3rd Annual Aging Conference: Cellular Mechanisms and Therapeutics

Starts On: 13/08/2018
Ends At: 14/08/2018
Country: United Arab Emirates
City: Dubai
Contact Email: aging@dermatologyconference.org
Contact Phone: +1-650-268-9744
Conference Website
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About Conference

Welcome you to the 3rd Annual Conference on Aging: Cellular Mechanism and Therapeutic Opportunities going to be held on August 13-14, 2018.

Aging Conference 2018 highlight the Theme ” Advancing in Aging Care Management and Exploring Therapeutic Opportunities.”

Hear enhance ideas in exploring new innovations on Therapeutic Opportunities on Aging. Join global Aging communities.

Important Dates:

Abstract Submission Opens January 15, 2018
Registration Opens January 22, 2018
Early Bird Registration March 23, 2018
On Spot Registration August 14, 2018


Track 1:Cellular Mechanism in Aging

Cellular Senescence is the aftereffect of a dynamic decrease in the proliferative limit and life expectancy of cells and the impacts of continuous exposure to exogenous influence that outcome in the the progressive accumulation of cellular and molecular damage. Mechanism of Cellular Agingincludes numerous Cellular, Molecular, Biochemical pathways. Various cellular function declines continuously with age.  Oxidative phosphorylation by mitochondria is decreases, as is synthesis of nucleic acids and structural and enzymatic proteins, cell receptors, and Transcription factors.  Senescent cells have a diminished limit with respect to take-up of nutrient and for repair of chromosomal damage. There are many  morphological modifications in aging cell includes irregular a lobed nuclei, pleomorphic vacuolated mitochondria, diffused endoplasmic reticulum, loss of cytoplasmic content, and distored  Golgi apparatus. Concomitantly, there is a steady accumulation of the pigment lipofuscin, represents a product of lipid peroxidation and evidence of oxidative damage; advanced glycation end products, which result from non-enzymatic glycosylation and are capable of cross-linking adjacent proteins; and the accumulation of abnormally folded proteins.

  • Track 1-1Decline in Protein synthesis
  • Track 1-2Stiffening in Collagen
  • Track 1-3Decline in energy Production
  • Track 1-4Change in fluidity and Permeability of Plasma membrane
  • Track 1-5Decrease in granular Endoplasmic reticulum
  • Track 1-6Degeneration of Chloroplast
  • Track 1-7Mutation in mitochondrial DNA

Track 2:Biological Mechanism in Aging

The mechanisms of biological aging, including the change or genome unsteadiness hypothesis, the free radical or oxidative pressure hypothesis, the mitochondrial hypothesis, the error catastrophe theory, the adjusted protein or protein homeostasis deregulation theory, the dedifferentiation or epigenetic hypothesis and the hyper function  theory. The creator has been associated with the improvement of some of these theories, which are in this manner depicted in more detail. An exchange on the meaning of maturing and general remarks on maturing theory, are incorporated. The most famous theory, of maturing, the free radical or oxidative theory was proposed over 50 years prior however has as of late confronted extreme feedback. To date, no single theory has possessed the capacity to effectively clarify the mechanisms of aging.

  • Track 2-1Accumulation of calcium ion
  • Track 2-2Loss of Ribosomal RNA
  • Track 2-3Decline in Transcription
  • Track 2-4Decline Translation
  • Track 2-5DNA scaffolding
  • Track 2-6DNA oxidation

Track 3:Somatic Stem cell Aging

Adult stem cells exist in most mammalian organs and tissues and are fundamental for ordinary tissue homeostasis and repair. In many tissues, there is an age-related decrease in undeveloped cell usefulness however not an exhaustion of undifferentiated cells. Such practical changes reflect malicious impacts of age on the genome, epigenome, and proteome, some of which emerge cell independently and others of which are forced by an age-related change in the nearby milieu or systemic environment. Outstandingly, a portion of the progressions, especially epigenomic and proteomic, are possibly reversible, and both natural and hereditary mediations can bring about the revival of matured undeveloped cells. Such discoveries have significant ramifications for the stem cell– based treatment of age-related illnesses.

  • Track 3-1Mesenchymal stem cell Aging
  • Track 3-2Hematopoietic Stem Cell Aging
  • Track 3-3Embryonic Stem Cell Aging
  • Track 3-4Follicular Stem Cell Aging
  • Track 3-5Pluripotent Stem Cell Aging
  • Track 3-6Epithelial Stem Cell Aging
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