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7th International Conference on Aging & Gerontology , will be organized around the theme “Theme - “Advancing in Aging Care Management and Exploring Therapeutic Opportunities.””

AGING CONFERENCE 2024 is comprised of keynote and speakers sessions on latest cutting edge research designed to offer comprehensive global discussions that address current issues in AGING CONFERENCE 2024

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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 Aging includes 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 1-2Follicular stem cell aging
  • Track 1-3DNA oxidation
  • Track 1-4DNA scaffolding
  • Track 1-5Decline translation
  • Track 1-6Decline in transcription
  • Track 1-7Loss of ribosomal RNA
  • Track 1-8Mutation in mitochondrial DNA
  • Track 1-9Degeneration of chloroplast
  • Track 1-10Decrease in granular endoplasmic reticulum
  • Track 1-11Change in fluidity and permeability of plasma membrane
  • Track 1-12Decline in energy production
  • Track 1-13Stiffening in collagen
  • Track 1-14Follicular stem cell 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

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 3-2Genomic instability
  • Track 3-3Genomic instability
  • Track 3-4Tissue regeneration
  • Track 3-5Oncogene induced senescence
  • Track 3-6Epithelial stem cell aging
  • Track 3-7Pluripotent stem cell aging
  • Track 3-8Embryonic stem cell aging
  • Track 3-9Hematopoietic stem cell aging
  • Track 3-10Aging and holistic medicine

Cells constantly encounter stress and damage from exogenous and endogenous sources, and their reactions range from complete recovery to cell death. Multiplying cells can start an extra reaction by embracing a condition of permanent cell-cycle capture that is named cell senescence. Understanding the causes and outcomes of cell senescence has given novel experiences into how cells respond to pressure, particularly genotoxic stress, and how this cell reaction can influence complex organismal procedures, for example, the advancement of cancer and ageing. Cell senescence may likewise advance tissue repair and fuel irritation related with aging and cancer progression. In this manner, cell senescence may take an interest in four complex natural procedures (tumour suppression, tumour promotion, aging, and tissue repair), some of which have clearly contradicting impacts. The test now is to comprehend the senescence reaction all around harness its advantages while stifling its disadvantages

  • Track 4-1Replicative senescence
  • Track 4-2DNA damage induced senescence
  • Track 4-3Change in fluidity and permeability of plasma membrane
  • Track 4-4Change in fluidity and permeability of plasma membrane
  • Track 4-5Decrease in granular endoplasmic reticulum
  • Track 4-6Degeneration of chloroplast
  • Track 4-7Mutation in mitochondrial DNA

Regeneration is a vital biological process that permits protecting tissue function in multi-cell living beings. Tissue-specific stem cells are vital to this procedure, as they keep up the capacity to divide and self-regenerate all through adulthood, bringing forth a group of specific daughter cell appear that can supplant damaged cells. The regenerative limit of stem cells and their daughter cells seems to diminish during aging, possibly causing the age-related functional decrease of numerous tissues. Moreover, damaged direction of regenerative procedures may represent the age-related increment in the occurrence of cancer. The centrality of regenerative decline for aging and age-related disorders, and the molecular systems causing this decrease, stay to be understood. The objective of regenerative medication is to re-establish the functionality of tissues, organs, or body parts damaged by injury, disease or aging.

  • Track 5-1Reparative regeneration
  • Track 5-2Pulmonary fibrosis
  • Track 5-3Dyskeratosis congentia
  • Track 5-4Tumour suppression
  • Track 5-5Mutation in telomerase gene
  • Track 5-6Loss of stem cell
  • Track 5-7Telomerase activity
  • Track 5-8Cell regeneration
  • Track 5-9Neuro regeneration
  • Track 5-10Aplastic anaemia

Cells of a multicellular living being are hereditarily homogeneous however fundamentally and practically heterogeneous attributable to the differential expression of genes. A considerable lot of these distinctions in gene expression emerge amid improvement and are consequently held through mitosis. Stable modifications of this kind are said to be 'epigenetic', in light of the fact that they are heritable temporarily however don't include transformations of the DNA itself. Research in the course of recent years has concentrated on two sub-atomic components that intervene epigenetic phenomena: DNA methylation and histone adjustments. Epigenetic impacts by methods for DNA methylation has a critical part being developed however can likewise emerge stochastically as creature’s age. Recognizable proof of proteins that intervene these impacts has given knowledge into this unpredictable procedure and maladies that happen when it is annoyed. Outer impacts on epigenetic forms are found in the impacts of eating regimen on long haul illnesses, for example, growth. Along these lines, epigenetic instruments appear to enable a living being to react to the earth through changes in gene expression.  The degree to which ecological impacts can incite epigenetic reactions speaks to an energizing zone of future research.

