title: A critical evaluation of neuroprotective and neurodegenerative MicroRNAs in Alzheimer's disease.
abstract: Currently, 5.4 million Americans suffer from AD, and these numbers are expected to increase up to 16 million by 2050. Despite tremendous research efforts, we still do not have drugs or agents that can delay, or prevent AD and its progression, and we still do not have early detectable biomarkers for AD. Multiple cellular changes have been implicated in AD, including synaptic damage, mitochondrial damage, production and accumulation of Aβ and phosphorylated tau, inflammatory response, deficits in neurotransmitters, deregulation of the cell cycle, and hormonal imbalance. Research into AD has revealed that miRNAs are involved in each of these cellular changes and interfere with gene regulation and translation. Recent discoveries in molecular biology have also revealed that microRNAs play a major role in post-translational regulation of gene expression. The purpose of this article is to review research that has assessed neuroprotective and neurodegenerative characteristics of microRNAs in brain samples from AD transgenic mouse models and patients with AD.
authors.affiliation: Garrison Institute on Aging Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Cell Biology & Biochemistry Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Neuroscience & Pharmacology Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Neurology Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Speech, Language and Hearing Sciences Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Garrison Institute on Aging, South West Campus, Texas Tech University Health Sciences Center, 6630 S. Quaker Suite E, MS 7495, Lubbock, TX 79413, United States. Electronic address: hemachandra.reddy@ttuhsc.edu.
authors.forename: P Hemachandra
authors.initials: PH
authors.lastname: Reddy
authors.affiliation: Garrison Institute on Aging Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States.
authors.forename: Sahil
authors.initials: S
authors.lastname: Tonk
authors.affiliation: Garrison Institute on Aging Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States.
authors.forename: Subodh
authors.initials: S
authors.lastname: Kumar
authors.affiliation: Garrison Institute on Aging Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States.
authors.forename: Murali
authors.initials: M
authors.lastname: Vijayan
authors.affiliation: Garrison Institute on Aging Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States.
authors.forename: Ramesh
authors.initials: R
authors.lastname: Kandimalla
authors.affiliation: Garrison Institute on Aging Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States.
authors.forename: Chandra Sekhar
authors.initials: CS
authors.lastname: Kuruva
authors.affiliation: Department of Internal Medicine, Texas Tech University Health Sciences Center, 3601 Fourth Street, MS 9424, Lubbock, TX 79430, United States. Electronic address: Arubala.reddy@ttuhsc.edu.
authors.forename: Arubala P
authors.initials: AP
authors.lastname: Reddy
mesh_terms: D000375:Aging / Q000235:genetics; D000818:Animals; D015415:Biomarkers / Q000097:blood; D016922:Cellular Senescence / Q000235:genetics; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D035683:MicroRNAs / Q000235:genetics*; D019636:Neurodegenerative Diseases / Q000235:genetics*; D000066829:Neuroprotection / Q000235:genetics*
chemical_list: D015415:Biomarkers; D035683:MicroRNAs
keywords: Alzheimer's disease; Mitochondrial dysfunction; Phosphorylated tau; Synaptic damage; microRNAs