Iron homeostasis plays an important role for the maintenance of human health. It is known that iron metabolism is tightly regulated by several key genes, including divalent metal transport-1(), transferrin receptor 1(), transferrin receptor 2(), ferroportin(), hepcidin(), hemojuvelin() and . Recently, it is reported that DNA methylation, histone acetylation, and microRNA (miRNA) epigenetically regulated iron homeostasis. Among these epigenetic regulators, DNA hypermethylation of the promoter region of , and bone morphogenetic protein 6 () genes result in inhibitory effect on the expression of these iron-related gene. In addition, histone deacetylase (HADC) suppresses gene expression. On the contrary, HADC inhibitor upregulates gene expression. Additional reports showed that miRNA can also modulate iron absorption, transport, storage and utilization via downregulation of and other genes. It is noteworthy that some key epigenetic regulatory enzymes, such as DNA demethylase TET2 and histone lysine demethylase JmjC KDMs, require iron for the enzymatic activities. In this review, we summarize the recent progress of DNA methylation, histone acetylation and miRNA in regulating iron metabolism and also discuss the future research directions.


Subject(s)
Epigenesis, Genetic , Gene Expression Regulation , Genetics , Homeostasis , Humans , Iron , Metabolism , Receptors, Transferrin
19.
Article in Chinese | WPRIM | ID: wpr-827181

ABSTRACT

OBJECTIVE@#To analyze the genome-wide DNA methylation differences in umbilical cord blood nucleated red blood cells (NRBCs) between term and preterm infants by using the methylation gene chip technology, and to screen the genes of differential methylation and biological signaling pathways which may be related to the expression of γ-globin gene (HBG).@*METHODS@#Umbilical cord bloods of eight term infants and eight preterm infants were collected, and NRBCs of each sample was isolated, then genome DNA was extracted and bisulfite conversion was performed. The DNA methylation sites were detected by using the Illumina 850K BeadChip. Differential DNA methylation sites were screened, and the function of genes with differential methylation was analyzed by using GO and KEGG enrichment analysis.@*RESULTS@#Compared with the preterm group, 4749 differential DNA methylation sites of term group were screened out, including 4359 hypomethylation sites and 390 hypermethylation sites. GO and KEGG analysis indicated that the function of genes with differential methylation mainly involved in the hemopoietic system, growth and development process, Wnt and Notch signal pathways.@*CONCLUSION@#The differentical methylation sites at genome-wide level in umbilicar cord blood NRBC of term and preterm infants have been obtained, and the signal pathway and genes which possibily related with swiching the expression of γ-globin gene to β-globin gene have been screened-out. This study provide the new targets for studing the mechamism regulating expression of HBG gene.


Subject(s)
DNA , DNA Methylation , Epigenesis, Genetic , Fetal Blood , Genome, Human , Humans , Infant, Newborn , Infant, Premature
20.
Acta Physiologica Sinica ; (6): 506-512, 2020.
Article in Chinese | WPRIM | ID: wpr-827036

ABSTRACT

Alzheimer's disease (AD) is currently the most prevalent neurodegenerative disease in the aging population. It is characterized by massive deposition of extracellular β-amyloid peptide and formation of intracellular neurofibrillary tangles. Cancer is also an age-related disease. Some epidemiological studies have shown an inverse relationship between AD and the onset of various types of cancers, that is, the risk of cancer in patients with AD is reduced, and vice versa. Epigenetic mechanisms play important roles in the development of AD and cancer. In this article, we will review the recent research advances on the epigenetic mechanisms of AD and cancer onset, and provide new ideas for rethinking the relevance of AD and cancer with a "holistic concept".


Subject(s)
Aged , Alzheimer Disease , Epigenesis, Genetic , Humans , Neoplasms , Neurodegenerative Diseases , Neurofibrillary Tangles
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