  • Track 6-1Genetic changes in genome
  • Track 6-2Deficiency in repair of DNA damage
  • Track 6-3Genomic instability
  • Track 6-4DNA methylation
  • Track 6-5Histone modification
  • Track 6-6Non coding DNA species
  • Track 6-7Gene transcription and silencing

Genome instability has for quite some time been involved as the principle causal factor in aging. Somatic cells are persistently presented to different wellsprings of DNA damage, from receptive oxygen species to UV radiation to natural mutagens. To adapt to the a huge number of compound sores brought into the genome of a normal cell every day, a complex  network system of genome support frameworks acts to remove damage and restore the correct base pair sequence. Every so often, nonetheless, repair is mistaken, and such blunders, and also the periodic inability to effectively recreate the genome amid cell division, are the reason for changes and epimutations. What isn't known, in any case, is whether the recurrence of these irregular changes is adequate to cause the phenotypic impacts for the most part connected with maturing. The exemption is growth, an age-related sickness caused by the gathering of transformations and epimutations. Here, we first audit current ideas with respect to the connection between DNA damage, repair, and change, and also the information seeing genome adjustments as a component of age. We at that point portray a model for how arbitrarily initiated DNA succession and epigenomic variations in the substantial genomes of creatures can bring about utilitarian decrease. At last, we examine the genetic qualities of genome instability in connection to life span to address the significance of changes in the substantial genome as a causal factor in maturing and to underscore the open doors gave by genetic ways to deal with create intercessions that lessen genome  instability, , decrease infection hazard, and increment life traverse.

  • Track 7-1DNA damage
  • Track 7-2Environmental mutagens
  • Track 7-3Role of epigenomic variants in somatic genome
  • Track 7-4Functional consequences of DNA mutation
  • Track 7-5Histone disruption
  • Track 7-6DNA misfolding
Latest research has demonstrated that Aging impacts profoundly our brain which leads to many cognitive disorders like Dementia, Alzheimer’s, depression, anxiety disorders, and psychosis are more typical . Clinical articulation of psychiatric disorders in old aged might be unique in relation to that observed in younger age group, with less and regularly milder side effects. Simultaneously, co-morbidity between various psychiatric disorders is immense, and in addition co-morbidity with cognitive disorder, psychiatric disorders in the elderly are regularly identified with cerebral neurodegeneration and cerebrovascular disease, despite the fact that psychosocial risk factors are additionally essential.
  • Track 8-1Aging and Dementia
  • Track 8-2Failure of adaptive stress response
  • Track 8-3Proteostasis regulation in aging
  • Track 8-4Misfolding of protein
  • Track 8-5Oxidative modification
  • Track 8-6Sources of protein damage
  • Track 8-7Aging and Stress
  • Track 8-8Aging and Alzheimers Disease
  • Track 8-9Aging and Delirium
  • Track 8-10Aging and Anxiety
  • Track 8-11Aging and Depression
  • Track 8-12Aging and Cognitive Impairment
  • Track 8-13Disruption of proteostasis by chorionic misfolding
Individual differences in the rate of aging are dictated by the ability with which a life form changes assets into metabolic energy consequently keeping up the homeostatic state of its cells and tissues. This observation has been incorporated with logical investigations of the metabolic procedure to infer the accompanying rule: The metabolic strength of administrative systems, that is the capacity of cells to keep up stable centralizations of Reactive Oxygen Species (ROS) and other basic metabolites is the prime determinant of life expectancy. The metabolic steadiness of an administrative system is dictated by the decent variety of the metabolic pathways or the level of availability of qualities in the system. These properties can be exactly assessed as far as transcriptional changes in quality gene expression. We utilize microarrays to explore the age-reliance of transcriptional changes of qualities in the insulin signalling, oxidative phosphorylation and glutathione metabolism pathways in mice. Our examinations portray age and tissue particular examples of transcriptional changes which are steady with the metabolic stability–longevity principle. This examination, what's more, rejects the free radical theory which proposes that the generation rate of ROS, and not its stability, determines life span.
  • Track 9-1Brain aging-endothelial cortex, superior frontal gyros
  • Track 9-2Meta-analysis study in aging
  • Track 9-3Transcriptional signature of aging
  • Track 9-4Dynamic RNA modifications in aging
  • Track 9-5Reactive Oxygen Species (ROS)

