title: MicroRNAs, Aging, Cellular Senescence, and Alzheimer's Disease.
abstract: Aging is a normal process of living being. It has been reported that multiple cellular changes, including oxidative damage/mitochondrial dysfunction, telomere shortening, inflammation, may accelerate the aging process, leading to cellular senescence. These cellular changes induce age-related human diseases, including Alzheimer's, Parkinson's, multiple sclerosis, amyotrophic lateral sclerosis, cardiovascular, cancer, and skin diseases. Changes in somatic and germ-line DNA and epigenetics are reported to play large roles in accelerating the onset of human diseases. Cellular mechanisms of aging and age-related diseases are not completely understood. However, recent discoveries in molecular biology have revealed that microRNAs (miRNAs) are potential indicators of aging, cellular senescence, and Alzheimer's disease (AD). The purpose of our chapter is to highlight recent advancements in miRNAs and their involvement in cellular changes in aging, cellular senescence, and AD. This chapter also critically evaluates miRNA-based therapeutic drug targets for aging and age-related diseases, particularly Alzheimer's.
authors.affiliation: Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, TX, United States; Texas Tech University Health Sciences Center, Lubbock, TX, United States. Electronic address: hemachandra.reddy@ttuhsc.edu.
authors.forename: P H
authors.initials: PH
authors.lastname: Reddy
authors.affiliation: Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, TX, United States.
authors.forename: J
authors.initials: J
authors.lastname: Williams
authors.affiliation: Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, TX, United States.
authors.forename: F
authors.initials: F
authors.lastname: Smith
authors.affiliation: Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, TX, United States; Department of Biotechnology, Sri Guru Gobind Singh College, Chandigarh, India.
authors.forename: J S
authors.initials: JS
authors.lastname: Bhatti
authors.affiliation: Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, TX, United States.
authors.forename: S
authors.initials: S
authors.lastname: Kumar
authors.affiliation: Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, TX, United States.
authors.forename: M
authors.initials: M
authors.lastname: Vijayan
authors.affiliation: Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, TX, United States.
authors.forename: R
authors.initials: R
authors.lastname: Kandimalla
authors.affiliation: Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, TX, United States.
authors.forename: C S
authors.initials: CS
authors.lastname: Kuruva
authors.affiliation: Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, TX, United States.
authors.forename: R
authors.initials: R
authors.lastname: Wang
authors.affiliation: Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, TX, United States.
authors.forename: M
authors.initials: M
authors.lastname: Manczak
authors.affiliation: Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, TX, United States.
authors.forename: X
authors.initials: X
authors.lastname: Yin
authors.affiliation: Texas Tech University Health Sciences Center, Lubbock, TX, United States.
authors.forename: A P
authors.initials: AP
authors.lastname: Reddy
mesh_terms: D000375:Aging / Q000235:genetics*; D000544:Alzheimer Disease / Q000235:genetics*; D000818:Animals; D016922:Cellular Senescence / Q000235:genetics*; D006801:Humans; D035683:MicroRNAs / Q000378:metabolism*; D009410:Nerve Degeneration / Q000235:genetics / Q000473:pathology; D015398:Signal Transduction / Q000235:genetics
chemical_list: D035683:MicroRNAs
keywords: Alzheimer's disease; MicroRNAs; Mitochondrial dysfunction; Phosphorylated tau; Synaptic damage