Gerontology
Gerontology
Introduction to
• Third level
• Fourth level
• Fifth level
gerontology
Dr. Safaa Hussein Ali
Associate professor of geriatric medicine
Ain Shams university
Cairo – Egypt
2018
ILOS
1. Biology of Aging and Longevity
WHAT IS AGING?
Aging as a Coordinated, Malleable Process
Key Themes from Studies of Invertebrate Models
Delayed Aging in Mice and Rats
AGING, CELLULAR SENESCENCE, TELOMERES,
AND CANCER
AGING RESEARCH AND PREVENTIVE MEDICINE
ANTIAGING RESEARCH: SOCIAL OBSTACLES AND
ETHICAL CONCERNS
2. Demography and
Epidemiology
Aging of the Population in the United States
Aging of the Population and Life Expectancy Around the World
Life Expectancy at Different Ages
Demographic Characteristics of the Aging Population
Employment
MORTALITY
Leading Causes of Death
DISEASE STATUS
Prevalence of Common Diseases
Health Care Utilization
DISABILITY
BEHAVIORAL RISK FACTORS
3. International Gerontology
IMPLICATIONS OF GLOBAL POPULATION AGING
FOR HEALTH AND HEALTH CARE
INTERNATIONAL COMPARISONS
Overall Organization and Services Available for Older
Adults (see Chapter 15)
Type of Health Care System
Overall Organization and Services Available for Elderly
Persons
Peculiarities
Difficulties/Solutions for a Typical Geriatric Patient
8
Characteristics of senescence are
as follows:
The universal process
The changes comes from
organism itself
The process occurred slowly
The process contribute to deficit
9
According to biological approaches,
biological aging can be divided into 3
types
Primary aging
Is the basic, shared, inevitable set of gains or
declines governed by some kind of
maturational process
Secondary aging
Is the product of environmental influences,
health habits, or disease and is neither
inevitable nor shared by all adults
Tertiary aging
Refers to quickly deficit in the last few years
prior to death
10
Life Expectancy at birth
Human Survivorship
through History
Theories of Aging
BIOLOGICAL THEORIES ON AGING
PROGRAMMED AGING RANDOM EVENTS
• Genetic life-span • Wear and tear theory
theory • Rate of living theory
• Genetic • Waste product
predisposition accumulation theory
theory • Cross-linking theory
• Telomere theory • Free radical theory
• Specific system • Autoimmune theory
theories
(Neuroendocrine • Error theories
theory) • Order to disorder 18
THE BIG QUESTION
DEVELOPMENTAL—
GENETIC THEORIES
ENVIRONMENTAL—
NON- GENETIC THEORIES
Genetic makeup Due to random events that
determines factors occur over time
directly affecting aging Aging caused by
Programmed & environmental damage
directed in the body Controlled extrinsically
Aging is
Predetermined
20
Programmed Ageing
Aging and death are genetically determined and
are ‘programmed’ in organisms
22
Telomere theory
Telomere is the tail of
23
Telomere theory
Telomere theory is based on
24
As the length of a telomere
decreases, changes may
occur in patterns of gene
expression that could affect
both the functioning of the
cell and the organ system in
which it operates.
25
Mutation accumulation theory
Peter Medawar
Nobel Laureate for the
discovery of immune
tolerance
Age
• Recurrent, deleterious, GERM LINE mutations occur
• Fewer bearers survive to express later-acting
mutations
• The force of natural selection against them declines
with age
• These mutations can therefore reach a higher
frequency under mutation-selection balance
Number alive
Age
George Williams
American
evolutionary
biologist
33
34
Cellular theories
Hayflict
Cells grown in laboratory culture
dishes only undergo a fixed
number of divisions at most before
dying, with the number of possible
divisions dropping depending on
the age of the donor organism
35
Cellular Theories
The Hayflick Limit (1961)
Pre-1961: “All metazoan cells are potentially
immortal. Ageing not cell autonomous”
Leonard Hayflick
Fibroblasts: connective tissue cells, e.g. from skin
37
‘Superoxide theory of ageing?’
Radicals Non-radicals
---------------------------------------------------------------------------
Superoxide, O2.- Hydrogen peroxide, H2O2
Hydroxyl, OH. Hypochlorous acid, HOCl
Peroxyl, RO2. Ozone, O3
Alkoxyl, RO. Peroxynitrite, ONOO-
Hydroperoxyl, HO2.
---------------------------------------------------------------------------
Reactive oxygen species (ROS)
Reactive nitrogen species (RNS)
Cynthia Kenyon
WHY SO MANY THEORIES?
“Number of hypotheses is
generally inversely
proportional to the clarity
of the problem.”
--Frolkis
Biology of Aging
Aging at the Cellular and Molecular Level
Interventions in the
Aging Process
Cell-based therapies
• Hormonal therapies
• Genetic manipulations
• Dietary therapies
• Other: hypothermia, exercise
Models of Accelerated Aging
• There are a small number of rare, inherited, diseases, of which Werner’s
syndrome and Hutchinson-Gilford syndrome are the most celebrated, that
have been mooted as possible examples of “accelerated” aging.
• Some of the physical features and symptoms of these diseases do
resemble, at least superficially, some of the changes that typically affect
older people, including in particular changes in skin and connective tissues.
• Hutchinson-Gilford syndrome, sometimes called “progeria,” is now known to
be caused by mutations in the gene for LaminA,a component of the nuclear
membrane.
• Werner’s syndrome patients usually have mutations in an enzyme (“WRN”)
that has activity as a DNA helicase (unwindingcoiledDNA) and as an
endonuclease.
• Patients with Hutchinson-Gilford syndrome typically survive to their early
teens, and Werner’s syndrome patients frequently survive to their mid-
forties, about 10 years after the age of typical diagnosis.
• Werner’s patients resemble elderly people in some ways: they frequently
suffer from cataracts and premature graying of the hair,and by their early
thirties often develop osteoporosis, diabetes,and atherosclerosis.
• On the othe Werner’s syndrome patients, for example, do not show signs of
Alzheimer’s disease or other amyloidoses, hypertension, or immune failure.
• Mesenchymal tumors, which are rare in normal people, are about100-fold
more frequent in Werner’s patients,but the epithelial and hematopoietic
tumors characteristic of normal aging are not seen in Werner’s syndrome
patients.
• it seems at least equally plausible that the WRN mutation, perhaps through
alteration of cells responsible for connective tissue maintenance, induces
multi-organ failure through processes quite distinct from the changes that
impair some of the same organs in normal aging.
Demography and Epidemiology
• 1 in 5 Individuals will
suffer from some
kind of disability