The gene expression profile of the maturing procedure was dissected in skeletal muscle of mice. Utilization of high-thickness oligonucleotide clusters speaking to 6347 qualities revealed that Aging brought about a differential gene expression design demonstrative of a marked pressure reaction and lower expression of metabolic and biosynthetic genes. Most adjustments were either totally or incompletely anticipated by caloric confinement, the main intercession known to hinder maturing in well evolved creatures. Transcriptional patterns of calorie-restricted creatures propose that caloric restriction decreases the aging procedure by causing a metabolic move toward expanded protein turnover and diminished macromolecular harm. Aging brought about a gene-expression profile characteristic of a provocative reaction, oxidative stress and decreased neurotropic bolster in both mind areas. At the transcriptional level, brain ageing in mice shows parallels with human neurodegenerative issue. Caloric confinement, which hinders the maturing procedure in well evolved creatures, specifically constricted the age-related enlistment of qualities encoding inflammatory and stress reactions.

  • Track 10-1Gene expression in human brain
  • Track 10-2Gene expression in endothelial cortex
  • Track 10-3Gene expression superior frontal gyros
  • Track 10-4Gene expression in skeletal muscles
  • Track 10-5Abundant DNA synthesis
  • Track 10-6Inhibitory messenger RNase
Social Gerontology is a sub-field of gerontology that spotlights on the social aspect of growing old. Experts in this field endeavour to enhance the connections between older adults and others, including relatives, companions, and medicinal services experts. They additionally attempt to help older adults to live more free and dynamic ways of life.
  • Track 11-1Aging and elderly care
  • Track 11-2Mitochondrial epigenome
  • Track 11-3Lipid adduct information
  • Track 11-4Lipid peroxidation
  • Track 11-5Mi-DNA dysfunction
  • Track 11-6Mi-DNA damage
  • Track 11-7Oxidative stress
  • Track 11-8Aging populations
  • Track 11-9Aging Sociology
  • Track 11-10Aging health care

Aging increases voluntarily with aged-associated diseases in all organisms. Basically, aging related diseases are complications emerging from senescence. Age-related disorders are to be recognized from the maturing procedure itself since every single grown-up creature age, exception in some uncommon special cases, however not every adult organism encounter all age-related diseases. Aging related diseases don't allude to age-specific diseases, for example, “chicken pox and measles. "Aging-associated disease" is utilized here to signify "disorders of the elderly". Nor should aging related diseases be mistaken for quickened aging diseases, which are all hereditary issue. Cases of maturing related infections are atherosclerosis and cardiovascular diseases, malignancy, joint inflammation, cancer, osteoporosis, type 2 diabetes, hypertension and Alzheimer's disease. The occurrence of these diseases increments quickly with aging (increments exponentially with age, on account of tumour).

  • Track 12-1Aging and movement disorders
  • Track 12-2Hearing impairment
  • Track 12-3Alzheimer and dementia
  • Track 12-4Vision disorder
  • Track 12-5Sleep disorder
  • Track 12-6Communicational disorder
  • Track 12-7Bariatric disorder

A Case Study includes a very close, top to bottom, and details examination of a subject (the case), and additionally its related relevant conditions. Contextual analyses show up with awesome recurrence all through famous works, with almost anyone ready to claim to have completed one. Contextual analyses additionally can be delivered by following a formal research strategy. These contextual investigations are probably going to show up in formal research scenes, for example, aging research conference and modern therapeutics, as opposed to well-known works. Aging population in UAE, Geriatric Psychiatry, Aging health care and other contextual analyses related to the aging mechanism are discussed.

