scholarly journals Targeting the Molecular & Cellular Pillars of Human Aging with Exercise

FEBS Journal ◽  
2021 ◽  
Author(s):  
Jorming Goh ◽  
Esther Wong ◽  
Janjira Soh ◽  
Andrea Maier ◽  
Brian Kennedy
Keyword(s):  
Human Aging

scholarly journals Normal human aging and early-stage schizophrenia share common molecular profiles

Aging Cell ◽  
2009 ◽  
Vol 8 (3) ◽  
pp. 339-342 ◽  
Author(s):  
Bin Tang ◽  
Wei-li Chang ◽  
Caroline M. Lanigan ◽  
Brian Dean ◽  
J. Gregor Sutcliffe ◽  
...  
Keyword(s):  
Early Stage ◽  
Human Aging ◽  
Normal Human ◽  
Molecular Profiles

scholarly journals Recruitment of inflammatory monocytes by senescent fibroblasts inhibits antigen-specific tissue immunity during human aging

Nature Aging ◽  
2021 ◽  
Vol 1 (1) ◽  
pp. 101-113
Author(s):  
Emma S. Chambers ◽  
Milica Vukmanovic-Stejic ◽  
Barbara B. Shih ◽  
Hugh Trahair ◽  
Priya Subramanian ◽  
...  
Keyword(s):  
Human Aging ◽  
Inflammatory Monocytes ◽  
Specific Tissue

scholarly journals Interactions Between Genes From Aging Pathways Significantly Influence Risk of Alzheimer’s Disease

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 142-143
Author(s):  
Svetlana Ukraintseva ◽  
Konstantin Arbeev ◽  
Hongzhe Duan ◽  
Igor Akushevich ◽  
Mary Feitosa ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Older Adults ◽  
Risk Factor ◽  
Human Aging ◽  
Cell Responses ◽  
Cell Cycle Reentry ◽  
Universal Feature ◽  
Igf I ◽  
Ad Prevention ◽  
Stress Damage

Abstract Age is major risk factor for AD; however, relationships between aging and AD are not well understood. Decline in physiological resilience is universal feature of human aging that may also play role in AD. Aging-related pathways (such as IGF-I/P53/mTOR-mediated) that are involved in tissue resilience work in concert to decide outcomes of cell responses to stress/damage, such as survival, apoptosis, autophagy, etc. We hypothesized that interplay among genes in these pathways may influence AD risk as result of epistasis (GxG). We estimated effects of pairwise epistasis between SNPs in 53 genes from respective pathways on AD risk in the LLFS compared with other data (HRS, CHS, LOADFS). We found significant (fdr<0.05) GxG effects on AD risk in older adults across datasets. The SNP rs11765954 in CDK6 gene was involved in top GxG effects on AD in all datasets, when paired with SNPs in BCL2 and PPARGC1A. The CDK6 role in AD could be pleiotropic, depending on its activity in neurons: CDK6 expression is needed for DNA repair and neuronal survival; however, CDK6 overexpression may lead to the cell cycle reentry in postmitotic neurons resulting in apoptosis, which may contribute to neurodegeneration. CDK6 was earlier found to interfere with BCL2 effects on apoptosis, and with PPARGC1A effects on energy metabolism, which might contribute to observed GxG between these genes. We conclude that interactions among genes from biologically connected aging pathways may significantly influence AD risk. Uncovering such GxG effects has a potential to yield new genetic targets for AD prevention/treatment.

Perspectives on Aging Human Aging: Biological Perspectives Augustine G. DiGiovanna

BioScience ◽  
1994 ◽  
Vol 44 (9) ◽  
pp. 639-640
Author(s):  
Avril D. Woodhead
Keyword(s):  
Human Aging

scholarly journals Genome and Epigenome Editing in Mechanistic Studies of Human Aging and Aging-Related Disease

Gerontology ◽  
2016 ◽  
Vol 63 (2) ◽  
pp. 103-117 ◽  
Author(s):  
Cia-Hin Lau ◽  
Yousin Suh
Keyword(s):  
Animal Models ◽  
Genetic Manipulation ◽  
Logic Gate ◽  
Therapeutic Interventions ◽  
Human Aging ◽  
Aging Research ◽  
Epigenome Editing ◽  
Related Disease ◽  
Age Related

The recent advent of genome and epigenome editing technologies has provided a new paradigm in which the landscape of the human genome and epigenome can be precisely manipulated in their native context. Genome and epigenome editing technologies can be applied to many aspects of aging research and offer the potential to develop novel therapeutics against age-related diseases. Here, we discuss the latest technological advances in the CRISPR-based genome and epigenome editing toolbox, and provide insight into how these synthetic biology tools could facilitate aging research by establishing in vitro cell and in vivo animal models to dissect genetic and epigenetic mechanisms underlying aging and age-related diseases. We discuss recent developments in the field with the aims to precisely modulate gene expression and dynamic epigenetic landscapes in a spatial and temporal manner in cellular and animal models, by complementing the CRISPR-based editing capability with conditional genetic manipulation tools including chemically inducible expression systems, optogenetics, logic gate genetic circuits, tissue-specific promoters, and the serotype-specific adeno-associated virus. We also discuss how the combined use of genome and epigenome editing tools permits investigators to uncover novel molecular pathways involved in the pathophysiology and etiology conferred by risk variants associated with aging and aging-related disease. A better understanding of the genetic and epigenetic regulatory mechanisms underlying human aging and age-related disease will significantly contribute to the developments of new therapeutic interventions for extending health span and life span, ultimately improving the quality of life in the elderly populations.

Sign in / Sign up

Export Citation Format

Share Document