  • Track 13-1Idiographic case studies
  • Track 13-2Inductive aging
  • Track 13-3Aging population
  • Track 13-4Demographic aging
  • Track 13-5Aging and puberty
  • Track 13-6Aging and public health
Clinical trials are a standout amongst the most advanced sciences in the aging research. A clinical trial is a particular sort of research frame work performed in people that is away to assess a helpful, surgical, or behavioural intercession. Most clinical trials test another treatment, like another pharmaceutical or eating standard or therapeutic contraption (for example, a pacemaker) as a method for treating a prosperity issue. Other clinical trials test ways to deal with find a sickness early, from time to time before there are even signs. A clinical trial may in like manner look at how to enhance life for people living with a presence undermining ailment or a perpetual prosperity issue. Clinical trials as a less than dependable rule focus with respect to parental figures or care groups.
  • Track 14-1Anti-aging medicine
  • Track 14-2Aging experimental research
  • Track 14-3Aging and new technologies
  • Track 14-4Anti-aging diet
  • Track 14-5Anti-aging anti-oxidants
  • Track 14-6Anti-aging supplements
  • Track 14-7Anti-aging technologies
  • Track 14-8Anti-aging therapies
  • Track 14-9Anti-aging exercise
  • Track 14-10Anti-aging telomerase
  • Track 14-11Aging and cosmetics
Increasing interest for “aesthetic” or cosmetic surgery (in the course of past 20 years) has been reflected in the changing dispositions to youth and beauty. As per the American Society of Plastic Surgeons, more than 8.7 million individuals experienced cosmetic surgery in 2003, an increment of 33% from the prior year, and a massive increment of 1698% since 1992 (ASPS 2004). In Australia, proper statistics for cosmetic/aesthetic systems are not available as there is no concentrated statistical specialist or statutory data collection necessities. In any case, in light of appraisals of 350 specialists, the New South Wales (NSW) Cosmetic Surgery Inquiry into Cosmetic Surgery (HCCC 1999) built up that the nearby business had multiplied over the 5 years going before 1998 with around 52 000 surgical products and 250 000 corrective medicinal systems performed in 1998 alone. This rate of development is respected practically identical per capita with that of the US, with cosmetic surgery now a standout amongst the most prevalent techniques available in Australia to accomplish and keep up a socially adequate appearance.
  • Track 15-1Plastic surgery in aging
  • Track 15-2Bariatric surgery in aging
  • Track 15-3Aging and liposuction
  • Track 15-4Aging and face lift treatment
  • Track 15-5Aging and Face lift Treatment
  • Track 15-6Blepharoplasty and aging

Medical science remains in a verge of finding the remedial measures to back off the senescence. ‘’Klotho’’ is an aging suppressor gene and increase life traverse when overexpressed in mice. Klotho protein was recently demonstrated to work as a hormone that restrains insulin/insulin-like growth factor-1 (IGF-1) signalling. Klotho-induced inhibition of insulin/IGF-1 signalling is related with increased protection from oxidative pressure, which conceivably adds to the counter anti-aging properties of klotho.Traditional and Regenerative medication is primarily focuses on the longevity of life by developing the anti-aging medicine. Standard medication incorporates therapeutic parts of regular data that made over periods inside various social requests previously the season of cutting edge prescription.

  • Track 16-1Aging and tissue engineering
  • Track 16-2Aging and herbal medicine
  • Track 16-3Stem cell treatment
  • Track 16-4Aging and Alternative Medicine

Various items, including diet, medications and supplements, are elevated to have anti-aging properties. Future anti-aging therapies and some counsel on healthy life style is also included. The main known intervention that may have the capacity to delay human aging is Caloric Restriction (CR). A portion of the most established and still most prominent anti-aging medications are hence in view of the thought that hormonal changes contribute to aging and turning around age-related hormonal changes will be helpful. The most renowned of these medications includes human Growth Hormone (HGH) injections. Development hormone has a long history as a hostile to anti-aging treatment and some evidence recommends HGH has gainful impacts in elderly individuals. To fight ROS(Reactive Oxygen Species), cells have a variety of barriers called  antioxidants, huge numbers of which can be isolated or extricated, purified for the most part in tablets, as anti-aging drugs  . Common antioxidants include vitamins A, C, and E and coenzyme Q10.

  • Track 17-1Anti-retroviral drug
  • Track 17-2Removal of senescence cell
  • Track 17-3Anti-arthrosclerosis drug
  • Track 17-4Role of chaperon in protein dissolving
  • Track 17-5Removal of damaged base pair
  • Track 17-6Restore the correct base pair
Related Conferences: Aging Congress | Gerontology Meetings | Palliative and Health Care Events | Aging Cellular Mechanism Conferences | Aging Care Events | Aging Therapeutic Research Conferences
  • 3rd International Conference On Aging & Gerontology July 18-19, 2018Atlanta, USA
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  • 5th World Congress on Hospice and Palliative Care  July 18-19,2018 Melbourne, Australia
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  • World Cosmetic and Dermatology Congress November 26-28, 2018 Bali, Indonesia
  • 19th World Dermatology Congress May 07-08, 2018 Tokyo, Japan
  • 14thInternational Conference and Exhibition on Cosmetic Dermatology and Hair Care August 13-14, 2018 Madrid, Spain
  • 17th European Dermatology Congress March 1-3, 2018 Paris, France
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  • International Federation on Ageing: 14th Global Conference Toronto, Canada August 8 -10,2018
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  • Ageing in an Unequal World: Shaping Environments for the 21st Century July 4-6, 2018 – Manchester, England
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  • Canadian Association on Gerontology Conference October 18-20 ,2018 – Vancouver, Canada.